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ACC/AHA CLINICAL DATA STANDARDS

2014 ACC/AHA Key Data Elementsand Definitions for CardiovascularEndpoint Events in Clinical TrialsA Report of the American College of Cardiology/American Heart Association Task Force onClinical Data Standards (Writing Committee to Develop Cardiovascular Endpoints Data Standards)

Writing Karen A. Hicks, MD, FACC, Chair*
CommitteeMembers*
James E. Tcheng, MD, FACC, Vice-Chair

Biykem Bozkurt, MD, PHD, FACC, FAHABernard R. Chaitman, MD, FACCDonald E. Cutlip, MD, FACCAndrew Farb, MD, FACC*Gregg C. Fonarow, MD, FACC, FAHAJeffrey P. Jacobs, MD, FACCMichael R. Jaff, DO, FACCJudith H. Lichtman, MPH, PHD

This document was approved by the American Heart Association Science A

College of Cardiology Board of Trustees on November 12, 2014.

The American College of Cardiology requests that this document be cited a

Fonarow GC, Jacobs JP, Jaff MR, Lichtman JH, Limacher MC, Mahaffey KW

elements and definitions for cardiovascular endpoint events in clinical trials:

Task Force on Clinical Data Standards (Writing Committee to Develop Cardi

This article has been copublished in Circulation.

Copies: This document is available on the World Wide Web sites of the

Association (my.americanheart.org). For copies of this document, please con

[email protected].

Permissions: Multiple copies, modification, alteration, enhancement, and

permission of the American College of Cardiology. Requests may be compl

author-agreement/obtaining-permission).

Marian C. Limacher, MD, FACC, FAHAKenneth W. Mahaffey, MD, FACCRoxana Mehran, MD, FACC, FAHASteven E. Nissen, MD, MACC, FAHAEric E. Smith, MD, MPH, FAHAShari L. Targum, MD, FACC*

*The findings and conclusions in this report are those of the authors and

do not necessarily represent the official positions of the U.S. Food and

Drug Administration.

ACC/AHA TaskForce on ClinicalData StandardsMembers

Biykem Bozkurt, MD, PHD, FACC, FAHA

William S. Weintraub, MD, MACC, FAHA, Chair

Gregg C. Fonarow, MD, FACC, FAHARobert C. Hendel, MD, FACC, FAHAyJeffrey P. Jacobs, MD, FACCHani H. Jneid, MD, FACC, FAHAMichael A. Kutcher, MD, FACC

Judith H. Lichtman, MPH, PHDEric E. Smith, MD, MPH, FAHAzJames E. Tcheng, MD, FACCTracy Y. Wang, MD, FACC, FAHA

yFormer Task Force Chair; current chair during the writing effort.

zFormer Task Force member; current member during the writing effort.

dvisory and Coordinating Committee on June 13, 2014, and by the American

s follows: Hicks KA, Tcheng JE, Bozkurt B, Chaitman BR, Cutlip DE, Farb A,

, Mehran R, Nissen SE, Smith EE, Targum SL. 2014 ACC/AHA key data

a report of the American College of Cardiology/American Heart Association

ovascular Endpoints Data Standards). J Am Coll Cardiol 2015;66:403-69.

American College of Cardiology (www.acc.org) and the American Heart

tact the Elsevier Inc. Reprints Department via fax (212) 633-3820 or e-mail

/or distribution of this document are not permitted without the express

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Hicks et al. J A C C V O L . 6 6 , N O . 4 , 2 0 1 5

Cardiovascular Endpoints Data Standards J U L Y 2 8 , 2 0 1 5 : 4 0 3 – 6 9

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TABLE OF CONTENTS

PREAMBLE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 404

FOREWORD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 406

1. INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 406

2. METHODOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 407

2.1. Writing Committee Composition . . . . . . . . . . . . . . 407

2.2. Relationships With Industry and Other Entities . 407

2.3. Review of Literature and ExistingData Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . 407

2.4. Development of Terminology Concepts . . . . . . . . 407

2.5. Consensus Development . . . . . . . . . . . . . . . . . . . 408

2.6. Relation to Other Standards . . . . . . . . . . . . . . . . 408

2.7. Peer Review, Public Review, andBoard Approval . . . . . . . . . . . . . . . . . . . . . . . . . . . 408

3. DATA ELEMENTS AND DEFINITIONS . . . . . . . . . . . . 408

3.1. Death Attribution . . . . . . . . . . . . . . . . . . . . . . . . . 408

3.1.1. Cardiovascular Cause of Death . . . . . . . . . . 409

3.1.2. Noncardiovascular Cause of Death . . . . . . . 409

3.1.3. Undetermined Cause of Death . . . . . . . . . . . 409

3.2. Myocardial Infarction . . . . . . . . . . . . . . . . . . . . . . 409

3.3. Hospitalization for Unstable Angina . . . . . . . . . . . 410

3.4. Transient Ischemic Attack and Stroke . . . . . . . . . 410

3.5. Heart Failure Event . . . . . . . . . . . . . . . . . . . . . . . . 411

3.6. Percutaneous Coronary Intervention . . . . . . . . . . 411

3.7. Peripheral Vascular Intervention . . . . . . . . . . . . . . 412

3.8. Stent Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . . 412

4. INFORMATICS OF CONTROLLED

VOCABULARIES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412

REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 413

APPENDIX 1

Author Relationships With Industry and Other Entities(Relevant)—2014 ACC/AHA Key Data Elements andDefinitions for Cardiovascular Endpoint Events inClinical Trials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416

APPENDIX 2

Reviewer Relationships With Industry and OtherEntities—2014 ACC/AHA Key Data Elements andDefinitions for Cardiovascular Endpoint Events inClinical Trials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417

APPENDIX 3

Death Attribution . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418

APPENDIX 4

Myocardial Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . 422

APPENDIX 5

Hospitalization for Unstable Angina . . . . . . . . . . . . . . . 428

APPENDIX 6

Transient Ischemic Attack and Stroke . . . . . . . . . . . . . 431

APPENDIX 7

Heart Failure Event . . . . . . . . . . . . . . . . . . . . . . . . . . . . 433

APPENDIX 8

Heart Failure Event: Additional Details . . . . . . . . . . . . 438

APPENDIX 9

Percutaneous Coronary Intervention . . . . . . . . . . . . . 440

APPENDIX 10

Cardiovascular Anatomy . . . . . . . . . . . . . . . . . . . . . . . . 456

APPENDIX 11

Peripheral Vascular Intervention . . . . . . . . . . . . . . . . . 463

PREAMBLE

The American College of Cardiology (ACC) and theAmerican Heart Association (AHA) support their mem-bers’ goal to improve the care of patients with car-diovascular disease through professional education,research, and development of guidelines and standardsand by fostering policies that support optimal patientoutcomes. The ACC and AHA recognize the importance ofthe use of clinical data standards for patient management,assessment of outcomes, and conduct of research, and theimportance of defining the processes and outcomes ofclinical care, whether in randomized trials, observationalstudies, registries, or quality-improvement initiatives.

Clinical data standards strive to define and standardizedata relevant to clinical concepts, with the primary goalof facilitating uniform data collection by providing aplatform of clinical terms with corresponding definitionsand data elements. Broad agreement on a commonvocabulary with reliable definitions used by all is vital topool and/or compare data across clinical trials to promote

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interoperability with electronic health records (EHRs) andto assess the applicability of research to clinical practice.The ultimate purpose of clinical data standards is tocontribute to the infrastructure necessary to accomplishthe ACC’s mission of fostering optimal cardiovascular careand disease prevention and the AHA’s mission of buildinghealthier lives, free of cardiovascular diseases and stroke.

The specific goals of clinical data standards are:

1. To establish a consistent, interoperable, and universalclinical vocabulary as a foundation for both clinicalcare and clinical research, including clinical trials

2. To promote the ubiquitous use of EHRs and facilitatethe exchange of data across systems through harmo-nized, standardized definitions of key data elements

3. To facilitate the further development of clinical regis-tries, quality- and performance-improvement pro-grams, outcomes evaluations, and clinical research,including the comparison of results within and acrossthese initiatives

The key elements and definitions are intended to facil-itate the consistent, accurate, and reproducible capture ofclinical concepts; standardize the terminology used todescribe cardiovascular diseases and procedures; create adata environment conducive to the assessment of patientmanagement and outcomes for quality and performanceimprovement and clinical and translational research; andincrease opportunities for sharing data across disparatedata sources. The ACC/AHA Task Force on Clinical DataStandards selects cardiovascular conditions and pro-cedures that will benefit from creation of a standarddataset. Subject matter experts are selected to examine/consider existing standards and develop a comprehensive,yet not exhaustive, standard dataset. When a data collec-tion effort is undertaken, only a subset of the elementscontained in a clinical data standards listing may beneeded, or conversely, users may want to considerwhether it may be necessary to collect some elements notlisted. For example, in the setting of a randomized clinicaltrial of a new drug, additional information would likely berequired regarding study procedures and drug therapies.

The ACC and AHA recognize that there are other nationalefforts to establish clinical data standards, and everyattempt is made to harmonize newly published standardswith existing standards. Writing Committees are instruc-ted to consider adopting or adapting existing nationallyand internationally recognized data standards if the defi-nitions and characteristics are useful and applicable to theset under development. In addition, the ACC and AHAare committed to continually expanding their portfolioof data standards andwill create new standards and updateexisting standards as needed to maintain their currencyand promote harmonizationwith other standards as healthinformation technology and clinical practice evolve.

The Writing Committee for the current effort wasintentionally expanded to include a regulatory perspec-tive. This reflects the key role of clinical event concepts inevaluating therapeutic safety and effectiveness in clinicaltrials. This unique collaboration between the regulatorysector and the ACC and AHA acknowledges the need toalign key clinical concepts for regulatory reporting andclinical care.

The Health Insurance Portability and AccountabilityAct privacy regulations, which went into effect in April2003, have heightened all practitioners’ awareness of ourprofessional commitment to safeguard our patients’ pri-vacy. The Health Insurance Portability and AccountabilityAct privacy regulations (1) specify which informationelements are considered “protected health information.”These elements may not be disclosed to third parties(including registries and research studies) without thepatient’s written permission. Protected health informa-tion may be included in databases used for healthcareoperations under a data use agreement. Research studiesusing protected health information must be reviewed byan institutional review board or a privacy board.

We have included identifying information in all clinicaldata standards to facilitate uniform collection of theseelements when appropriate. For example, a longitudinalclinic database may contain these elements because ac-cess is restricted to the patient’s caregivers. Conversely,registries may not contain protected health informationunless specific permission is granted by each patient.These fields are indicated as protected health informationin the data standards.

In clinical care, caregivers communicate with eachother through a common vocabulary. In an analogousfashion, the integrity of clinical research depends on firmadherence to prespecified procedures for patient enroll-ment and follow-up; these procedures are guaranteedthrough careful attention to definitions enumerated inthe study protocol, case report forms, and clinical eventcommittee charters. When data elements and definitionsare standardized across studies, comparison, pooledanalysis, and meta-analysis are enabled, thus deepeningour understanding of individual studies.

The recent development of quality-performance mea-surement initiatives, particularly those for which thecomparison of providers is an implicit or explicit aim, hasfurther raised awareness about the importance of datastandards. Indeed, a wide audience, including nonmed-ical professionals such as payers, regulators, and con-sumers, may draw conclusions about care and outcomes.To understand and compare care patterns and outcomes,the data elements that characterize them must be clearlydefined, consistently used, and properly interpreted.

William S. Weintraub, MD, MACC, FAHAChair, ACC/AHA Task Force on Clinical Data Standards



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FOREWORD

This publication, commissioned by the ACC/AHA, is theproduct of a novel collaboration between the ACC andAHA, the US Food and Drug Administration (FDA), and theStandardized Data Collection for Cardiovascular TrialsInitiative (SCTI). The aim of the collaboration is to pro-mulgate, for regulatory submissions, clinical data stan-dards for key cardiovascular and stroke endpoint eventsin clinical trials. The Writing Committee for this particulardata standard is unique in that it was convened to achievethe following goals: to address issues particular to regu-latory submissions and to provide a framework of datastandards that would simplify the design and conduct ofclinical trials for those considering regulatory sub-missions. The intent of this Writing Committee is notto be overly prescriptive. For example, the stroke dataelements are minimal by design to allow for flexibilityneeded to conduct global clinical trials for drugs anddevices. In a trial focused on the treatment of stroke,investigators may define additional outcomes and dataelements for a particular stroke treatment or indica-tion. The Writing Committee recognizes that thesestandards may be used for other types of clinical trialsand clinical care processes where appropriate. Thesedata standards are a first step in developing a uni-versal language for clinical trials and other types ofhealth-related research.

1. INTRODUCTION

Effective communication is a cornerstone of the health-care enterprise. A prerequisite for providing seamlesscare is the universal and consistent use of medicalvocabularies (2). Cardiovascular endpoints such as death,myocardial infarction, stroke, and revascularization arecritical in assessing diagnostic and therapeutic ap-proaches in the clinical care, research, and regulatorydomains. With the adoption of EHR solutions has comethe opportunity to manage health-related information asdiscrete data (3). Therefore, the ACC/AHA Task Force onClinical Data Standards established this Writing Commit-tee to identify and harmonize the common data elementsinvolved in key cardiovascular endpoint events. Doing sowill allow this vocabulary to be used to improve theassessment of process, performance, and outcomes acrossmultiple dimensions of health care.

In this work, the term “vocabulary” includes the ter-minology concept, the concept definition, a suggestedlabel for the corresponding data element, permissiblevalues of the data element, and definitions for thepermissible values.

The Writing Committee identified the ongoing work ofthe SCTI as the foundation for the development of this

vocabulary. The Writing Committee’s task was to review,refine, and advance as a clinical standard the cardiovas-cular endpoint terminology set developed by the SCTI.This terminology set largely reflects endpoints related tothe symptoms, manifestations, treatment, and conse-quences of coronary artery disease in both cardiovascularand noncardiovascular drug and device trials. Endpointconcepts related to carotid/cerebral revascularization,peripheral surgical revascularization, and treatmentof diseases of the aorta are beyond the scope of thisdocument.

First convened in 2009 by the FDA, the SCTI is aworking group formed to improve the quality and ef-ficiency of clinical trials. It includes representativesfrom academia, professional societies, the Clinical DataInterchange Standards Consortium, Health Level 7, theClinical Trials Transformation Initiative, pharmaceuticaland cardiovascular device manufacturers, and the FDA(which includes the Center for Drug Evaluation andResearch and the Center for Devices and RadiologicalHealth). The original goal of the working group was toimprove the quality and efficiency of cardiovascularclinical trials (e.g., acute coronary syndrome trials,percutaneous coronary intervention [PCI] trials). Sub-sequently, in recognition of the growing interest incardiovascular events in noncardiovascular trials (e.g.,diabetes control trials, weight loss trials), this focusexpanded to include noncardiovascular trials. To ach-ieve its goal, the SCTI acknowledged the need for aconsistent cardiovascular and stroke endpoint vocabu-lary comprising terms defined by objective criteriaand reported uniformly (4). This framework of stan-dardized key data elements in clinical trials (andpotentially the clinical care domain), could also facili-tate the conduct of meta-analyses to assess cardiovas-cular safety and compare the effectiveness of drug anddevice products.

The SCTI-developed working draft “StandardizedDefinitions for Cardiovascular and Stroke EndpointEvents in Clinical Trials” is the source document for thedata standards in this publication (4). This source docu-ment identifies the cardiovascular and stroke endpointterms relevant to clinical trials and regulatory sub-missions. The Writing Committee evaluated and harmo-nized these endpoint terms, categorized the attributes ofeach data element, developed permissible (i.e., allowed)values, and tabulated the content to facilitate computa-tional interoperability and the use of the terminologyregulatory domains.

The objective is to use this controlled terminology,initially developed for clinical trials and regulatorysubmissions, to standardize event reporting and datacollection when determinations must be made aboutcardiovascular and stroke endpoints in the context of


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clinical care processes, registries, EHRs, and longitudinaldrug or device surveillance.

Nonetheless, the Writing Committee recognizes thatthis terminology is not applicable to all dimensions ofhealth care and that some of these definitions are notapplicable to clinical care processes. For example, the“Hospitalization for Unstable Angina” definition may notbe optimal for the Centers for Medicare and MedicaidServices because other clinical scenarios could beconsistent with unstable angina but not fulfill all thecriteria needed to define this endpoint in a clinical trial.Similar scenarios could be relevant to other nonfatalendpoint definitions.

To avoid ambiguity, we recommend maintaining thecardiovascular and stroke endpoint vocabulary describedin this document as “regulatory specific” distinct fromother vocabularies. Although endpoint definitions mayevolve over time, a period in which definitions remainstatic is needed for terms to be used successfully toconduct a meta-analysis. Furthermore, the ACC/AHA TaskForce on Clinical Data Standards should include regula-tory data standards experts—in addition to members ofthis Writing Committee, SCTI representatives, and otherclinical trial experts—as an integral part of any necessarydefinition revision process, because such experts under-stand the requirements for evaluating drug and deviceproducts.

2. METHODOLOGY

2.1. Writing Committee Composition

The ACC/AHA Task Force on Clinical Data Standardsselected the members of the Writing Committee. Thecommittee consisted of 16 people with domain expertisein internal medicine, cardiovascular medicine, neurology,clinical research, epidemiology, invasive and interven-tional therapies, outcomes assessment, medical infor-matics, health information management, and healthcareservices research and delivery.

2.2. Relationships With Industry and Other Entities

The ACC/AHA Task Force on Clinical Data Standardsmakes every effort to avoid actual or potential conflicts ofinterest that might arise as a result of an outside rela-tionship or a personal, professional, or business interestof any member of the Writing Committee. Specifically, allmembers of the Writing Committee are required to com-plete and submit a disclosure form showing all such re-lationships that could be perceived as real or potentialconflicts of interest. These statements are reviewed by theACC/AHA Task Force on Clinical Data Standards andupdated when changes occur. Authors’ and peer re-viewers’ relationships with industry and other entitiespertinent to this data standards document are disclosed in

Appendixes 1 and 2, respectively. In addition, for com-plete transparency, the disclosure information of eachWriting Committee member—including relationshipsnot pertinent to this document—is available as anonline supplement at http://jaccjacc.cardiosource.com/acc_documents/Comprehesive_RWI_CV_Endpointsv1.pdf.The work of the Writing Committee was supportedexclusively by the ACC and AHA without commercialsupport. Writing Committee members volunteered theirtime for this effort. Meetings of the Writing Committeewere confidential and attended only by committeemembers and staff.

2.3. Review of Literature and Existing Data Definitions

Cardiovascular endpoint concepts have long been used inclinical care and research to ascertain and assess out-comes of diagnostic and therapeutic approaches. A seriesof reference publications provided the foundation for thecardiovascular endpoint concepts identified by the SCTIand developed by the Writing Committee (5–14). Whatmakes this work unique is that it reviews and refines theterms as developed by the SCTI explicitly for use inreporting clinical trial results and in regulatory sub-missions, and it delineates where these concepts could orshould not be used as the foundational vocabulary inroutine clinical care.

2.4. Development of Terminology Concepts

The terminology set addressed in this body of work in-cludes cardiovascular endpoints of universal interest inclinical care, research, and regulatory review: death(specifically attribution of the cause of death), myocardialinfarction, stroke, transient ischemic attack (TIA), coro-nary intervention (including stent thrombosis), periph-eral vascular intervention, hospitalization for unstableangina, and acute heart failure (HF) events.

The Writing Committee aggregated, reviewed, harmo-nized, and extended these terms to develop a controlled,semantically interoperable, machine-computable termi-nology set that would be usable, as appropriate, inas many contexts as possible. As necessary, theWriting Committee identified the contexts where indi-vidual terms required differentiation depending on theirproposed use (i.e., research/regulatory versus clinical carecontexts).

The Writing Committee tabulated the content andprovided sufficient structure to build and model theinformatics formalisms to achieve computational inter-operability. The resulting appendices (Appendixes 3–7and 9–11) list the “terminology concept” in the firstcolumn, followed by a clinical definition (“conceptdefinition”) of the terminology concept in the secondcolumn. A data element label is suggested for forms-basedapproaches to data capture. The allowed responses

http://jaccjacc.cardiosource.com/acc_documents/Comprehesive_RWI_CV_Endpointsv1.pdf

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(“permissible values”) for each terminology conceptin the next column are the acceptable “answers” forcapturing the information. For terminology conceptswith multiple permissible values, a bulleted list of thepermissible values is provided in the same row as theterminology concept, with successive rows listing eachpermissible value and corresponding permissible valuedefinition. The process of converting the prose descrip-tion of an endpoint into this tabular format can be seen bycomparing the source text for a HF endpoint event(Appendix 8, an excerpt from the SCTI draft document)and the tabular representation of the same concept inAppendix 7. Where possible, clinical definitions of end-points (and the corresponding permissible values) arerepeated verbatim as defined by the SCTI or as previouslypublished in reference documents.

2.5. Consensus Development

The ACC/AHA Task Force on Clinical Data Standardsestablished the Writing Committee in November 2012,according to the processes described in the Task Forceon Clinical Data Standards’ methodology statement (15).As described previously, the responsibility of theWriting Committee was to review and refine the list ofcandidate terms identified by the SCTI and to harmo-nize the attributes and other informatics formalismsrequired to attain interoperability of the terms. Duringthe first 6 months of 2013, the work of the WritingCommittee was accomplished through a series of tele-conference and Web conference meetings, along withextensive correspondence by e-mail. The review workwas distributed among subgroups of the Writing Com-mittee on the basis of their interest and expertise inthe components of the terminology set. The proceedingsof the work groups were then assembled, resulting inthe vocabulary and associated descriptive prose inSection 3. All members reviewed and approved the finalvocabulary.

2.6. Relation to Other Standards

The Writing Committee reviewed the work of the SCTIalong with available published data standards, specifi-cally those developed for death, acute myocardialinfarction, stroke, TIA, unstable angina/non–ST-elevationmyocardial infarction, HF, PCI, and peripheral vascularintervention (4–13,16–21). Existing published definitionswere adjusted to eliminate verbiage not relevant to anactual definition (e.g., instructions such as the phrase“indicate whether the patient has.” have beeneliminated).

Through the affirmation and refinement of existingdata standards, the Writing Committee anticipates thatthe vocabulary will facilitate the uniform adoption ofthese terms, where appropriate, by the clinical care,

clinical and translational research, regulatory, quality andoutcomes, and EHR communities.

2.7. Peer Review, Public Review, and Board Approval

The “2014 ACC/AHA Key Data Elements and Definitionsfor Cardiovascular Endpoint Events in Clinical Trials”statement was reviewed by official reviewers nominatedby the ACC and AHA. To increase its applicability further,the document was posted on the ACC Web site for a30-day public comment period. This document wasapproved for publication by the ACC Board of Trustees onNovember 12, 2014, and by the AHA Science Advisory andCoordinating Committee on June 13, 2014. The WritingCommittee anticipates that these data standards willrequire review and updating in the same manner as otherpublished guidelines, performance measures, and appro-priate use criteria. The Writing Committee will thereforereview the set of data elements periodically, startingwith the anniversary of publication of the standards, toascertain whether modifications should be considered.

3. DATA ELEMENTS AND DEFINITIONS

As described above, the SCTI identified candidate car-diovascular and stroke endpoint event terms in the draftdocument “Standardized Definitions for Cardiovascularand Stroke Endpoint Events in Clinical Trials.” Thedocument delineated the following cardiovascular andneurological endpoint events in the context of clinicaltrials and regulatory reporting:

1. Cardiovascular death2. Noncardiovascular death3. Undetermined cause of death4. Myocardial infarction5. Hospitalization for unstable angina6. Transient ischemic attack and stroke7. Heart failure event8. Percutaneous coronary intervention9. Peripheral vascular intervention10. Stent thrombosis

The SCTI envisioned that data collection and exchangestandards for these endpoint events would allow indi-vidual investigators and clinical research organizationsto collect and exchange research data consistently andefficiently. It also envisioned that adoption of thecontrolled terminology within the research and regula-tory sectors could facilitate consistency across the clinicalcare domain.

3.1. Death Attribution

Death is classified into 1 of 3 categories: 1) cardiovasculardeath; 2) noncardiovascular death; and 3) undeterminedcause of death. The intent of the classification schema is


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to identify one, and only one, of the categories as theunderlying cause of death. The key priority is differenti-ating between cardiovascular and noncardiovascularcauses of death (Appendix 3).

Collection of appropriate source documentation iscritical for rigorous adjudication of the cause of death.Although death certificates establish that the patientdied, reliance on information included in death certifi-cates may be problematic; several studies have demon-strated inaccurate coding in the death certificate whendeath certificates were compared with adjudicated out-comes (22,23). In contrast, autopsy reports are oftenvaluable in assessing the cause of death and should beused whenever possible.

For sudden deaths, even when witnessed, death attri-bution may be difficult if only limited information isavailable. Frequently, these deaths are attributed toeither sudden cardiac death (cardiovascular death) ordeath due to an undetermined cause. Sensitivity analysesmay be helpful in determining the effect of these eventson the primary and major secondary endpoints in aparticular clinical trial or development program.

3.1.1. Cardiovascular Cause of Death

Frequently, the cardiovascular death category is notdivided further into subcategories such as death resultingfrom an acute myocardial infarction, sudden cardiacdeath, or HF, because the cause of death is so often un-known or ambiguous (e.g., Does a death after a myocar-dial infarction count as a myocardial infarction, suddendeath, arrhythmic death, or HF death?). Moreover, theunderlying cause of death and the mode of death (i.e.,most proximate event associated with death) may overlapsubstantially. In contrast, precision is more achievablewith respect to nonfatal events.

However, in cases where subclassification is desired,the Writing Committee recommends a uniform approachfor categorizing the attributable cause (and not just theproximate event) for cardiovascular death. The suggestedsubcategories for attribution of death to a cardiovascularetiology are acute myocardial infarction, sudden cardiacdeath, HF, stroke, cardiovascular procedure, cardio-vascular hemorrhage, and other cardiovascular causes.“Death due to other cardiovascular causes” refers to acardiovascular death not included in the above categoriesbut with a specific known cause, such as a pulmonaryembolism or peripheral arterial disease. In addition,“death due to cardiovascular hemorrhage” refers to adeath related to hemorrhage such as a nonstroke intra-cranial hemorrhage, nonprocedural or nontraumaticvascular rupture (e.g., aortic aneurysm), or pulmonaryhemorrhage from a pulmonary embolism. In contrast,if a pulmonary hemorrhage were a result of a contusionfrom a motor vehicle accident, the cause of death

would be noncardiovascular (death due to trauma).Although these subcategories may not be applicable toall study populations, therapeutic areas, or drug anddevice development programs, the events in these sub-categories occur relatively frequently in the generalpopulation and probably contribute to mortality in anyobservation. In some trials, subclassification of cardio-vascular causes of death may prove helpful in under-standing pathophysiology in the context of drug ordevice programs.

3.1.2. Noncardiovascular Cause of Death

Identifying noncardiovascular causes of death is impor-tant when assessing competing mortality risks in bothcardiovascular and noncardiovascular trials. The pro-posed schema for noncardiovascular causes of death ismore general than that for cardiovascular causes of death.This noncardiovascular schema could be expanded tocapture other causes for specific trials in particular ther-apeutic areas or for specific drug or device developmentprograms if a specific toxicity has been identified innonclinical work or early clinical trials. When death isclearly due to a noncardiovascular cause, a cardiovascularcause of death is excluded. The proposed values repre-sent commonly used noncardiovascular categories.

3.1.3. Undetermined Cause of Death

In general, this category of death should apply to fewpatients in well-run clinical trials. Attribution of causal-ity may be limited or impossible if information availableat the time of death is minimal or nonexistent. In suchcases, the date of death may be the only data elementcaptured.

The key priority is to prespecify how these deathswill be classified and to implement a uniform approachthroughout the conduct of the trial. Occasionally, it maynot be possible to determine exact causality when 2 lethalconditions contribute to death equally. In this circum-stance, 1 condition should be chosen, with considerationof the issue being studied. For example, if cardiac safetyis under consideration and the competing causes ofdeath are cardiovascular and noncardiovascular, cardio-vascular death should take precedence.

3.2. Myocardial Infarction

The categorization and definitions of the types ofmyocardial infarction are derived from the “Third Uni-versal Definition of Myocardial Infarction” (13,14), the“2012 ACCF/AHA Guideline for the Management of Un-stable Angina/Non-ST-Elevation Myocardial Infarction”(12), and the “2013 ACCF/AHA Guideline for the Manage-ment of ST-Elevation Myocardial Infarction” (18).

The key recommendation is to base thresholdsfor biomarker detection of myocardial infarction on



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99th percentile values (i.e., the upper reference limit)rather than on “upper limit of normal” values. Multipleassays exist for cardiac troponin and the MB fraction ofcreatine kinase (CK-MB), and assay characteristics vary bymanufacturer. Some assays reported by local laboratoriesprovide the 99th percentile and a higher “decision limit”or upper limit of normal above which myocardial infarc-tion should be considered. The “Third Universal Defini-tion of Myocardial Infarction” (13,14) recommends theuse of the 99th percentile upper reference limit as thereference standard. The data elements developed inAppendix 4 allow both the 99th percentile and the upperlimit of normal (or both) to be captured, depending on thereporting approach used in the central or local laboratory.Instead of listing every cardiac biomarker assay inAppendix 4, we have elected to represent all assays withthe generic term [cardiac biomarker]. The actualbiomarker assay used should replace the generic term[cardiac biomarker]. Collection of serial biomarker valuesto capture all measurements (and to reflect rise or fall ofthe biomarker) would recursively use the same dataelement construct as the approach for capturing a singlevalue. Cardiac troponin is the preferred biomarker. Iftroponin values are not available, then CK-MB mass isused as an alternative.

The terminology set includes data elements for stentrestenosis without occlusion as a type of acute myocardialinfarction (type 4c) and asymptomatic postbaselinemyocardial infarction detected during follow-up. Thedata elements that reflect old or prior myocardial infarc-tion at baseline are not included here but can be found inthe “2013 ACCF/AHA Key Data Elements and Definitionsfor Measuring the Clinical Management and Outcomes ofPatients With Acute Coronary Syndromes and CoronaryArtery Disease” (16).

The Writing Committee acknowledges that there isdisagreement about how to define a “clinically relevantmyocardial infarction” after coronary revascularization(PCI or coronary artery bypass graft). An expert consensusgroup from the Society for Cardiovascular Angiographyand Interventions (24) proposes the use of CK-MB insteadof troponin and different cut points from those includedin the “Third Universal Definition of Myocardial Infarc-tion” (13,14). A detailed discussion of these differences isbeyond the scope of this publication but is provided byWhite (25). At this time, the Writing Committee continuesto support the “Third Universal Definition of MyocardialInfarction” (13) for harmonization purposes but recog-nizes that this matter requires further study. As longas cardiac biomarker values (both cardiac troponin andCK-MB) and 99th percentile upper reference limit valuesare recorded, virtually any definition of periproceduralmyocardial infarction can be applied and examined withrespect to outcome.

3.3. Hospitalization for Unstable Angina

Hospitalization for unstable angina is a commonly usedendpoint in clinical trials evaluating the efficacy orsafety of cardiovascular therapies such as lipid-modifyingagents, antihypertensive drugs, antithrombotic therapies,and coronary interventions. Unlike traditional endpointssuch as death, myocardial infarction, or stroke, hospital-ization for unstable angina, by necessity, involves somedegree of subjective assessment of the most likely etiol-ogy of symptoms resulting in hospital admission. Theterminology set for unstable angina (Appendix 5) focuseson data elements needed for determining whethersymptoms truly represent cardiovascular ischemia, in-cluding the character and duration of the presentingsymptoms, the proximity of symptom onset to hospitali-zation, and the duration of hospitalization. Electrocar-diographic abnormalities are pivotal to the diagnosis.Such abnormalities include the presence or absence ofdeviations in the ST segment, morphology of ST-segmentchanges (horizontal or downsloping versus upsloping),and the magnitude of the deviation. Many patientswithout high-risk features (i.e., patients with low TIMI[Thrombolysis in Myocardial Infarction] or GRACE [GlobalRegistry of Acute Coronary Events] risk scores) undergoprovocative testing for inducible myocardial ischemia,requiring measurement of ST elevation or depressionduring electrocardiographic monitoring. Alternatively,exercise or pharmacological stress testing may involveassessment of wall motion abnormalities on echocar-diography and/or reversible perfusion defects by nuclearscintigraphy or magnetic resonance imaging. Other im-portant data elements include angiographic evidence ofthe severity of coronary stenosis or presence of coronarythrombus in a vessel believed to be responsible for theischemic signs and symptoms. Additional data elementsinclude the need for coronary revascularization by PCI orcoronary bypass surgery of lesion(s) believed responsiblefor the hospitalization.

The need for escalation of pharmacological therapy(nitrates, beta-blockers, or other antianginal therapy)may provide supportive evidence for a diagnosis ofunstable angina. Last, to fulfill the criteria for un-stable angina, cardiac biomarkers must be negativeand there can be no evidence of acute myocardialinfarction.

3.4. Transient Ischemic Attack and Stroke

TIA and stroke endpoints (Appendix 6) are designed tocapture the incidence of new TIA and stroke, type ofstroke (i.e., ischemic, hemorrhagic, or undetermined),and severity of stroke (i.e., mortality and level of func-tional disability). The modified Rankin Scale (26) is rec-ommended as the measure of disability. Hemorrhagicstroke may be further subcategorized as intracerebral


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hemorrhage or subarachnoid hemorrhage if there issufficient information to make this determination.

The Writing Committee proposes the following defini-tion of TIA: “a transient episode of focal neurologicaldysfunction caused by brain, spinal cord, or retinalischemia, without acute infarction.” This definition isidentical to that adopted by the SCTI (FDA Stroke Team)and is based on one previously proposed in an AHA/American Stroke Association (ASA) scientific statement(9) with one subtle but important difference: as definedby the scientific statement, TIA is “a transient episode ofneurological dysfunction caused by focal brain, spinalcord, or retinal ischemia, without acute infarction.” TheSCTI definition that the Writing Committee has adoptedemphasizes the clinical presentation rather than theanatomic location of the TIA and may be more appropriatefor clinical trial use because the availability of imagingmodalities may vary greatly from one study center tothe next.

In contrast to TIA, stroke is defined on the basis of thepresence of acute infarction as demonstrated by imagingor based on the persistence of symptoms. The WritingCommittee acknowledges that the categorization of TIAversus ischemic stroke depends partly on the sensitivityof the diagnostic assessments for brain infarction. Forexample, patients with symptoms of short duration(e.g., <24 hours) but evidence of infarction on magneticresonance imaging could be categorized as having had anischemic stroke. In contrast, in the absence of highlysensitive magnetic resonance imaging evidence, the samepatient could be categorized as having had a TIA. Thepresence of persisting symptoms should be consideredsufficient evidence for stroke rather than TIA. Primarilyon the basis of consensual practice (rather than objectiveevidence), the AHA/ASA has recommended the existenceof symptoms for at least 24 hours as an operational defi-nition of persisting symptoms to indicate stroke ratherthan TIA (19). However, the time cut point that best dis-criminates between infarction and the absence of infarc-tion remains largely undefined. Accordingly, for anyclinical trial that plans to use the duration of symptompersistence to operationally discriminate between TIAand stroke, the Writing Committee and SCTI recommendprespecifying the particular duration in the protocol,although both acknowledge that a duration $24 hoursis frequently used.

Depending on the trial objectives, additional optionalinformation could be recorded for analysis, includingphysical examination findings (e.g., using the AHA/ASAguideline–recommended National Institutes of HealthStroke Scale), presumed mechanism of ischemic stroke,and impact on additional patient-centered outcomessuch as basic or instrumental activities of daily living.Investigators interested in collecting more detailed

information on stroke outcomes should consider usingthe National Institute of Neurological Disordersand Stroke Common Data Elements, available online atwww.commondataelements.ninds.nih.gov.

3.5. Heart Failure Event

HF is a common outcome of many different etiologies andmay be associated with cardiovascular and non-cardiovascular treatment modalities. Accurate recogni-tion of HF events is important because of the pooroutcomes associated with them and because of theirincreasing prevalence and societal burden. In clinical tri-als, when a specific uniform definition is lacking, theconcurrence between the initial and adjudicated assess-ment of HF is lower than is the case with adjudications ofmyocardial infarction and/or stroke (27). This lack ofconcurrence illustrates the challenges investigators facein classifying HF events and underlines the importanceof a standardized definition of event. A consistent defi-nition will ensure that all HF events are accuratelyreported in all clinical trials and registries.

The proposed HF endpoint event (Appendix 7) hasbeen constructed independent of whether the exacerba-tion of HF results in hospitalization, recognizing thatexacerbation of HF can often be managed on an out-patient basis such as with an urgent or unscheduledoutpatient office/practice or emergency room visit.Instead, the key characteristic of a HF event is the needfor a resource-intensive response to failure of the primarytherapeutic management strategy. The terminology setfor a HF event requires both subjective and objectivefindings, including worsening symptoms and signs, aswell as laboratory evidence supporting the diagnosis ofworsening HF. Also incorporated into the definition isthe requirement for a substantive intensification in HFtherapies, whether pharmacological, mechanical, or both.For additional details, see Appendix 8 (28–40).

3.6. Percutaneous Coronary Intervention

The vast majority of catheter-based interventional cardi-ology procedures are performed to treat atheroscleroticcoronary artery lesions.

For coronary revascularization procedures, it isimportant to determine whether the procedure was per-formed to treat symptoms of myocardial ischemia orbased solely on coronary anatomic characteristics. It isalso important to document whether the Heart Teamconsidered the patient to be inappropriate for surgicalrevascularization due to prohibitive comorbidities. Med-ical records that include a description of symptoms andobjective assessments of ischemia should be reviewedto determine whether the revascularization procedurewas clinically indicated. Imaging reviews by indepen-dent core laboratories (e.g., angiography, intravascular

http://www.commondataelements.ninds.nih.gov



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ultrasonography, optical coherence tomography) areparticularly useful for reducing potential bias.

The terminology set for PCI (Appendix 9) concentrateson PCI status, procedural success, target lesion failure,target lesion revascularization, and both intraproceduraland vascular complications. Of specific note, the WritingCommittee identified limitations in the nomenclature ofthe coronary arteries as described for the Coronary ArterySurgery Study (CASS) (41), which has subsequently beenupdated by the Bypass Angioplasty Revascularization In-vestigators (BARI) (42) and is currently used by the ACCNational Cardiovascular Data Registry. For example, thenomenclature does not address the concepts of ostial orbifurcation disease and does not follow a consistentconvention for naming coronary segments. The WritingCommittee therefore proposes an update to the CASS/BARI/National Cardiovascular Data Registry coronaryartery nomenclature (Appendix 10) to better capture dataevaluating treatment approaches to ostial and bifurcationdisease, improve the consistency and completeness ofcoronary artery nomenclature, include the Medina Clas-sification (43,44) as a standard, and reflect universalconventions and terminology currently used by angiog-raphy core laboratories. Finally, as new classes ofintracoronary therapy (e.g., drug-coated balloons, bio-resorbable drug-eluting stents/scaffolds) are developed,novel mechanisms of failure may be identified that willrequire modification and addition to this controlledvocabulary.

3.7. Peripheral Vascular Intervention

Peripheral artery disease (PAD) is widespread. Of all theatherosclerotic syndromes, the clinical relevance of PADis poorly appreciated by primary care physicians, cardio-vascular specialists, and patients alike. Not only doesPAD reduce the physical functioning of affected patients,but it is associated with a marked increase in all-causeand cardiovascular mortality.

Although vascular disease is defined as “all diseasesof the arteries, veins, and lymphatic vessels” (10), forsimplicity, this vocabulary for peripheral vascular inter-vention endpoints focuses on data elements that describerevascularization interventions involving the peripheralarterial circulation. These data standards concentrateon PAD involving the infrarenal aorta, iliac, and infrain-guinal arteries and carotid, renal, mesenteric, and aorticinterventions. Of note, upper extremity or intracranialvascular diseases are beyond the scope of thispublication.

Appendix 11 lists the vocabulary to facilitate uniformreporting of endovascular and surgical interventions forpatients with PAD, thereby allowing comparisons of drug,device, and surgical treatments for PAD. Included areharmonized definitions of success and failure that are

derived from the coronary revascularization terminology,including concepts of target lesion and target vesselrevascularization. Although somewhat arbitrary, theproposed construct includes the division of the lowerextremity arterial circulation into the 3 “vessel” terri-tories, or levels (aorto-iliac, femoral-popliteal, and tibio-peroneal) analogous to the division of the 3 coronaryvessel territories.

As new classes of endovascular therapy (e.g., drug-coated balloons, bioresorbable drug-eluting stents/scaf-folds) are developed, novel mechanisms of failure maybe identified that will require modification and additionto this controlled vocabulary.

3.8. Stent Thrombosis

According to the classification proposed by the AcademicResearch Consortium, stent thrombosis is defined asdefinite, probable, or possible (7). Definite stent thrombosisis defined as occurring when clinical presentation isconsistent with acute coronary syndrome and angiog-raphy or autopsy examination confirm stent occlusion orthrombus. Probable stent thrombosis is defined as deathoccurring within 30 days that cannot be attributed toanother cause or when myocardial infarction occurs at anytime point and is attributable to the target vessel inthe absence of angiography confirming another culpritlesion. Finally, possible stent thrombosis is defined asoccurring when the patient dies after >30 days and deathis not explained by another cause. The terminology set(Appendix 9) focuses on data elements required forconfirmation of stent thrombosis. To classify these eventsaccordingly, the following information is required: clinicaldetails surrounding the acute event; dates and proceduralinformation for all prior stent procedures; serial electro-cardiograms at the time of the event and for appropriateduration of follow-up; serial cardiac biomarkers; results ofcoronary angiography with review by an independentangiographic core laboratory or independent clinicalevents committee; and clinical details surrounding alldeaths, including death certificate and autopsy report ifapplicable. When available data support >1 classification,the highest level of certainty should be reported.

4. INFORMATICS OF CONTROLLED

VOCABULARIES

Variability in the definitions, formatting, and encoding ofclinical concepts hinders the use, exchange, and analysisof information in health care. Efficient use of healthcareinformation requires both syntactic interoperability (i.e.,standards and protocols for formatting, packaging, andtransmission required for computer-to-computer datatransfer) and semantic interoperability (i.e., the capacityof computer systems to transmit data with unambiguous,


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shared meaning, enabling machine-computable logic, datafederation, inferential processing, and knowledge discov-ery) (45,46). To achieve these forms of interoperability,the Writing Committee specified the attributes of theendpoint concepts relevant to the informatics of con-trolled vocabularies. These attributes (terminologyconcept, concept definition, permissible values, permis-sible value definitions) are only a subset of those needed tocharacterize data elements. Other attributes are stillneeded to fully qualify a terminology set as a controlledvocabulary; these include preferred abbreviation, conceptunique identifier, data type, data format, relationships toother terms, use of case context describing where andwhen a concept is assessed, and concept steward. Theneed to be explicit is particularly relevant because theclass of endpoint events represents summative conceptsmore useful for assessing responses and outcomes totherapeutic approaches and treatments. The use of sum-mative concepts contrasts with the emphasis in EHRsolutions on diagnoses as classified by taxonomies suchas the International Classification of Disease and theSystemized Nomenclature of Medicine—Clinical Terms.

Under FDA grant 1R24FD004411-01, this terminologyset has been developed as a controlled vocabulary in thecardiovascular domain of the Clinical Data Acquisitionand Standards Harmonization, and the tabular repre-sentation of this work is available for download athttp://jaccjacc.cardiosource.com/acc_documents/CVEndpointTestData_20NOV2014.xlsx and http://jaccjacc.acc.org/Clinical_Document/CVEndpoints_Data_Element_Spreadsheet_MASTER.xlsx. The terminology set will also be devel-oped in an International Organization for Standardiza-tion/International Electrotechnical Commission 11179standard metadata repository; this specification pro-vides a standardized grammar and syntax for describingdata elements and associated metadata, resulting inunambiguous representation and interpretation of data(47,48). Specifically, the endpoint concepts will be rep-resented in the National Institutes of Health/National

Cancer Institute Data Standards Registry and Repositoryto facilitate the use of the terminology set across theclinical care, research, and regulatory domains. Finally, itis intended for this terminology set to be developed andballoted through the HL7 EHR System Functional Modelprocess to further foster adoption in EHR systems.

The Writing Committee acknowledges that cardiovas-cular and stroke endpoint event concepts are a subset ofa larger set of cardiovascular endpoints. In particular,additional concepts such as those describing carotid/cerebral revascularization, peripheral surgical revascu-larization, aortic dissection, abdominal aortic aneurysm,aortic surgery, and valvular heart disease remain to bedeveloped.

STAFF

American College of Cardiology

Patrick T. O’Gara, MD, FACC, PresidentShalom Jacobovitz, Chief Executive OfficerLara E. Slattery, MHS, Team Leader, ACC Scientific

ReportingAmelia Scholtz, PhD, Publications Manager, Clinical

Policy and PathwaysAmerican College of Cardiology/American Heart Association

Maria Lizza D. Isler, BSMT, Associate, Clinical DataStandards

American Heart Association

Elliott Antman, MD, FAHA, PresidentNancy Brown, Chief Executive OfficerRose Marie Robertson, MD, FACC, FAHA, Chief Science

OfficerGayle R. Whitman, PhD, RN, FAHA, FAAN, Senior Vice

President, Office of Science OperationsMelanie B. Turner, MPH, Science and Medicine Advisor,

Office of Science OperationsJody Hundley, Production Manager, Scientific Publications,

Office of Science Operations

RE F E RENCE S

1. Health Insurance Portability and Accountability Actof 1996. Public Law 104–191. 1996.

2. Hammond WE. Seamless care: what is it; what is itsvalue; what does it require; when might we get it? StudHealth Technol Inform. 2010;155:3–13.

3. Cimino JJ. Desiderata for controlled medical vocab-ularies in the twenty-first century. Methods Inf Med.1998;37:394–403.

4. Hicks KA, Hung HM, Mahaffey KW, et al. Standard-ized Definitions for Cardiovascular and Stroke End PointEvents in Clinical Trials. Available at: http://www.cdisc.org/therapeutic. Accessed August 20, 2014.

5. Anderson JL, Adams CD, Antman EM, et al. ACC/AHA2007 guidelines for the management of patients with

unstable angina/non ST-elevation myocardial infarc-tion: a report of the American College of Cardiology/American Heart Association Task Force on PracticeGuidelines (Writing Committee to Revise the 2002Guidelines for the Management of Patients With Un-stable Angina/Non ST-Elevation Myocardial Infarction):Developed in collaboration with the American Collegeof Emergency Physicians, the Society for CardiovascularAngiography and Interventions, and the Society ofThoracic Surgeons. J Am Coll Cardiol. 2007;50:e1–157.

6. Campeau L. Letter: grading of angina pectoris.Circulation. 1976;54:522–3.

7. Cutlip DE, Windecker S, Mehran R, et al. Clinical endpoints in coronary stent trials: a case for standardizeddefinitions. Circulation. 2007;115:2344–51.

8. Dickstein K, Cohen-Solal A, Filippatos G, et al. ESCguidelines for the diagnosis and treatment of acute andchronic heart failure 2008: the Task Force for theDiagnosis and Treatment of Acute and Chronic HeartFailure 2008 of the European Society of Cardiology.Developed in collaboration with the Heart FailureAssociation of the ESC (HFA). Eur J Heart Fail. 2008;10:933–89.

9. Easton JD, Saver JL, Albers GW, et al. Definition andevaluation of transient ischemic attack: a scientificstatement for healthcare professionals from theAmerican Heart Association/American Stroke Associa-tion Stroke Council; Council on Cardiovascular Surgeryand Anesthesia; Council on Cardiovascular Radiologyand Intervention; Council on Cardiovascular Nursing;

http://jaccjacc.cardiosource.com/acc_documents/CVEndpointTestData_20NOV2014.xlsx

http://jaccjacc.cardiosource.com/acc_documents/CVEndpointTestData_20NOV2014.xlsx

http://jaccjacc.acc.org/Clinical_Document/CVEndpoints_Data_Element_Spreadsheet_MASTER.xlsx



http://www.cdisc.org/therapeutic




414

and the Interdisciplinary Council on Peripheral VascularDisease. Stroke. 2009;40:2276–93.

10. Hiatt WR, Goldstone J, Smith SC Jr., et al.Atherosclerotic Peripheral Vascular Disease Sympo-sium II: nomenclature for vascular diseases. Circulation.2008;118:2826–9.

11. Hunt SA, Abraham WT, Chin MH, et al. 2009Focused update incorporated into the ACC/AHA 2005guidelines for the diagnosis and management of heartfailure in adults: a report of the American College ofCardiology Foundation/American Heart AssociationTask Force on Practice Guidelines. Developed incollaboration with the International Society for Heartand Lung Transplantation. J Am Coll Cardiol. 2009;53:e1–90.

12. Jneid H, Anderson JL, Wright RS, et al.2012 ACCF/AHA focused update of the guideline forthe management of patients with unstable angina/non-ST-elevation myocardial infarction (updatingthe 2007 guideline and replacing the 2011 focusedupdate): a report of the American College of Cardi-ology Foundation/American Heart Association TaskForce on Practice Guidelines. J Am Coll Cardiol. 2012;60:645–81.

13. Thygesen K, Alpert JS, Jaffe AS, et al. Third uni-versal definition of myocardial infarction. Circulation.2012;126:2020–35.

14. Thygesen K, Alpert JS, Jaffe AS, et al. Third uni-versal definition of myocardial infarction. J Am CollCardiol. 2012;60:1581–98.

15. Hendel RC, Bozkurt B, Fonarow GC, et al. ACC/AHA2013 methodology for developing clinical data stan-dards: a report of the American College of Cardiology/American Heart Association Task Force on Clinical DataStandards. J Am Coll Cardiol. 2014;63:2323–34.

16. Cannon CP, Brindis RG, Chaitman BR, et al. 2013ACCF/AHA key data elements and definitions formeasuring the clinical management and outcomes ofpatients with acute coronary syndromes and coronaryartery disease: a report of the American College ofCardiology Foundation/American Heart AssociationTask Force on Clinical Data Standards (Writing Com-mittee to Develop Acute Coronary Syndromes andCoronary Artery Disease Clinical Data Standards). J AmColl Cardiol. 2013;61:992–1025.

17. Creager MA, Belkin M, Bluth EI, et al. 2012 ACCF/AHA/ACR/SCAI/SIR/STS/SVM/SVN/SVS key data ele-ments and definitions for peripheral atheroscleroticvascular disease: a report of the American Collegeof Cardiology Foundation/American Heart AssociationTask Force on Clinical Data Standards (Writing Com-mittee to develop Clinical Data Standards for Periph-eral Atherosclerotic Vascular Disease). J Am CollCardiol. 2012;59:294–357.

18. O’Gara PT, Kushner FG, Ascheim DD, et al.2013 ACCF/AHA guideline for the management ofST-elevation myocardial infarction: a report of theAmerican College of Cardiology Foundation/AmericanHeart Association Task Force on Practice Guidelines.J Am Coll Cardiol. 2013;61:485–510.

19. Sacco RL, Kasner SE, Broderick JP, et al. Anupdated definition of stroke for the 21st century:a statement for healthcare professionals from theAmerican Heart Association/American Stroke Associa-tion. Stroke. 2013;44:2064–89.

20. Weintraub WS, Karlsberg RP, Tcheng JE, et al.ACCF/AHA 2011 key data elements and definitions of

a base cardiovascular vocabulary for electronic healthrecords: a report of the American College of Cardiol-ogy Foundation/American Heart Association TaskForce on Clinical Data Standards. J Am Coll Cardiol.2011;58:202–22.

21. Zannad F, Garcia AA, Anker SD, et al. Clinicaloutcome endpoints in heart failure trials: a EuropeanSociety of Cardiology Heart Failure Associationconsensus document. Eur J Heart Fail. 2013;15:1082–94.

22. Lloyd-Jones DM, Martin DO, Larson MG, et al.Accuracy of death certificates for coding coronaryheart disease as the cause of death. Ann Intern Med.1998;129:1020–6.

23. Every NR, Parsons L, Hlatky MA, et al. Use andaccuracy of state death certificates for classificationof sudden cardiac deaths in high-risk populations. AmHeart J. 1997;134:1129–32.

24. Moussa ID, Klein LW, Shah B, et al. Considerationof a new definition of clinically relevant myocardialinfarction after coronary revascularization: an expertconsensus document from the Society for Cardiovas-cular Angiography and Interventions (SCAI). J Am CollCardiol. 2013;62:1563–70.

25. White H. Avatar of the universal definition ofperiprocedural myocardial infarction. J Am Coll Cardiol.2013;62:1571–4.

26. Rankin J. Cerebral vascular accidents in patientsover the age of 60. II. Prognosis. Scott Med J. 1957;2:200–15.

27. Ives DG, Fitzpatrick AL, Bild DE, et al. Surveil-lance and ascertainment of cardiovascular events.The Cardiovascular Health Study. Ann Epidemiol.1995;5:278–85.

28. Binanay C, Califf RM, Hasselblad V, et al. Evalua-tion study of congestive heart failure and pulmonaryartery catheterization effectiveness: the ESCAPE trial.JAMA. 2005;294:1625–33.

29. Butman SM, Ewy GA, Standen JR, et al. Bedsidecardiovascular examination in patients with severechronic heart failure: importance of rest or induciblejugular venous distension. J Am Coll Cardiol. 1993;22:968–74.

30. Dao Q, Krishnaswamy P, Kazanegra R, et al. Utilityof B-type natriuretic peptide in the diagnosis ofcongestive heart failure in an urgent-care setting. J AmColl Cardiol. 2001;37:379–85.

31. Davis M, Espiner E, Richards G, et al. Plasma brainnatriuretic peptide in assessment of acute dyspnoea.Lancet. 1994;343:440–4.

32. Drazner MH, Rame JE, Stevenson LW, et al. Prog-nostic importance of elevated jugular venous pressureand a third heart sound in patients with heart failure.N Engl J Med. 2001;345:574–81.

33. Drazner MH, Hellkamp AS, Leier CV, et al. Value ofclinician assessment of hemodynamics in advancedheart failure: the ESCAPE trial. Circ Heart Fail. 2008;1:170–7.

34. Kirkpatrick JN, Vannan MA, Narula J, et al. Echo-cardiography in heart failure: applications, utility, andnew horizons. J Am Coll Cardiol. 2007;50:381–96.

35. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapidmeasurement of B-type natriuretic peptide in theemergency diagnosis of heart failure. N Engl J Med.2002;347:161–7.

36. Moe GW, Howlett J, Januzzi JL, et al. N-terminalpro-B-type natriuretic peptide testing improves themanagement of patients with suspected acute heartfailure: primary results of the Canadian prospectiverandomized multicenter IMPROVE-CHF study. Circula-tion. 2007;115:3103–10.

37. Mueller C, Scholer A, Laule-Kilian K, et al. Use ofB-type natriuretic peptide in the evaluation and man-agement of acute dyspnea. N Engl J Med. 2004;350:647–54.

38. Nagueh SF, Appleton CP, Gillebert TC, et al. Rec-ommendations for the evaluation of left ventriculardiastolic function by echocardiography. Eur J Echo-cardiogr. 2009;10:165–93.

39. Nagueh SF, Bhatt R, Vivo RP, et al. Echocardio-graphic evaluation of hemodynamics in patients withdecompensated systolic heart failure. Circ CardiovascImaging. 2011;4:220–7.

40. van Kimmenade RR, Pinto YM, Bayes-Genis A,et al. Usefulness of intermediate amino-terminal pro-brain natriuretic peptide concentrations for diagnosisand prognosis of acute heart failure. Am J Cardiol.2006;98:386–90.

41. Austen WG, Edwards JE, Frye RL, et al. A reportingsystem on patients evaluated for coronary artery dis-ease. Report of the Ad Hoc Committee for Grading ofCoronary Artery Disease, Council on CardiovascularSurgery, American Heart Association. Circulation. 1975;51:5–40.

42. Alderman EL, Stadius M. The angiographic defini-tions of the bypass angioplasty revascularization inves-tigation. Coronary Artery Disease. 1992;3:1189–207.

43. Louvard Y, Thomas M, Dzavik V, et al. Classificationof coronary artery bifurcation lesions and treatments:time for a consensus! Catheter Cardiovasc Interv.2008;71:175–83.

44. Medina A, Suarez de Lezo J, Pan M. [A new clas-sification of coronary bifurcation lesions]. Rev EspCardiol. 2006;59:183.

45. Hammond WE. eHealth interoperability. StudHealth Technol Inform. 2008;134:245–53.

46. Mead CN. Data interchange standards in health-care IT–computable semantic interoperability: nowpossible but still difficult, do we really need a bettermousetrap? J Healthc Inf Manag. 2006;20:71–8.

47. Fragoso G, de Coronado S, Haber M, et al. Over-view and utilization of the NCI thesaurus. Comp FunctGenomics. 2004;5:648–54.

48. Komatsoulis GA, Warzel DB, Hartel FW, et al.caCORE version 3: implementation of a model driven,service-oriented architecture for semantic interopera-bility. J Biomed Inform. 2008;41:106–23.

49. CDISC Glossary. Available at: http://cdisc.org/therapeutic. Accessed December 12, 2014.

50. LOINC Test. Available at: http://www.loinc.org.Accessed December 12, 2014.

51. van Swieten JC, Koudstaal PJ, Visser MC, et al.Interobserver agreement for the assessment of hand-icap in stroke patients. Stroke. 1988;19:604–7.

52. Radford MJ, Arnold JM, Bennett SJ, et al. ACC/AHAkey data elements and definitions for measuring theclinical management and outcomes of patients withchronic heart failure: a report of the American College ofCardiology/American Heart Association Task Force onClinical Data Standards (Writing Committee to Develop

http://cdisc.org/therapeutic

http://cdisc.org/therapeutic

http://www.loinc.org


415

Heart Failure Clinical Data Standards). Developed incollaboration with the American College of Chest Phy-sicians and the International Society for Heart and LungTransplantation. J Am Coll Cardiol. 2005;46:1179–207.

53. NCDR CathPCI Registry v4.4 Coder’s DataDictionary. Available at: https://www.ncdr.com/WebNCDR/docs/public-data-collection-documents/cathpci_v4_codersdictionary_4-4.pdf?sfvrsn¼2. AccessedDecember 12, 2014.

54. Levine GN, Bates ER, Blankenship JC, et al. 2011ACCF/AHA/SCAI guideline for percutaneous coronaryintervention. A report of the American College ofCardiology Foundation/American Heart AssociationTask Force on Practice Guidelines and the Society forCardiovascular Angiography and Interventions. J AmColl Cardiol. 2011;58:e44–122.

55. Butman SM, editor. Complications of PercutaneousCoronary Interventions. New York, NY: Springer, 2010.

56. National Heart, Lung, and Blood Institute.Coronary artery angiographic changes after percuta-neous transluminal coronary angioplasty. In: Manualof Operations: NHLBI PTCA Registry. Bethesda, MD:National Heart, Lung, and Blood Institute, 1985:6–9.

57. Capone G, Wolf NM, Meyer B, et al. Frequency ofintracoronary filling defects by angiography in anginapectoris at rest. Am J Cardiol. 1985;56:403–6.

58. Cannon CP, Braunwald E, McCabe CH, et al. TheThrombolysis in Myocardial Infarction (TIMI) trials: thefirst decade. J Interv Cardiol. 1995;8:117–35.

59. STS/ACC TVT Registry v2.0 Coder’s Data Dictionary.Available at: https://www.ncdr.com/TVT/Libraries/TVT_

Library/2_0_CoderDataDictionary.sflb.ashx. AccessedDecember 12, 2014.

60. Diehm N, Pattynama PM, Jaff MR, et al.Clinical endpoints in peripheral endovascularrevascularization trials: a case for standardizeddefinitions. Eur J Vasc Endovasc Surg. 2008;36:409–19.

KEY WORDS ACC Data Standards,cardiovascular endpoints, clinical events,clinical trials, death, heart failure, myocardialinfarction, percutaneous coronary intervention,peripheral vascular intervention, stroke,unstable angina

https://www.ncdr.com/WebNCDR/docs/public-data-collection-documents/cathpci_v4_codersdictionary_4-4.pdf?sfvrsn=2




https://www.ncdr.com/TVT/Libraries/TVT_Library/2_0_CoderDataDictionary.sflb.ashx




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APPENDIX 1. AUTHOR RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES (RELEVANT)—

2014 ACC/AHA KEY DATA ELEMENTS AND DEFINITIONS FOR CARDIOVASCULAR ENDPOINT

EVENTS IN CLINICAL TRIALS

Name Employment ConsultantSpeakersBureau

Ownership/Partnership/Principal Research

Institutional,Organizational,

or Other FinancialBenefit

ExpertWitness

Karen A. Hicks, Chair FDA None None None None None None

James E. Tcheng,Vice-Chair

Duke UniversityMedical Center

None None None � NIH � Duke UniversityMedical Center—Philips MedicalSystems

None

Judith H. Lichtman,TFDS Liaison

Yale University Schoolof Medicine,

Department ofEpidemiology and

Public Health

None None None None None None

Marian C. Limacher,AHA Representative

University of Florida,Division of

CardiovascularMedicine


Biykem Bozkurt Michael E. DeBakey VAMedical Center


Bernard R. Chaitman St. Louis UniversitySchool of Medicine,Core ECG Laboratory


Donald E. Cutlip Beth Israel DeaconessMedical Center,InterventionalCardiology


Andrew Farb FDA None None None None None None

Gregg C. Fonarow Ahmanson-UCLACardiomyopathy

Center, Division ofCardiology


Jeffrey P. Jacobs Cardiac SurgicalAssociates


Michael R. Jaff Massachusetts GeneralHospital


Kenneth W. Mahaffey Stanford UniversitySchool of Medicine


Roxana Mehran Mount Sinai MedicalCenter


Steven E. Nissen Cleveland ClinicFoundation,

Department ofCardiovascular

Medicine


Eric E. Smith Calgary Stroke Program,Department of Clinical

Neurosciences


Shari L. Targum FDA None None None None None None

This table represents the relationships of committee members with industry and other entities that were determined to be relevant to this document. These relationships werereviewed and updated in conjunction with all meetings and/or conference calls of the Writing Committee during the document development process. The table does not necessarilyreflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of 5% or more of thevoting stock or share of the business entity, or ownership of $10,000 or more of the fair market value of the business entity; or if funds received by the person from the business entityexceed 5% of the person’s gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in thistable are modest unless otherwise noted.

ACC indicates American College of Cardiology; AHA, American Heart Association; ECG, electrocardiography; FDA, US Food and Drug Administration; TFDS, Task Force on DataStandards; UCLA, University of California Los Angeles; and VA, Veterans Affairs.


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APPENDIX 2. REVIEWER RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES—2014 ACC/AHA KEY

DATA ELEMENTS AND DEFINITIONS FOR CARDIOVASCULAR ENDPOINT EVENTS IN CLINICAL TRIALS

Name Representation Employment ConsultantSpeakersBureau

Ownership/Partnership/Principal Research

Institutional,Organizational,

or OtherFinancialBenefit

ExpertWitness

AthenaPoppas

ACC—Boardof Trustees

Rhode IslandHospital,Division of

Cardiology, andBrown Medical

School—AssociateProfessor ofMedicine


DhanunjayaLakkireddy

ACC—Board ofGovernors

University ofKansas

Hospital—Professor ofMedicine

� St. Jude � BoehringerIngelheim

� Jansen

None None None None

Jean-PierreBassand

ACC—Assemblyof International

Governors

UniversityHospital

Jean-MinjozPole CoeurPoumon

� Bayer � AstraZeneca� GlaxoSmithKline

None None None None

HaroldAdams

AHA—OfficialReviewer

University ofIowa Hospitals &Clinics—Professor,

Neurology


Steven J.Kittner

AHA—OfficialReviewer

University ofMaryland Schoolof Medicine—Professor ofNeurology


Tracy Y.Wang

ACC/AHA TaskForce on DataStandards Lead

Reviewer

Duke UniversitySchool ofMedicine—Associate

Professor ofMedicine

� ACC� AstraZeneca

None None � ASNC� Eli Lilly/Daiichi

Sankyo Alliance� Gilead� GlaxoSmithKline

None None

Kelly P.Anderson

ContentReviewer

MarshfieldClinic


Alfred A. Bove ContentReviewer

Temple UniversityHospital—

Professor ofMedicine

� InsightTele-health,LLC

� WorldHealthNetworks,Inc.

None � InsightTelehealth,LLC

� MerckScheringPlough

None None

VirginiaHoward

ContentReviewer

University ofAlabama at

Birmingham—

Professor

� BayerHealthcare

None None � NIH PrincipalInvestigator

None � Chantixand Risk ofAdverseEvents,2012—Defendant

Ileana L. Pina ContentReviewer

MontefioreMedical

Center—AssociateChief for

Academic Affairs

� GEHealthcare

� Novartis

None None None None None

Diane Reeves ContentReviewer

National CancerInstitute—AssociateDirector, Biomedical

Data Standards


Peter Smith ContentReviewer

MarshfieldClinic


This table represents the relationships of committee members with industry and other entities that were determined to be relevant to this document. These relationships werereviewed and updated in conjunction with all meetings and/or conference calls of the Writing Committee during the document development process. The table does not necessarilyreflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of 5% or more of thevoting stock or share of the business entity, or ownership of $10,000 or more of the fair market value of the business entity; or if funds received by the person from the business entityexceed 5% of the person’s gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in thistable are modest unless otherwise noted.

ACC indicates American College of Cardiology; AHA, American Heart Association; ASNC, American Society of Nuclear Cardiology; and NIH, National Institutes of Health.

TerminologyConcept Concept Definition

Suggested DataElement Label Permissible Values Permissible Value Definit Citations and References

Death—SystemAttribution

Classification of the causeof death by physiologicalsystem.Note: Classification maybe difficult because thisclassificationschema encompassesboth underlying cause(e.g., acute MI) and modeof death concepts(sudden/arrhythmic,progression of HF),and they overlapsubstantially.

Primary Cause of Death � CV: acute MI� CV: sudden cardiac death� CV: HF� CV: stroke� CV: CV procedure� CV: CV hemorrhage� CV: other� Pulmonary� Renal� Gastrointestinal� Hepatobiliary� Pancreatic� Infection� Inflammatory/ immune

(including autoimmune)� Hemorrhage� Non-CV procedure or surgery� Trauma� Suicide� Nonprescription drug reaction or

overdose� Prescription drug reaction or

overdose� Neurological� Malignancy� Other non-CV

http://www.cdisc.org/therapeutic (49)

CV: acute MI Death by any cardiovascular mechanism a,sudden death, HF, stroke, pulmonary em )within 30 d after an acute MI, related to iateconsequences of the MI, such as progrerecalcitrant arrhythmia. There may be a(attributable) mechanisms of cardiovascduring this time period, but for simplicitcardiovascular death occurs within 30 d MI,it will be considered a death due to MI.Note: Acute MI should be verified to the sibleby the diagnostic criteria outlined for ac yautopsy findings showing recent MI or r arythrombosis. Death resulting from a proce t anMI (PCI or CABG), or to treat a complica ngfrom MI, should also be considered dea uteMI. Death resulting from an elective coro dureto treat myocardial ischemia (i.e., chroni ina)or death due to an MI that occurs as a dconsequence of a cardiovascular investigprocedure/operation should be consider thdue to a cardiovascular procedure.

Continued on the next page

APPENDIX 3. DEATH ATTRIBUTION

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ions

(arrhythmibolus, PADthe immed

ssive HF orssessableular deathy, if theof an acute

extent posute MI or becent corondure to treation resultith due to acnary procec stable angirectation/ed as a dea



Suggested DataElement Label Permissible Values Permissible Value Definitions Citations and References

CV: sudden cardiac death Death that occurs unexpectedly and not within 30 d ofan acute MI.Note: Sudden cardiac death includes the followingscenarios:� Death witnessed and occurring without new or

worsening symptoms� Death witnessed within 60 min of the onset of

new or worsening cardiac symptoms unless thesymptoms suggest acute MI

� Death witnessed and attributed to an identifiedarrhythmia (e.g., captured on an electrocardio-graphic recording, witnessed on a monitor, orunwitnessed but found on ICD review)

� Death after unsuccessful resuscitation from car-diac arrest (e.g., ICD unresponsive sudden cardiacdeath, pulseless electrical activity arrest)

� Death after successful resuscitation from cardiacarrest and without identification of a specificcardiac or noncardiac etiology

� Unwitnessed death in a subject seen alive andclinically stable #24 h before being found deadwithout any evidence supporting a specific non-cardiovascular cause of death (information aboutthe patient’s clinical status preceding deathshould be provided if available)

Unless additional information suggests an alternatespecific cause of death (e.g., Death due to Other Car-diovascular Causes), if a patient is seen alive #24 hbefore being found dead, sudden cardiac death (criterion2f) should be recorded. For patients who were notobserved alive within 24 h of death, undetermined causeof death should be recorded (e.g., a subject found deadin bed but who had not been seen by family members for>24 h).

CV: HF Death associated with clinically worsening symptomsand/or signs of HF, regardless of HF etiologyNote: Deaths due to HF can have various etiologies,including single or recurrent MIs, ischemic ornonischemic cardiomyopathy, hypertension, or valvulardisease.

CV: stroke Death after a stroke that is either a direct consequenceof the stroke or a complication of the stroke.Note: Acute stroke should be verified to the extentpossible by the diagnostic criteria outlined for stroke.


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Suggested DataElement Label Permissible Values Permissible Value Defi Citations and References

CV: CV procedure Death caused by the immediate com aCardiovascular procedure

CV: CV hemorrhage Death related to hemorrhage such aintracranial hemorrhage (e.g., subdunonprocedural or nontraumatic vasc g.,aortic aneurysm), or hemorrhage catamponade

CV: other Cardiovascular death not included incategories but with specific, known c AD)

Pulmonary Noncardiovascular death attributabl thelungs (excludes malignancy)

Renal Noncardiovascular death attributabl e

Gastrointestinal Noncardiovascular death attributabl theesophagus, stomach, or intestines (emalignancy)

Hepatobiliary Noncardiovascular death attributabl theliver, gall bladder, or biliary ducts (ex ncy)

Pancreatic Noncardiovascular death attributabl thepancreas (excludes malignancy)

Infection Noncardiovascular death attributabl usdisease.Note: Includes sepsis.

Inflammatory/immune(including autoimmune)

Noncardiovascular death attributablinflammatory or immune-mediated d ssNote: Includes SIRS, immunological, nediseases and disorders. Includes anaenvironmental (e.g., food) allergies.

Hemorrhage Noncardiovascular death attributable at isnot considered cardiovascular hemoaccording to this classification schem

Non-CV procedure or surgery Death caused by the immediate com anoncardiovascular procedure or surg

Trauma Noncardiovascular death attributablIncludes homicide.

Suicide Noncardiovascular death attributabl

Nonprescription drug reaction oroverdose

Noncardiovascular death attributablnonprescription drug reaction or ove



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nitions

plication(s) of

s a nonstrokeral hematoma)ular rupture (e.using cardiac

the aboveause (e.g., PE, P

e to disease of

e to renal failur

e to disease ofxcludes

e to disease ofcludes maligna

e to disease of

e to an infectio

e to anisease or proceand autoimmuphylaxis from

to bleeding thrrhage or strokea

plication(s) ofery

e to trauma.

e to suicide

e to ardose


Suggested DataElement Label Permissible Values Permissible Value Definitions Citations and References

Prescription drug reaction or overdose Noncardiovascular death attributable to a prescriptiondrug reaction or overdose.Note: Includes anaphylaxis.

Neurological Noncardiovascular death attributable to disease of thenervous system (excludes malignancy).Note: Excludes cardiovascular death from ischemicstroke, hemorrhagic stroke, or undetermined cause ofstroke, or cardiovascular hemorrhage of central nervoussystem

Malignancy Noncardiovascular death attributable to leukemia,lymphoma, or other malignancy.

Other non-CV; specify Noncardiovascular death attributable to a cause otherthan those listed in this classification (specify organsystem)

Death—Date–Time

Date and time of death Death Date_Time � Date–time

CABG indicates coronary artery bypass graft; CV, cardiovascular; HF, heart failure; ICD, implantable cardioverter-defibrillator; MI, myocardial infarction; PAD, peripheral artery disease; PCI, percutaneous coronary intervention; PE, pulmonary embolism;and SIRS, systemic inflammatory response syndrome.


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Terminology Concept Concept DefinitionSuggested DataElement Label Permissible Values Permissible Value Definitions Citations and References

Acute MI Clinical syndrome where thereis evidence of myocardialnecrosis in a clinical settingconsistent with acutemyocardial ischemia.

Acute MyocardialInfarction Indicator

� Yes� No

Thygesen K, Alpert JS, Jaffe AS, et al.Third universal definition of myocardialinfarction. J Am Coll Cardiol.2012;60:1581–98 (14).Thygesen K, Alpert JS, Jaffe AS, et al.Third universal definition of myocardialinfarction. Circulation. 2012;126:2020–35 (13).

Acute MI—Date–Time Date and time of onset ofacute MI.

Acute MyocardialInfarctionDate_Time

� Date–time

Acute MI—Type Type of acute MI, classifiedaccording to the Joint ESC/ACCF/AHA/WHF Joint TaskForce for the UniversalDefinition of MyocardialInfarction.Note: cTn-I or -T is thepreferred biomarker. If a cTnassay is not available, the bestalternative is CK-MB(measured by mass assay).

Acute MyocardialInfarction Type

� Type 1: spontaneous� Type 2: ischemic

imbalance� Type 3: death, no

biomarkers� Type 4a: PCI related� Type 4b: stent

thrombosis� Type 4c: stent

restenosis� Type 5: CABG related


Type 1: spontaneous Spontaneous clinical syndrome related to atheroscleroticplaque rupture, ulceration, fissuring, erosion, or dissection,with resulting intraluminal thrombus, and leading todecreased myocardial blood flow or distal platelet emboliwith ensuing myocyte necrosis. This classification requiresa) Detection of a rise and/or fall of [cardiac biomarker]

values (preferably cTn) with at least 1 value >99thpercentile of the URL and

b) At least 1 of the following:1) Symptoms of myocardial ischemia2) New or presumed new significant ST-segment–

T wave (ST–T) changes or new LBBB on the ECG3) Development of pathological Q waves on the ECG4) Imaging evidence of new loss of viable myocardium

or new regional wall motion abnormality5) Identification of an intracoronary thrombus by

angiography or autopsy.Notes: One or more coronary arteries may be involved. Thepatient may have underlying severe CAD but on occasionmay have nonobstructive CAD.


APPENDIX 4. MYOCARDIAL INFARCTION

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Type 2: ischemicimbalance

Spontaneous clinical syndrome where a condition other thanCAD contributes to an imbalance between myocardialoxygen supply and/or demand (e.g., coronary endothelialdysfunction, coronary artery spasm, coronary embolism,tachy-/bradyarrhythmias, anemia, respiratory failure,hypotension, and hypertension with or without LVH). Thisclassification requiresa) Detection of a rise and/or fall of [cardiac biomarker]

values (preferably cTn) with at least 1 value >99thpercentile of the URL and

b) At least 1 of the following:1) Symptoms of myocardial ischemia2) New or presumed new significant ST-segment–

T wave (ST–T) changes or new LBBB on the ECG3) Development of pathological Q waves on the ECG4) Imaging evidence of new loss of viable myocardium

or new regional wall motion abnormality.

Type 3: death, nobiomarkers

Death where symptoms suggestive of myocardial ischemiaare present, and with (presumed) new ischemic changes ornew LBBB on ECG, but where death occurs before cardiacbiomarkers can be obtained or could rise or (in rare cases)were not collected.

Type 4a: PCI related MI associated with and occurring within 48 h of PCI, withelevation of cardiac biomarker values to >5 � 99thpercentile of the URL in patients with normal baseline values(#99th percentile URL), or a rise of [cardiac biomarker]values $20% if baseline values are elevated and are stableor falling. This classification also requires at least 1 of thefollowing:a) Symptoms suggestive of myocardial ischemia

(i.e., prolonged ischemia $20 min)b) New ischemic changes on ECG or new LBBBc) Angiographic loss of patency of a major coronary

artery or a side branch or persistent slow flow or noflow or embolization

d) Imaging evidence of new loss of viable myocardium ornew regional wall motion abnormality.

Type 4b: stentthrombosis

MI associated with stent thrombosis as detected by coronaryangiography or at autopsy, where symptoms suggestive ofmyocardial ischemia are present, and with a rise and/or fallof [cardiac biomarker] values, with at least 1 value >99thpercentile of the URL.



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Terminology Concept Concept DefinitionSuggested DataElement Label Permissible Values Permissible Value Defini Citations and References

Type 4c: stent restenosis MI associated with stent restenosis as de ronaryangiography or at autopsy, occurring >48 ,without evidence of stent thrombosis bu omssuggestive of myocardial ischemia, and w of[cardiac biomarker] values to >99th perc URL.This classification also requires the followa) Does not meet criteria for any other n

of MIb) Presence of a $50% stenosis at the ious

successful stent PCI or a complex le othersignificant obstructive CAD of greatfollowing1) Initially successful stent deploym2) Dilation of a coronary artery sten alloon

angioplasty to <50% stenosisNote: Type 4c is described in the text of t iversalDefinition of Myocardial Infarction.”

Type 5: CABG related MI associated with and occurring within 4surgery, with elevation of [cardiac bioma to>10 � 99th percentile of the URL in pat rmalbaseline cardiac biomarker values (#99th RL).This classification also requires at least 1 ing:a) New pathological Q waves, new LBBb) Angiographic new graft or new nativ artery

occlusionc) Imaging evidence of new loss of viab ium or

new regional wall motion abnormal

Acute MI—Symptoms,Acute

Presence of acute symptomsof myocardial ischemia, suchas chest, upper extremity,mandibular, or epigastricdiscomfort, or an ischemicequivalent such as dyspnea orfatigue. This is one of thenoncardiac marker criteriasupporting the diagnosis ofacute MI types 1, 2, 3, 4a, 4b,and 4c.

Myocardial IschemiaAcute SymptomIndicator

� Yes� No


Acute MI—SymptomOnset Date–Time

Date and time of onset ofsymptoms of acute MI.

Myocardial IschemiaSymptom OnsetDate_Time

� Date–time


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tions

tected by coh after PCI

t with symptith elevationentile of theing:classificatio

site of prevsion and noer severity

ent, orosis with b

he “Third Un

8 h of CABGrker] valuesients with nopercentile Uof the followB on ECGe coronary

le myocardity.


Acute MI—Acute IschemicChangeson ECG

Presence of new or presumednew significant ST-segment–Twave (ST-T) changes or newLBBB consistent with acutemyocardial ischemia. This isone of the noncardiac markercriteria supporting thediagnosis of acute MI types 1,2, 3, and 4.

Acute Ischemic ECGChange Type

� Ischemic changes onECG

� LBBB


Ischemic changes on ECG In the absence of LVH and LBBB pattern (or otherconfounder such as a paced rhythm) on ECG, either a) new(or presumed new) ST elevation at the J point in 2contiguous leads with the following cut points: $0.1 mV inall leads other than leads V2 to V3 where the following cutpoints apply: $0.2 mV in men $40 y of age; $0.25 mV inmen <40 y of age, or $0.15 mV in women; or b) new (orpresumed new) horizontal or downsloping ST-segmentdepression $0.05 mV in 2 contiguous leads and/or Tinversion $0.1 mV in 2 contiguous leads with prominent Rwave or R/S ratio >1.

LBBB New (or presumed new) LBBB pattern on ECG.

Acute MI—New Q Waveson ECG

Presence of new or presumednew pathological Q wavesconsistent with MI. This is oneof the noncardiac markercriteria supporting thediagnosis of acute MI types 1,2, 4, and 5.

ECG Change, NewQ-Wave Indicator

� New Q waves New (or presumed new) a) Q wave in leads V2 toV3 $0.02 s or QS complex in leads V2 and V3; b) Qwave $0.03 s and $0.1 mV deep or QS complex in leads I, II,aVL, aVF, or V4 to V6 in any 2 leads of a contiguous leadgrouping (I, aVL; V1 to V6; II, III, aVF; V7 to V9); or c) Rwave $0.04 s in V1 to V2 and R/S $1 with a concordantpositive T wave in the absence of a conduction defect.


Acute MI—CoronaryThrombus Present

Presence of thrombus in amajor epicardial vesselconsistent with an acute MI.This is one of the noncardiacmarker criteria supporting thediagnosis of acute MI type 1.

Identification ofCoronary ArteryThrombus WithAcute MyocardialInfarction

� Thrombus onangiography

� Thrombus at autopsy


Thrombus onangiography

In the patient with a presumed acute STEMI, theangiographic appearance of thrombus (typically a fillingdefect) on angiography. This includes the aspiration ofthrombus from the infarct vessel before coronaryintervention during primary PCI for acute STEMI.

Thrombus at autopsy Identification of thrombus in a major epicardial vessel atautopsy.


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Acute MI—Change inNoninvasive Imaging

Demonstration of a newchange in myocardial viabilityor function consistent withMI. This is one of thenoncardiac marker criteriasupporting the diagnosis ofacute MI types 1, 2, 4a, and 5.

Change in Non-Invasive ImagingType

� New loss of viablemyocardium

� New regional wallmotion abnormality


New loss of viablemyocardium

Noninvasive imaging evidence of a loss of viable myocardiumwhen compared with the most recent previous noninvasiveimaging study.

New regional wall motionabnormality

Noninvasive imaging evidence of a decrease in regional wallmotion contractility compared with the most recent previousnoninvasive imaging study.

Acute MI—PCIAngiographicComplication

Occurrence of an adverseangiographic finding duringPCI consistent with acutemyocardial ischemia. This isone of the noncardiac markercriteria supporting thediagnosis of acute MI type 4a.

PCI AcuteAngiographicComplication

� Loss of majorcoronary

� Loss of side branch� Slow flow/no flow/

embolization


Loss of major coronary Angiographic loss of patency of a major epicardial vessel.

Loss of side branch Angiographic loss of patency of a side branch.

Slow flow/no flow/embolization

Angiographic reduction of flow into the coronarymicrocirculation.

Acute MI—Acute VesselOcclusion After CABG

Angiographic documentationof a new CABG or new nativecoronary artery occlusionwithin 48 h of CABG surgery.This is one of the noncardiacmarker criteria supporting thediagnosis of acute MI type 5.

Vessel OcclusionAfter CoronaryArtery Bypass GraftSurgery Indicator

� Yes� No



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Prior MI Presence of any one of thefollowing criteria meets thediagnosis for prior MI (beforestudy initiation):a) Pathological Q waves

with or without symp-toms in the absence ofnonischemic causes

b) Imaging evidence of aregion of loss of viablemyocardium that is thin-ned and/or fails to con-tract, in the absence of anonischemic cause

c) Pathological findings of aprior MI.

Prior MyocardialInfarction Indicator

� Yes� No


Cardiac Biomarker—Name Name of cardiac biomarkertest, per LOINC nomenclature.

Cardiac BiomarkerTest

� LOINC Test Name LOINC�. Available at www.loinc.org(50).

Cardiac Biomarker—Value Serum concentration result ofa cardiac biomarker test.

Cardiac BiomarkerValue

� Value

Cardiac Biomarker—Unit Unit of measure of the resultof a cardiac biomarker test.

Cardiac BiomarkerUnit

� nanogram per liter� nanogram per

milliliter� pictogram per

milliliter

Cardiac Biomarker—Date–Time

Date and time a specimen wasobtained for the assay of acardiac biomarker.

Cardiac BiomarkerDate_Time

� Date–time

Cardiac Biomarker—99%URL

The 99% URL of a cardiacbiomarker.

Cardiac Biomarker99% URL Value

� Value

Cardiac Biomarker—99%URL Unit

Unit of measure of the 99%URL of a cardiac biomarker.

Cardiac Biomarker99% URL Unit



milliliter

Cardiac Biomarker—ULN The ULN of a cardiacbiomarker.

Cardiac BiomarkerULN Value

� Value

Cardiac Biomarker—ULNUnit

Unit of measure of the ULN ofa cardiac biomarker.

Cardiac BiomarkerULN Unit



milliliter

ACC indicates American College of Cardiology; ACCF, American College of Cardiology Foundation; AHA, American Heart Association; CABG, coronary artery bypass graft; CAD, coronary artery disease; CK-MB, creatinine kinase MB; cTn, cardiac troponin;ECG, electrocardiogram; ESC, European Society of Cardiology; HF, heart failure; ICD, implantable cardioverter-defibrillator; LBBB, left bundle-branch block; LOINC, Logical Observation Identifiers Names and Codes; LVH, left ventricular hypertrophy;MI, myocardial infarction; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction; ULN, upper limit of normal; URL, upper reference limit; and WHF, World Heart Federation.


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APPENDIX 5. HOSPITALIZATION FOR UNSTABLE ANGINA

Terminology Concept Concept Definition

SuggestedData Element

LabelPermissible

ValuesPermissible Value

DefinitionsCitations andReferences

UA Hospitalization Unscheduledhospitalization for themanagement of UA,occurring within 24 hof the most recentsymptoms.Hospitalization is definedas an admission to aninpatient unit or a visit toan ED that results in atleast a 24-h stay (or achange in calendar date ifthe hospital admission ordischarge times are notavailable).This classification requiresthat 4 separate criteria bemet:a) Worsening ischemic

discomfortb) Unscheduled

hospitalizationc) Objective evidence of

myocardial ischemiad) Negative cardiac

biomarkersNote: Escalation of phar-macotherapy for myocar-dial ischemia, whileconsidered supportiveevidence, is not sufficientto qualify as UA hospital-ization without objectiveevidence of ischemia.Admission for suspectedUA does not qualify as aUA hospitalization if anoncardiac or non-ischemic etiology is sub-sequently identified.An ischemic eventmeeting the criteria foracute MI is not a UA hos-pitalization.Planned hospitalization orrehospitalization for per-formance of an electiverevascularization proce-dure (e.g., positive stresstest, staged revasculari-zation) is not a UA hospi-talization.Hospitalization withrevascularization of CADidentified during electivecardiac catheterizationdoes not qualify as a UAhospitalization.

Unstable AnginaEvent Indicator

� Yes� No

Adapted from CannonCP, Brindis RG,Chaitman BR, et al.2013 ACCF/AHA keydata elements anddefinitions formeasuring the clinicalmanagement andoutcomes of patientswith acute coronarysyndromes andcoronary artery disease.A report of theAmerican College ofCardiology Foundation/American HeartAssociation Task Forceon Clinical DataStandards (WritingCommittee to DevelopAcute CoronarySyndromes andCoronary ArteryDisease Clinical DataStandards). J AmColl Cardiol.2013;61:992–1025 (16).

UA Hospitalization—Date–Time

Date and time of thepresentation of thepatient to the hospital formanagement of UA.Date and time ofpresentation is defined asthe date and time ofregistration in the ED (orhospital, if the patient isnot seen in the ED).

Unstable AnginaHospitalizationDate_Time

� Date–time



429




LabelPermissible



UA Hospitalization—Symptoms ofIschemia

Documentation ofischemic discomfort(angina, or symptomsthought to beequivalent) $10 min induration occurring eithera) At rest, orb) In an accelerating

pattern withfrequent episodesassociated with pro-gressively decreasingexercise capacity.

Unstable AnginaIschemic DiscomfortIndicator

� Yes� No

Adapted from CannonCP, Brindis RG,Chaitman BR, et al.2013 ACCF/AHA keydata elements anddefinitions formeasuring the clinicalmanagement andoutcomes of patientswith acute coronarysyndromes andcoronary artery disease.A report of theAmerican College ofCardiology Foundation/American HeartAssociation Task Forceon Clinical DataStandards (WritingCommittee to DevelopAcute CoronarySyndromes andCoronary ArteryDisease Clinical DataStandards). J Am CollCardiol. 2013;61:992–1025 (16).

UA Hospitalization—Evidence ofIschemia

Documentation ofobjective evidence of newor worsening coronaryischemia.

Unstable AnginaIschemic EvidenceType

� Changes onresting ECG

� Induciblemyocardialischemia

� Coronary lesionon angiography

� Coronaryrevascularization

Changes onresting ECG

New or worsening STor T-wave changes onresting ECG (in theabsence of confounders,such as LBBB or LVH),defined as eithera) Transient ST elevation

(duration <20 min):new ST elevation at theJ point $0.1 mV in any2 contiguous leads(other than leads V2

to V3); in leads V2 to V3,the following cutpoints apply: $0.2 mVin men $40 y ofage, $0.25 mV inmen <40 y of age,and $0.15 mV inwomen.

b) ST depression andT-wave changes:new horizontal ordownsloping STdepression $0.05 mVin 2 contiguousleads and/or new Tinversion $0.3 mV in2 contiguous leads withprominent R wave orR/S ratio >1.




LabelPermissible



Inducible myocardialischemia

Definite evidence ofinducible myocardialischemia believed tobe responsible for themyocardial ischemicsymptoms/signs,demonstrated by anyof the following:a) An early positive

exercise stress testresult, defined asST elevation or $2 mmST depression before5 METs

b) Stress echocardi-ography (reversiblewall motionabnormality)

c) Myocardial scinti-graphy (reversibleperfusion defect)

d) MRI (myocardialperfusion deficitunder pharmacologicalstress)

Coronary lesion onangiography

Angiographic evidenceof new or worseninglesion $70% ($50% forleft main coronary arterylesion) and/or thrombus inan epicardial coronaryartery believed to beresponsible for themyocardial ischemicsymptoms/signs.

Coronary revascularization Need for coronaryrevascularization procedure(PCI or CABG) for thepresumed culprit lesion(s).This criterion would befulfilled if revascularizationwas undertaken duringthe unscheduledhospitalization orsubsequent to transferto another institutionwithout intercedinghome discharge.

UA Hospitalization—MI Excluded

Exclusion of the diagnosisof MI as the reason forhospitalization, includingnegative cardiacbiomarkers and no otherevidence of acute MI.

Myocardial InfarctionExclusion Indicator

� Yes� No

ACCF indicates American College of Cardiology Foundation; AHA, American Heart Association; CABG, coronary artery bypass graft; CAD, coronary artery disease; ECG, electrocar-diogram; ED, emergency department; LBBB, left bundle-branch block; LVH, left ventricular hypertrophy; METs, metabolic equivalents; MI, myocardial infarction, MRI, magneticresonance imaging; PCI, percutaneous coronary intervention; and UA, unstable angina.




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431

APPENDIX 6. TRANSIENT ISCHEMIC ATTACK AND STROKE


Suggested DataElement Name

PermissibleValues

Permissible ValueDefinitions

Citations andReferences

Stroke An acute episode of focalor global neurologicaldysfunction caused by brain,spinal cord, or retinal vascularinjury as a result ofhemorrhage or infarction.

Stroke Indicator � Yes� No

Adapted from Sacco RL,Kasner SE, Broderick JP, et al.An updated definition ofstroke for the 21st century: astatement for healthcareprofessionals from theAmerican Heart Association/American Stroke Association.Stroke. 2013;44:2064–89(19).

Stroke—Date–Time Date and time of the onset ofa stroke.

Stroke Date_Time � Date–time

Stroke—Type Categorical description ofstroke type, classified into1 of 3 mutually exclusivecategories (ischemic,hemorrhagic, undetermined).

Stroke Type � Ischemic� Hemorrhagic� Undetermined

Adapted from Sacco RL,Kasner SE, Broderick JP, et al.An updated definition ofstroke for the 21st century: astatement for healthcareprofessionals from theAmerican Heart Association/American Stroke Association.Stroke. 2013;44:2064–89(19).

Ischemic An acute episode of focalcerebral, spinal, or retinaldysfunction caused byinfarction of central nervoussystem tissue.Note: Hemorrhage may be aconsequence of ischemicstroke. In this situation, thestroke is an ischemic strokewith hemorrhagictransformation and not ahemorrhagic stroke.

Hemorrhagic Hemorrhagic: An acuteepisode of focal or globalcerebral or spinal dysfunctioncaused by intraparenchymal,intraventricular, orsubarachnoid hemorrhage.Note: Subdural hematomasare intracranial hemorrhagicevents and not strokes.

Undetermined Undetermined: An acuteepisode of focal or globalneurological dysfunctioncaused by presumed brain,spinal cord, or retinal vascularinjury as a result ofhemorrhage or infarction butwith insufficient informationto allow categorization aseither ischemic orhemorrhagic.

Modified RankinScale

Validated scale forassessment of disabilityfollowing a stroke.Note: Measure disability withthe modified Rankin Scale ateach visit and 90 d after theevent.

Modified RankinScale Value

� 0� 1� 2� 3� 4� 5� 6

Rankin J. Cerebral vascularaccidents in patients over theage of 60. Scott Med J.1957;2:200–15 (26).van Swieten J, Koudstaal P,Visser M, et al. Interobserveragreement for the assessmentof handicap in stroke patients.Stroke. 1988;19:604–7 (51).




PermissibleValues



0 No symptoms at all.

1 No significant disabilitydespite symptoms; able tocarry out all usual duties andactivities.

2 Slight disability; unable toperform all previous activitiesbut able to look after ownaffairs without assistance.

3 Moderate disability; requiringsome help but able to walkwithout assistance.

4 Moderately severe disability;unable to walk withoutassistance and unable toattend to own bodily needswithout assistance.

5 Severe disability; bedridden,incontinent, and requiringconstant nursing care andattention.

6 Dead.

Modified RankinScale—Date–Time

Date and time of neurologicalassessment to determinemodified Rankin scale grade.

Rankin Scale Date_Time Date–time

TIA Transient episode of focalneurological dysfunctioncaused by brain, spinal cord,or retinal ischemia withoutacute infarction.Note: Persistence ofsymptoms is an acceptableindicator of acute infarction. Ifit is used, duration ofsymptom persistence that willbe used to distinguishbetween transient ischemiaand acute infarction should bedefined for any clinical trial inwhich it is used.Note: AHA/ASA recommendsduration $24 h as anoperational definition ofpersisting symptoms of strokerather than TIA, based mostlyon consensual practice ratherthan objective evidence.

Transient Ischemic AttackIndicator

� Yes� No

Easton JD, Saver JL, AlbersGW, et al. Definition andevaluation of transientischemic attack: a scientificstatement for healthcareprofessionals from theAmerican Heart Association/American Stroke AssociationStroke Council; Council onCardiovascular Surgery andAnesthesia; Council onCardiovascular Radiology andIntervention; Council onCardiovascular Nursing; andthe Interdisciplinary Councilon Peripheral VascularDisease. Stroke.2009;40:2276–93 (9).Sacco RL, Kasner SE,Broderick JP, et al. Anupdated definition of strokefor the 21st century: astatement for healthcareprofessionals from theAmerican Heart Association/American Stroke Association.Stroke. 2013;44:2064–89(19).

TIA—Date–Time Date and time of the onset ofa TIA.

Transient Ischemic AttackDate_Time

Date–time

AHA indicates American Heart Association; ASA, American Stroke Association; and TIA, transient ischemic attack.




432

PPENDIX 7. HEART FAILURE EVENT


433

A

Terminology Concept Concept DefinitionSuggested DataElement Name

PermissibleValues



HF Event Presentation of the patientfor an urgent, unscheduledclinic/office/ED visit orhospital admission, with aprimary diagnosis of HF,where the patient exhibitsnew or worseningsymptoms of HF onpresentation, has objectiveevidence of new orworsening HF, and receivesinitiation or intensificationof treatment specificallyfor HF.Objective evidence consistsof at least 2 physicalexamination findings OR atleast 1 physical examinationfinding and at least 1laboratory criterion of newor worsening HF onpresentation.

Heart FailureEndpoint Event

� Yes� No


HF Event—Date–Time Date and time of thepresentation of a patientfor management of aHF event.

Heart FailureEndpoint EventDate_Time

� Date–time

HF Event—EncounterType

The type of healthcareencounter of a patientwho presents for themanagement of new-onsetor worsening HF.

Heart FailureEndpoint EventHealthcareEncounter Type

� HF hospitalization� Urgent HF visit


HF hospitalization An event where thepatient is admitted to thehospital with a primarydiagnosis of HF where thelength of stay is at least24 h (or extends over acalendar date if thehospital admission anddischarge times areunavailable), where thepatient exhibits new orworsening symptoms ofHF on presentation, hasobjective evidence of newor worsening HF, andreceives initiation orintensification oftreatment specificallyfor HF.

Urgent HF visit An event where thepatient has an urgent,unscheduled office/practice/ED visit for aprimary diagnosis of HFbut is not admitted to thehospital, where the patientexhibits new or worseningsymptoms of HF onpresentation, has objectiveevidence of new orworsening HF,and receives initiationor intensification oftreatment specifically forHF, with the exceptionthat changes to oraldiuretic therapy do notqualify as initiation orintensification oftreatment.







PermissibleValues



HF Event—Symptoms,New or Worsening

Documentation of new orworsening symptoms of HFon patient presentation.Criterion for new orworsening symptoms due toHF is to have at least 1 ofthe following onpresentation:a) Dyspneab) Decreased exercise

tolerancec) Fatigued) Worsened end-organ

perfusione) Volume overload

Heart Failure Symptoms,New or Worsening

� Dyspnea� Decreased exercise

tolerance� Fatigue� Worsened end-organ

perfusion� Volume overload

Adapted from RadfordMJ, Arnold JM, BennettSJ, et al. ACC/AHA keydata elements anddefinitions for measuringthe clinical managementand outcomes of patientswith chronic heartfailure: a report of theAmerican College ofCardiology/AmericanHeart Association TaskForce on Clinical DataStandards (WritingCommittee to DevelopHeart Failure ClinicalData Standards).Developed incollaboration with theAmerican College ofChest Physicians and theInternational Society forHeart and LungTransplantation.Circulation.2005;112:1888–916 (52).

Dyspnea Includes dyspnea onexertion, dyspnea at rest,orthopnea, andparoxysmal nocturnaldyspnea.

Decreased exercisetolerance

Decreased exercisetolerance: reduced abilityto withstand or participatein activities that inducephysical or mentalexertion.

Fatigue Unusual tiredness andinability to perform usualactivities.

Worsened end-organperfusion

Decreased blood supply tothe vital organs (kidney,liver, lungs, heart, andbrain).Note: Parameters must bespecified and described bythe study protocol.

Volume overload Excessive accumulation ofintravascular fluidresulting fromcompromised regulatorymechanisms.Note: Parameters must bespecified and described bythe study protocol.

HF Event—PhysicalExamination, New orWorsening

Documentation of new orworsening physicalexamination findings of HFon patient presentation.Criterion for new orworsening objectivefindings due to HF includesat least 2 physicalexamination findings OR 1physical examinationfinding and at least 1laboratory criterion.Physical examinationfindings include new orworsened:

Heart Failure PhysicalExamination Findings,New or Worsening

� Peripheral edema� Increasing abdominal

distention or ascites� Pulmonary rales/

crackles/crepitations� Increased jugular

venous pressure and/or hepatojugularreflux

� S3 gallop� Clinically significant

or rapid weight gain

Adapted from RadfordMJ, Arnold JM, BennettSJ, et al. ACC/AHA keydata elements anddefinitions for measuringthe clinical managementand outcomes of patientswith chronic heartfailure: a report of theAmerican College ofCardiology/AmericanHeart Association TaskForce on Clinical DataStandards (WritingCommittee to Develop





434


PermissibleValues



a) Peripheral edemab) Increasing abdominal

distention or ascitesc) Pulmonary rales/

crackles/crepitationsd) Increased jugular

venous pressure and/orhepatojugular reflux

e) S3 gallopf) Clinically significant or

rapid weight gainthought to be relatedto fluid retention

Heart Failure ClinicalData Standards).Developed incollaboration with theAmerican College ofChest Physicians and theInternational Society forHeart and LungTransplantation.Circulation.2005;112:1888–916 (52).

Peripheral edema Increased tissue fluidindicated by perceptiblepitting indentation onlower leg, foot, or sacrumafter palpation.

Increasing abdominaldistention or ascites

Intra-abdominal fluidaccumulation asdetermined by physicalexamination (in theabsence of primary hepaticdisease).

Pulmonary rales/crackles/crepitations

Pulmonary rales/crackles/crepitations: Abnormalbreath sounds caused bythe accumulation of fluidin the lungs.

Increased jugular venouspressure and/orhepatojugular reflux

Increase in the estimatedheight of the mean jugularvenous waveform abovethe right atrium incentimeters.Note: When expressed ascentimeters withoutfurther description, thenumber should berecorded as written. Whenit is expressed ascentimeters above thesternal angle, 5 cm shouldbe added to the numberrecorded. In the absenceof a numerical estimate ofjugular venous pressure,“JVD,” “distended neckveins,” and “halfway to thejaw” or “to the angle ofthe jaw” would berecorded as positive forelevated jugular venouspressure.

S3 gallop Presence of an S3 mid-diastolic heart sound.

Clinically significantor rapid weight gain

Weight gain thought to berelated to fluid retention.

HF Event—LaboratoryData, New orWorsening

Documentation of new orworsening laboratoryevidence of HF obtainedwithin 24 h of patientpresentation.Criterion for new orworsening objectivefindings due to HF includesat least 2 physicalexamination findings OR 1physical examinationfinding and at least 1laboratory criterion.Laboratory criteria includenew or worsened:

Heart Failure LaboratoryFindings, New orWorsening

� Increase in HFbiomarker

� Radiological evi-dence of pulmonarycongestion

� Noninvasive diag-nostic evidence of HF

� Invasive diagnosticevidence of HF

Adapted from: RadfordMJ, Arnold JM, BennettSJ, et al. ACC/AHA keydata elements anddefinitions for measuringthe clinical managementand outcomes of patientswith chronic heartfailure: a report of theAmerican College ofCardiology/AmericanHeart Association TaskForce on Clinical DataStandards (WritingCommittee to Develop




435


PermissibleValues



a) Increased BNP/NT-proBNP

b) Radiological evidenceof pulmonarycongestion

c) Noninvasive diagnosticevidence of HF

d) Invasive diagnostic ev-idence of HF

Heart Failure ClinicalData Standards).Developed incollaboration with theAmerican College ofChest Physicians and theInternational Society forHeart and LungTransplantation.Circulation.2005;112:1888–916 (52).

Increase in HF biomarker Biomarker increase BNP/NT-pro BNP withdecompensation of HF(such as BNP >500 pg/mLor NT-proBNP >2,000pg/mL). In patients withchronically elevatednatriuretic peptides, asignificant increase abovebaseline is required.

Radiological evidence ofpulmonary congestion

Radiological evidence ofpulmonary congestion:imaging findingsconsistent with increasedintravascular bloodvolume in the lungs.

Noninvasive diagnosticevidence of HF

Noninvasive diagnosticevidence of HF:Noninvasive diagnosticevidence of clinicallysignificant elevated left-or right-sided ventricularfilling pressure or lowcardiac output. Forexample,echocardiographic criteriacould include E/e’ >15 orD-dominant pulmonaryvenous inflow pattern,plethoric inferior venacava with minimal collapseon inspiration, ordecreased LVOT minutestroke distance (TVI).

Invasive diagnosticevidence of HF

Invasive diagnosticevidence with right-sidedcatheterization of heartshowing a PCWP(pulmonary arteryocclusion pressure) $18mmHg, central venouspressure $12 mmHg,or a cardiacindex <2.2 L/min/m2.

HF Event—TreatmentIntensification

Initiation or intensificationof treatment specificallyfor HF. The criterion is thatthe patient receives initiationor intensification oftreatment specifically forHF, including at least 1of the following:a) Augmentation in oral

diuretic therapyb) Intravenous diuretic or

vasoactive agent (e.g.,inotrope, vasopressor,or vasodilator)

c) Mechanical or surgicalintervention

Heart Failure Therapy,Intensification

� Augmentation of oraldiuretic therapy

� Intravenous diuretic,inotrope, or vasodi-lator therapy

� Mechanical or surgi-cal intervention

Adapted from RadfordMJ, Arnold JM, BennettSJ, et al. ACC/AHA keydata elements anddefinitions for measuringthe clinical managementand outcomes of patientswith chronic heartfailure: a report of theAmerican College ofCardiology/AmericanHeart Association TaskForce on Clinical DataStandards (WritingCommittee to DevelopHeart Failure ClinicalData Standards).





436


PermissibleValues



Developed incollaboration with theAmerican College ofChest Physicians and theInternational Society forHeart and LungTransplantation.Circulation.2005;112:1888–916 (52).

Augmentation of oraldiuretic therapy

Initiation or intensificationof orally administeredmedication(s) thatpromote diuresis totreat HF.

Intravenous diuretic,inotrope, vasopressor, orvasodilator therapy

Initiation or intensificationof medication(s)administered by vein totreat HF, increaseproduction of urine,increase cardiacperformance, and/orreduce cardiac preload orafterload.

Mechanical or surgicalintervention

Mechanical circulatorysupport (e.g., intra-aorticballoon pump, ventricularassist device,extracorporeal membraneoxygenation, total artificialheart) or mechanical fluidremoval (e.g.,ultrafiltration,hemofiltration, dialysis).

Cardiogenic Shock Sustained (>30 min)episode of systolicBP <90 mmHg and/orcardiac index <2.2 L/min/m2 determined to besecondary to cardiacdysfunction, and/or therequirement for parenteralinotropic or vasopressoragents or mechanicalsupport (e.g., intra-aorticballoon pump,extracorporeal circulatorysupport, ventricular assistdevice) to maintain BP andcardiac index above thosespecified levels.

Cardiogenic ShockIndicator

� Yes� No

Cannon CP, Brindis RG,Chaitman BR, et al.2013 ACCF/AHA key dataelements and definitionsfor measuring the clinicalmanagement andoutcomes of patientswith acute coronarysyndromes and coronaryartery disease: a reportof the American Collegeof CardiologyFoundation/AmericanHeart Association TaskForce on Clinical DataStandards (WritingCommittee to DevelopAcute CoronarySyndromes and CoronaryArtery Disease ClinicalData Standards). J AmColl Cardiol.2013;61:992–1025 (16).

ACCF indicates American College of Cardiology Foundation; AHA, American Heart Association; BNP, B-type natriuretic peptide; BP, blood pressure; cm, centimeter; ED, emergencydepartment; HF, heart failure; JVD, jugular venous distention; L/min/m2, liter per minute per square millimeter; LVOT, left ventricular outflow tract; mmHg, millimeters of mercury;NT-pro BNP, N-terminal pro B-type natriuretic peptide; PCWP, pulmonary capillary wedge pressure; and TVI, time velocity integral.



437

� A Heart Failure Event includes hospitalization for HF and may include urgent, unscheduled outpatient office/practice or ED visits.– A Heart Failure Hospitalization is defined as an event in which the patient is admitted to the hospital with a primary diagnosis of HF, the length of stay is

at least 24 h (or extends over a calendar date), the patient exhibits new or worsening symptoms of HF on presentation, has objective evidence of new orworsening HF, and receives initiation or intensification of treatment specifically for HF.

– An Urgent Heart Failure Visit is defined as an event in which the patient has an urgent, unscheduled office/practice or ED visit for a primary diagnosis ofHF but is not admitted to the hospital and exhibits new or worsening symptoms of HF on presentation, has objective evidence of new or worsening HF,and receives initiation or intensification of treatment specifically for HF. Note that changes to oral diuretic therapy do not qualify as initiation orintensification of treatment.

� Heart Failure Symptoms: The patient may present with new or worsening symptoms due to HF on presentation. To be defined as having new or worseningsymptoms due to HF, the patient should have at least at least 1 of the following on presentation:– Dyspnea (dyspnea with exertion, dyspnea at rest, orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough in supine position, tachypnea);– Decreased exercise tolerance (reduced ability to perform activities that involve dynamic movement of large skeletal muscles because of symptoms of

dyspnea or fatigue);– Fatigue (usually described as feeling a lack of energy and motivation in both mental and physical activities, easily tiring and not being able to complete

usual activities, and sometimes accompanied by dizziness, lightheadedness);– Worsened end-organ perfusion (worsening cerebral, renal, liver, abdominal or gastrointestinal, peripheral circulatory function manifested by symptoms

such as dizziness, lightheadedness, syncope, confusion, altered mental status, restlessness, decline in cognitive state, nausea, vomiting, abdominal pain,abdominal fullness, abdominal discomfort or abdominal tenderness, cold clammy extremities, discoloration of extremities or lips, jaundice, pain inextremities, reduced urine output, darkening of urine color, chest pain, and/or palpitations); or

– Other symptoms of volume overload (swelling of lower extremities; swelling or indentation of pressure marks in areas of fluid accumulation such as thelegs, ankles, or lower back; an increase in abdominal girth, right-sided abdominal fullness, discomfort, or tenderness; an increase in body weight; oozingand development of skin breakdown in lower extremities).

� Heart Failure Signs: The patient may present with objective evidence of new or worsening HF. The objective evidence or signs of new or worsening HFshould consist of at least 2 physical examination findings OR 1 physical examination finding and at least 1 laboratory criterion. Physical examination findingsconsidered to be due to HF include new or worsened:– Peripheral edema (swelling or pitting indentation when pressed in feet, ankles, legs, thighs, upper extremities, scrotum, presacral area, or abdominal

wall).– Increasing abdominal distention or ascites (in the absence of primary hepatic disease)– Pulmonary rales/crackles/crepitations– Increased jugular venous pressure and/or hepatojugular reflux– S3 gallop– Clinically significant or rapid weight gain thought to be related to fluid retention (usually >3–4 lb in 3–4 d).Other physical findings such as the following may also support the diagnosis: a decline in systolic or diastolic blood pressure; orthostatic hypotension; cool,mottled or clammy skin; lip discoloration and cyanosis; tachypnea; irregular or periodic breathing pattern (e.g., Cheyne-Stokes respirations); tachycardia orbradycardia; arrhythmia; irregular pulse; pulsus alternans; displaced point of maximum impulse of cardiac apex; RV heave; loud S2; diminished S1; S4;valvular murmurs; reduced urine output; liver enlargement; physical findings compatible with pleural effusion such as decreased breath sounds and ordecreased egophony; narrow pulse pressure; abnormal arterial pulse pressure response during the strain phase of the Valsalva maneuver; weight loss;and/or wheezing (29,32,33). Because these physical findings are not as common, sensitive, specific, or easily reproducible for HF as those listed in the bulletpoints above, they are not included in the required physical findings criteria.

� Laboratory Evidence of HF: Laboratory evidence of new or worsening HF should be obtained within 24 h of presentation.Laboratory criteria include new or worsened:

– Increased BNP or NT-proBNP concentrations. In patients with suspected new onset of HF, or in patients with dyspnea but uncertainty of HF,measurement of BNP or NT-proBNP is useful to support the clinical diagnosis of HF (30,31,35,39,40). In acute decompensated HF, natriuretic peptidelevels are usually significantly elevated (e.g., BNP >500 pg/mL or NT-proBNP >2,000 pg/mL). The exclusion threshold differs for patients presentingwith acute onset or worsening of symptoms and for those presenting with more gradual onset of symptoms. For patients presenting with acute onset orworsening of symptoms, the optimal exclusion cut-off points are usually quoted as 300 pg/mL for NT-proBNP and 100 pg/mL for BNP levels. Lowervalues of natriuretic peptides usually make the diagnosis of HF less likely, and higher values have reasonably high positive predictive value in diagnosingHF, especially in dyspneic patients presenting to urgent care or ED settings. That being said, elevated plasma levels of natriuretic peptides can be seenwith a variety of other cardiac and noncardiac causes. Other causes of elevated natriuretic peptide levels in the acute setting are acute coronarysyndrome, atrial or ventricular arrhythmias, pulmonary embolism, cor pulmonale, renal failure, and sepsis. Other causes of an elevated natriuretic level inthe nonacute setting are old age (>75 y), atrial arrhythmias, LV hypertrophy, chronic obstructive pulmonary disease, and chronic kidney disease.Conversely, natriuretic peptide levels can be lower in obese patients. In patients with chronically elevated natriuretic peptides, levels usually correlatewith HF severity and prognosis, and an increase above the baseline is usually noted during acute decompensated HF. Current evidence suggests there isno specific cut-off point for an absolute or relative rise above the baseline level to diagnose a HF event in patients with chronically elevated natriureticpeptide levels.

– Radiological evidence of pulmonary congestion (CXR or other imaging modality such as CT or MRI with evidence of pulmonary venous or alveolarcongestion, interstitial or pulmonary edema, pleural effusion, or cephalization of venous flow. It is important to note that CXR may also reflect evidenceof cardiomegaly.)

– Noninvasive diagnostic evidence of HF (echocardiography, cardiac MRI, cardiac PET scan, and nuclear imaging) can provide information about cardiacanatomy such as LV or RV function, volumes, geometry, wall motion, or valvular function, and other findings such as elevated filling pressures by Dopplerechocardiography) supporting the diagnosis and etiology of HF. In systolic HF, LV ejection fraction (<50%) and LV fractional shortening are reduced(<25%). There may be regional LV wall motion abnormalities, especially in patients with ischemic HF. In patients with chronic systolic HF, LV end-diastolic size is usually increased (diameter $60 mm, >32 mm/m2, LV volume >97 mL/m2), as is LV end-systolic size (diameter >45 mm/>25 mm/m2,volume >43 mL/m2). Cardiac output is usually reduced, and LV outflow tract velocity time integral is reduced (<15 cm). LV diastolic dysfunctionparameters may reflect abnormalities of the mitral inflow pattern, with tissue velocities (e) or the E/e’ ratio indicating the presence and degree of LVdiastolic dysfunction. In cases of diastolic dysfunction, e’ is decreased (<8 cm/s septal, <10 cm/s lateral, or <9 cm/s average), suggesting delayed LVrelaxation. High E/e’ ratios (>15) usually indicate high LV filling pressures, whereas low E/e’ ratios (<8) usually indicate normal LV filling pressures. Amitral inflow E/A ratio >2 suggests restrictive, high LV filling pressures. In contrast, a mitral inflow E/A ratio of <1 suggests delayed LV relaxation withnormal LV filling pressures. An E/A ratio of 1–2 may be inconclusive or pseudonormal. Mitral inflow during the Valsalva maneuver may reflect a changefrom the pseudonormal to the impaired relaxation pattern (with a decrease in E/A ratio >0.5), suggesting high LV filling pressures (unmasked throughValsalva). An A-wave duration >30 ms usually suggests high LV filling pressures. In patients with elevated filling pressures, left atrial volume index is


APPENDIX 8. HEART FAILURE EVENT: ADDITIONAL DETAILS



438

usually increased (volume >34 mL/m2) (34,38,39) In HF, LV mass index is usually increased to >95 g/m2 in women and >115 g/m2 in men. Valvularstructure and function may reveal valvular stenosis or regurgitation, especially aortic stenosis and mitral regurgitation, and may be the cause, result, or acomplicating factor of HF (secondary mitral regurgitation). RV function (e.g., TAPSE) may be reduced (TAPSE <16 mm). Tricuspid regurgitation peakvelocity may be increased (>3.4 m/s), suggesting increased RV systolic pressures. Systolic pulmonary artery pressure may be increased (>50 mmHg)with pulmonary hypertension. The inferior vena cava may be dilated, with no respiratory collapse, suggesting increased right atrial pressures, RVdysfunction, volume overload, or pulmonary hypertension.

– Invasive diagnostic evidence of HF (right-sided heart catheterization) may reveal elevated PCWP, reduced cardiac output or cardiac index, elevated rightatrial pressure, or reduced mixed venous oxygen saturation. Left-sided heart catheterization may reveal elevated LVEDP. In patients with LV failure,PCWP or LVEDP is usually elevated over 18 mmHg. In patients with decompensated HF, right atrial pressure or central venous pressure is usually >12mmHg, and cardiac index is usually <2.2 L/min/m2 (28).

All results from diagnostic tests should be reported if available, even if they do not meet the above criteria, because they provide important information forthe adjudication of these events.

� Initiation or Intensification of HF Treatment: The criterion is that the patient receives initiation or intensification of treatment specifically for HF, includingat least 1 of the following:1) Augmentation in oral diuretic therapy (increase in oral diuretic dose or addition of another oral diuretic)2) Intravenous diuretic or intravenous vasoactive therapy. Vasoactive therapy may include an intravenous inotrope, vasodilator, or vasopressor.3) Mechanical or surgical intervention, including:

� Mechanical circulatory support (e.g., intra-aortic balloon pump, ventricular assist device, extracorporeal membrane oxygenation, total artificial heart)� Mechanical fluid removal (e.g., ultrafiltration, hemofiltration, dialysis)

BNP indicates B-type natriuretic peptide; CT, computed tomography; CXR, chest X-ray; ED, emergency department; HF, heart failure; LV, left ventricular; LVEDP, left ventricular end-diastolic pressure; MRI, magnetic resonance imaging; NT-proBNP, N-terminal pro-B-type natriuretic peptide; PCWP, pulmonary capillary wedge pressure; PET, positron emissiontomography; RV, right ventricular; and TAPSE, Tricuspid Annular Plane Systolic Excursion.



439


PermissibleValues



PCI PCI is the placement ofan angioplastyguidewire, balloon, orother device (eg stent,atherectomy,brachytherapy, orthrombectomycatheter) into a nativecoronary artery or CABGfor the purpose ofmechanical coronaryrevascu larization. Theassessment of coronarylesion severity byintravascularultrasonography,coronary flow reserve,or fractional flowreserve is notconsidered a PCIprocedure.

Percutaneous CoronaryIntervention Indicator

� Yes� No

NCDR CathPCI Registryv4.4 Coder’s DataDictionary (53),seq. #7020.Available at: https://www.ncdr.com/WebNCDR/docs/public-data-collection-documents/cathpci_v4_codersdictionary_4-4.pdf?sfvrsn¼2. AccessedDecember 12, 2014.

PCI—Status Classification of theurgency of a PCIprocedure at the timethe operator decides toperform the PCI.

Percutaneous CoronaryIntervention Status

� Elective� Urgent� Emergency� Salvage

NCDR CathPCI Registryv4.4 Coder’s DataDictionary (53), seq.#7020. Available at:https://www.ncdr.com/WebNCDR/docs/public-data-collection-documents/cathpci_v4_codersdictionary_4-4.pdf?sfvrsn¼2. AccessedDecember 12, 2014.

Elective A procedure that can beperformed on anoutpatient basis orduring a subsequenthospitalization withoutsignificant risk of MI ordeath. For stableinpatients, a PCIprocedure that isperformed during thehospitalization forconvenience and ease ofscheduling and notbecause the patient’sclinical situationdemands that theprocedure be performedbefore discharge.

Urgent A procedure that shouldbe performed on aninpatient basis andbefore dischargebecause of significantconcerns about the riskof myocardial ischemia,MI, and/or death.Patients who areoutpatients or in the EDat the time that thecardiac catheterization isrequested wouldwarrant hospitaladmission based onclinical presentation.


APPENDIX 9. PERCUTANEOUS CORONARY INTERVENTION



440








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http://https://www.ncdr.com/WebNCDR/docs/public-data-collection-documents/cathpci_v4_codersdictionary_4-4.pdf?sfvrsn=2


PermissibleValues



Emergency A procedure that shouldbe performed as soon aspossible because ofsubstantial concernsthat ongoing myocardialischemia and/or MIcould lead to death. “Assoon as possible” refersto a patient whosecondition is sufficientlyacute that the providerwould 1) cancel ascheduled case toperform the procedureimmediately in the nextavailable room duringbusiness hours or 2)would activate the on-call team if this were tooccur during off-hours.

Salvage A procedure that is a lastresort. The patient is incardiogenic shock whenthe PCI begins (i.e., thetime at which the firstguidewire orintracoronary device isintroduced into acoronary artery orbypass graft for thepurpose of mechanicalrevascularization) orwithin the last 10 minbefore the start of thecase; or during thediagnostic portion of thecase, the patientreceived chestcompressions or was onunanticipatedcirculatory support (e.g.,intra-aortic balloonpump, extracorporealmembrane oxygenation,or cardiopulmonarysupport).

PCI—Procedure Success Achievement of <30%residual diameterstenosis of all treatedlesions as assessed byvisual inspection orQCA, without an in-hospital major adversecardiac event (death,MI, or repeat coronaryrevascularization of thetarget lesion).Note: For some deviceinterventions (e.g.,balloon angioplasty),achievement of <50%diameter stenosis byvisual inspection or QCAis an acceptabledefinition for proceduresuccess.

Percutaneous CoronaryIntervention ProcedureSuccess Indicator

� Yes� No

Levine GN, Bates ER,Blankenship JC, et al.2011 ACCF/AHA/SCAIguideline forpercutaneous coronaryintervention. A report ofthe American College ofCardiology Foundation/American HeartAssociation Task Force onPractice Guidelines andthe Society forCardiovascularAngiography andInterventions. J AmColl Cardiol.2011;58:e44–122 (54).




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PCI—Target LesionSegment

Name of the coronaryartery segment wherePCI was performed thatis the subject of clinicalinvestigation. In thecontext of clinicalinvestigation, any lesiontreated or for whichtreatment wasattempted with a deviceor technique beingstudied. The length ofthe target lesion isinclusive of the arterialsection treated with thestudy device (e.g., astent) and the 5 mmproximal and 5 mmdistal to the treatedsection.

Percutaneous CoronaryIntervention TargetLesion Segment Name

Coronary artery segment(see Appendix 7)

Revised from AldermanEL, Stadius M.Angiographic definitionsof the Bypass AngioplastyRevascularizationInvestigation. CoronArtery Dis. 1992;3:1189–207 (42).

PCI—Target LesionProcedure Success

Achievement of <30%residual diameterstenosis of the targetlesion as assessed byvisual inspection orQCA, without an in-hospital major adversecardiac event (death,MI, or repeat coronaryrevascularization of thetarget lesion). For somedevice interventions(e.g., balloonangioplasty),achievement of <50%diameter stenosis byvisual inspection or QCAis an acceptabledefinition for technical(angiographic) success.In the context of clinicalinvestigation, ideallythe assessment of theresidual stenosis at theend of the procedureshould be performed byan angiographic corelaboratory.

Percutaneous CoronaryIntervention TargetLesion Procedure SuccessIndicator

� Yes� No

Adapted from Levine GN,Bates ER, Blankenship JC,et al. 2011 ACCF/AHA/SCAI guideline forpercutaneous coronaryintervention. A report ofthe American College ofCardiology Foundation/American HeartAssociation Task Force onPractice Guidelines andthe Society forCardiovascularAngiography andInterventions. J AmColl Cardiol.2011;58:e44–122 (54).

PCI—Abrupt Closure New intraproceduralseverely reduced flow(TIMI grade 0–1) withinthe target vessel thatpersists and requiresintervention by stentingor other treatment orresults in MI or death.Abrupt closure requiresan association with avascular dissection,thrombus, or severespasm at the treatmentsite or within theinstrumented vessel.

Coronary Artery AbruptClosure

� Yes� No

Adapted from ButmanSM, ed. Complications ofPercutaneous CoronaryInterventions. New York,NY: Springer; 2010 (55).

PCI—Dissection New appearance ofcontrast and/orradiolucencies duringPCI inconsistent withthe expected luminal

Coronary ArteryDissection Grade

� Grade A� Grade B� Grade C� Grade D� Grade E

Adapted from NationalHeart, Lung, and BloodInstitute. Coronary arteryangiographic changesafter percutaneous





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dimensions of a lesionand/or vessel.

� Grade F transluminal coronaryangioplasty. In: Manual ofOperations: NHLBI PTCARegistry. Bethesda, MD:National Heart, Lung, andBlood Institute; 1985:6–9(56).

Grade A Minor radiolucencieswithin the lumen duringcontrast injection withno persistence after dyeclearance.

Grade B Parallel tracts or doublelumen separated by aradiolucent area duringcontrast injection withno persistence after dyeclearance.

Grade C Extraluminal cap withpersistence of contrastafter dye clearance fromthe lumen.

Grade D Spiral luminal fillingdefect with delayed butcomplete distal flow.

Grade E New persistent fillingdefect with delayedantegrade flow. Mayrepresent thrombus.

Grade F Non–A-E types withtotal coronary occlusionand no distal antegradeflow. May representthrombus.

PCI—No Reflow New acute reduction incoronary flow (TIMIgrade 0–1) in theabsence of dissection,thrombus, spasm, orhigh-grade residualstenosis at the originalPCI lesion site.

Coronary Artery NoReflow Indicator

� Yes� No


PCI—CoronaryThrombosis

New acute developmentof compromise of a PCIvessel by coronaryartery thrombus (bloodclot) occurring at anytime during a procedureand independent ofevidence of stenosis ordissection.Criteria for anintraproceduralthrombosis eventinclude $1 of thefollowing:a) Development of

new or increasingcoronary thrombus

b) Abrupt vesselclosure

c) No reflow (fromTIMI flow 3/2 to 1/0) or slow reflow(from TIMI 3 to 2)

d) Distal embolization

Coronary ArteryThrombosis, Intra-Procedural Indicator

� Yes� No





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PCI—IntraproceduralStent Thrombosis

Occlusion of the lumenof a newly implantedstent by thrombus(blood clot) during theindex stentimplantation procedure.

Stent Thrombosis Intra-Procedural Indicator

� Yes� No


PCI—Stent Thrombosis Compromise of thelumen of a coronarystent by thrombus(blood clot) and not as aresult of restenosis oratherosclerosis aftercompletion of the stentimplantation procedure.Note: Angiographicnonocclusiveintracoronary thrombusis defined as a (spheric,ovoid, or irregular)noncalcified fillingdefect or lucencysurrounded by contrastmaterial (on 3 sides orwithin a coronarystenosis) seen inmultiple projections, orpersistence of contrastmaterial within thelumen, or a visibleembolization ofintraluminal materialdownstream.Angiographic occlusivethrombus is defined asthe presence of TIMI0 or TIMI 1 flowintrastent or proximalto a stent up to themost adjacent proximalside branch or mainbranch (if it originatesfrom the side branch).Pathologicalconfirmation of stentthrombosis is evidenceof recent thrombuswithin the stentdetermined at autopsyor by examination oftissue retrievedfollowingthrombectomy.

Stent Thrombosis,Coronary, Indicator

� Yes� No

Cutlip DE, Windecker S,Mehran R, et al. Clinicalendpoints in coronarystent trials: a case forstandardized definitions.Circulation. 2007;115:2344–51 (7).

PCI—Stent ThrombosisDate–Time

Date and time of theonset of stentthrombosis.

Stent Thrombosis,Coronary, Date_Time

� Date–time

PCI—Stent ThrombosisARC Grade

Probability thatcoronary artery stentthrombosis hasoccurred, according toARC grading criteria.Note: The incidentalangiographicdocumentation of stentocclusion in the absenceof clinical signs orsymptoms is notconsidered a confirmedstent thrombosis (silentocclusion).

Stent Thrombosis,Coronary, ARC grade

� Definite� Probable� Possible






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Definite Definite stentthrombosis is consideredto have occurred whenthere is eitherangiographic orpathologicalconfirmation.Angiographicconfirmation is thepresence of a thrombusat coronary angiographythat originates in thestent or in the segment5 mm proximal or distalto the stent, with thepresence of at least 1 of3 clinical criteria within a48-h time window:a) Acute onset of

ischemic symptomsat rest

b) New ischemicchanges on ECGthat suggest acuteischemia

c) Typical rise and fallin cardiac bio-markers. Patholog-ical confirmation isevidence of recentthrombus within thestent determined atautopsy or by ex-amination of tissueretrieved followingthrombectomy.

Probable Probable stentthrombosis is consideredto have occurred afterintracoronary stenting inthe following situations:a) Any unexplained

death within thefirst 30 d (forstudies of patientswith an ST-segmentelevation MI,exclusion ofunexplained deathwithin 30 d asevidence ofprobable stentthrombosis)

b) irrespective of thetime after the indexprocedure, any MIthat is related todocumented acuteischemia in the ter-ritory of theimplanted stentwithout angio-graphic confirma-tion of stentthrombosis and inthe absence of anyother obviouscause.

Possible Possible: Possible stentthrombosis is consideredto have occurred withany unexplained death>30 d afterintracoronary stenting.




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PCI—Stent ThrombosisARC Timing

Timing of the detectionof stent thrombosisaccording to the ARCgrading criteria, withtime 0 defined as thetime when the patientdeparts thecatheterizationlaboratory after a stentimplantation procedure.Note: The combinationof acute or subacutestent thrombosis can bereplaced by the termearly stent thrombosis(0–30 d).

Stent Thrombosis,Coronary, ARC timing

� Acute� Subacute� Late� Very late


Acute 0–24 h after stentimplantation

Subacute >24 h to 30 d afterstent implantation

Late >30 d to 1 y after stentimplantation

Very late >1 y after stentimplantation

PCI—Stent Restenosis Renarrowing of a stentimplanted at a lesionsite to treat a priorstenosis, to a diameterstenosis of >50%within the stent,inclusive of the originaltreated site plus theadjacent vascularsegments 5 mmproximal and 5 mmdistal to the stent.

Percutaneous CoronaryIntervention Restenosis,In-Stent, AngiographicBinary Indicator

� Yes� No


PCI—Lesion Restenosis Renarrowing of a lesionsite following treatmentof a prior stenosis, to adiameter stenosis of>50% at the previouslytreated lesion site,inclusive of the originaltreated site plus theadjacent vascularsegments 5 mmproximal and 5 mmdistal to the treatedsegment.

Percutaneous CoronaryIntervention, Restenosis,Lesion AngiographicBinary Indicator

� Yes� No


PCI—TLR Repeat percutaneousintervention of a targetlesion, or surgicalbypass of a targetvessel, performed forrestenosis or othercomplication involving

Percutaneous CoronaryIntervention, TargetVessel RevascularizationIndicator

� Yes� No

Cutlip DE, Windecker S,Mehran R, et al. Clinicalendpoints in coronarystent trials: a case forstandardized definitions.Circulation.2007;115:2344–51 (7).





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the target lesion. Thelength of the targetlesion is inclusive of thetreated section and the5 mm proximal anddistal to the treatedsection.In the assessment ofTLR, angiograms shouldbe assessed by anangiographic corelaboratory (ifdesignated) and madeavailable to the CEC forreview on request.

PCI—Ischemia Before TLR Criteria for clinical orfunctional ischemiainclude any of thefollowing:a) History of angina

pectoris, presum-ably related to thetarget vessel

b) Objective signs ofischemia at rest(electrocardio-graphic changes) orduring exercise test(or equivalent),presumably relatedto the target vessel

c) Abnormal results ofany invasive func-tional diagnostictest (e.g., CFR orFFR)

Percutaneous CoronaryIntervention TargetLesion RevascularizationIschemia Indicator

� Yes� No


PCI—Clinically Driven TLR PCI–TLR is clinicallydriven if the targetlesion diameter stenosisis >50% by QCA andthe subject has clinicalor functional ischemiathat cannot beexplained by anothernative coronary orbypass graft lesion. TLRof a >70% diameterstenosis by QCA in theabsence of the abovesigns or symptoms maybe considered clinicallydriven. In the absenceof QCA data or if astenosis #50% ispresent, TLR may beconsidered clinicallydriven if severe ischemicsigns and symptomsattributed to the targetlesion are present.

Percutaneous CoronaryIntervention TargetLesion RevascularizationClinically Driven Indicator

� Yes� No


PCI—TLF The composite ofischemia-driven targetlesion revascularization,MI related to the targetvessel, or cardiac deathrelated to the targetvessel. If it cannot bedetermined withcertainty whether an MIor death was related tothe target vessel, it isconsidered a TLF.

Percutaneous CoronaryIntervention TargetLesion Failure Indicator

� Yes� No





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PCI—Target Vessel In the context of clinicalinvestigation, the majornative coronary artery(e.g., left main coronaryartery, LAD coronaryartery, left circumflexcoronary artery, or rightcoronary artery) orbypass graft containingthe target lesion. Anative coronary arterytarget vessel includesthe arterial segmentsupstream anddownstream from thetarget lesion plus majorside branches.

Percutaneous CoronaryIntervention TargetVessel Name

� Left main artery� LAD artery� Left circumflex artery� Ramus intermedius

artery� Right coronary artery

Adapted from AldermanEL, Stadius M.Angiographic definitionsof the Bypass AngioplastyRevascularizationInvestigation. CoronaryArtery Disease.1992;3:1189–207 (42).

Left main artery Left main coronaryartery.

SNOMED-CT: 3227004

LAD artery LAD coronary artery,including septal anddiagonal branches.

SNOMED-CT: 59438005

Left circumflex artery Left circumflex coronaryartery, includingmarginal branches; ifmixed dominance, alsoincluding leftposterolateral branches;if left dominant, alsoincluding posterolateraland posteriordescending branches.

SNOMED-CT: 57396003

Ramus intermedius artery Ramus intermediuscoronary branch.

SNOMED-CT: 244252004

Right coronary artery Right coronary arteryand its branches; ifmixed dominance, alsoincluding posteriordescending branch; ifright dominant, alsoincluding rightposterolateral andposterior descendingbranches.

SNOMED-CT: 13647002

PCI—TVR Repeat PCI or surgicalbypass of any segmentof a coronary arterycontaining a targetlesion. A target vessel isdefined as the entiremajor coronary vesselproximal and distal to atarget lesion, includingupstream anddownstream branchesand the target lesionitself.In the assessment ofTVR, angiograms shouldbe assessed by anangiographic corelaboratory (ifdesignated) and madeavailable to the CEC forreview on request.

Percutaneous CoronaryIntervention TargetVessel RevascularizationIndicator

� Yes� No






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PCI—TVF The composite ofischemia-driven TVR, MIrelated to the targetvessel, or cardiac deathrelated to the targetvessel. If it cannot bedetermined withcertainty whether theMI or death was relatedto the target vessel, it isconsidered a TVF.

Percutaneous CoronaryIntervention TargetVessel Failure Indicator

� Yes� No


PCI—Nontarget LesionSegment

Name of a coronaryartery segment wherePCI was performed thatis NOT the subject ofclinical investigation. Inthe context of clinicalinvestigation, any lesionnot treated or for whichno attempt at treatmentwas made with thedevice or techniquebeing studied. Thisincludes lesions treatedwith (nonstudy) PCI andlesions managedmedically.

Percutaneous CoronaryIntervention Non-TargetLesion Segment Name

� Coronary arterysegment (seeAppendix 10)

Revised from AldermanEL, Stadius M.Angiographic definitionsof the Bypass AngioplastyRevascularizationInvestigation. CoronaryArtery Disease.1992;3:1189–207 (7).

PCI—Nontarget LesionRevascularization

Any (de novo or repeat)PCI of a nontargetlesion or surgical bypassof a nontarget vessel.This includesrevascularization at thetime of an index (study)PCI of a separate targetlesion and subsequentrevascularization afterthe index (study) PCI.

Percutaneous CoronaryIntervention Non-TargetLesion RevascularizationIndicator

� Yes� No

Cutlip DE, Windecker S,Mehran R, et al. Clinicalendpoints in coronarystent trials: a case forstandardized definitions.Circulation.2007;115:2344–51 (7).

PCI—Nontarget Vessel In the context of clinicalinvestigation, any majornative coronary artery(e.g., left main coronaryartery, LAD coronaryartery, left circumflexcoronary artery, or rightcoronary artery) orbypass graft not treatedor for which no attemptat treatment was madewith a device ortechnique beingstudied. This includesvessels treated with(nonstudy) PCI andvessels managedmedically.

Percutaneous CoronaryIntervention Non-TargetVessel Name

� Left main artery� LAD artery� Left circumflex artery� Ramus intermedius

artery� Right coronary artery

Adapted from AldermanEL, Stadius M.Angiographic definitionsof the Bypass AngioplastyRevascularizationInvestigation. CoronaryArtery Disease.1992;3:1189–207 (42).

Left main artery Left main coronaryartery.

SNOMED-CT: 3227004

LAD artery LAD coronary artery,including septal anddiagonal branches.

SNOMED-CT: 59438005

Left circumflex artery Left circumflex coronaryartery, includingmarginal branches; ifmixed dominance, alsoincluding left

SNOMED-CT: 57396003




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posterolateral branches;if left dominant, alsoincluding posterolateraland posteriordescending branches.

Ramus intermedius artery Ramus intermediuscoronary branch.

SNOMED-CT: 244252004

Right coronary artery Right coronary arteryand its branches; ifmixed dominance, alsoincluding posteriordescending branch; ifright dominant, alsoincluding rightposterolateral andposterior descendingbranches.

SNOMED-CT: 13647002

PCI—Nontarget VesselRevascularization

Any (de novo or repeat)PCI or surgical bypass ofany segment of anontarget vessel.This includesrevascularization at thetime of an index (study)PCI of a separate targetlesion and subsequentrevascularization afterthe index (study) PCI.

Percutaneous CoronaryIntervention Non-TargetVessel RevascularizationIndicator

� Yes� No


Coronary Angiography—TIMI Flow Grade

Grading scale todescribe coronaryepicardial blood flow asvisualized duringangiography accordingto the classificationdescribed by the TIMIGroup.

tIMIFlowGrade � Grade 0� Grade 1� Grade 2� Grade 3

Cannon CP, Brindis RG,Chaitman BR, et al. 2013ACCF/AHA key dataelements and definitionsfor measuring the clinicalmanagement andoutcomes of patients withacute coronarysyndromes and coronaryartery disease. A report ofthe American College ofCardiology Foundation/American HeartAssociation Task Force onClinical Data Standards(Writing Committee toDevelop Acute CoronarySyndromes and CoronaryArtery Disease ClinicalData Standards). J AmColl Cardiol.2013;61:992–1025 (16).

Grade 0 No perfusion. There isno antegrade flowbeyond the point ofocclusion.

Grade 1 Penetration withoutperfusion. Contrastmaterial passes beyondthe area of obstructionbut “hangs up” and failsto opacify the entirecoronary bed distal tothe obstruction for theduration of thecineangiographic filmingsequence.





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Grade 2 Partial perfusion. Thecontrast material passesacross the obstructionand opacifies thecoronary bed distal tothe obstruction.However, the rate ofentry of contrastmaterial into the vesseldistal to the obstructionor its rate of clearancefrom the distal bed (orboth) is perceptiblyslower than its entryinto or clearance fromcomparable areas notperfused by thepreviously occludedvessel (e.g., theopposite coronary arteryor the coronary bedproximal to theobstruction).

Grade 3 Complete perfusion.Antegrade flow into thebed distal to theobstruction occurs aspromptly as into the bedproximal to theobstruction, andclearance of contrastmaterial from theinvolved bed is as rapidas from an uninvolvedbed in the same vesselor the opposite artery.

Coronary Angiography—Coronary ArteryThrombus

A discrete, mobile,intraluminal fillingdefect with definedborders with or withoutassociated contraststaining.

Coronary ArteryThrombus Indicator

� Yes� No

Adapted from Capone G,Wolf NM, Meyer B,Meister SG. Frequency ofintracoronary fillingdefects by angiography inangina pectoris at rest.Am J Cardiol.1985;56:403–6 (57).

Coronary Angiography—TIMI Thrombus Grade

Grading scale todescribe coronarythrombus as visualizedduring angiography perthe classificationdescribed by the TIMIGroup.

TIMI Coronary ThrombusGrade

� Grade 1� Grade 2� Grade 3� Grade 4� Grade 5

Cannon CP, Braunwald E,McCabe CH, et al.The Thrombolysis inMyocardial Infarctiontrials: the first decade.J Interv Cardiol. 1995;8:117–35 (58).

Grade 1 Possible thrombuspresent: angiographydemonstratescharacteristics such asreduced contrastdensity, haziness,irregular lesion contour,or a smooth convex“meniscus” at the site oftotal occlusionsuggestive, but notdiagnostic, of thrombus.

Grade 2 Small definite thrombus,with the greatestdimension less than orequal to one-half of thevessel diameter.




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Grade 3 Moderate definitethrombus, with thegreatest lineardimension greater thanone-half but <2 vesseldiameters.

Grade 4 Large definite thrombus,with the greatestdimension $2 vesseldiameters.

Grade 5 Total vessel occlusion.

CardiovascularCatheterization—Access SiteHematoma

Development of a new,localized collection ofblood at a vascularaccess site sufficient toproduce a palpablemass within 72 h of aprocedure.

Access Site HematomaIndicator

� Yes� No


CardiovascularCatheterization—Arteriovenous Fistula

Development of a new,unintendedcommunicationbetween an artery and avein occurring at avascular access sitewithin 72 h of aprocedure.

Arteriovenous FistulaIndicator

� Yes� No


CardiovascularCatheterization—Peripheral Ischemia

Development of newarterial insufficiencysufficient to produceclinical signs orsymptoms of ischemia(pallor, pain,paresthesia) distal to avascular access sitewithin 72 h of aprocedure.

Peripheral IschemiaIndicator

� Yes� No


CardiovascularCatheterization—Peripheral NerveInjury

Development of newsensory or motor loss ofperipheral nervefunction from externalnerve compression(e.g., as a result ofpositioning during aprocedure), or internalcompression or directnerve damage from theprocedure, occurringwithin 72 h of aprocedure.

Peripheral Nerve InjuryIndicator

� Yes� No


CardiovascularCatheterization—Pseudoaneurysm

Development of a newlocalized collection ofblood with a persistentcommunication (neck)originating at a vascularaccess site andoccurring within 72 h ofa procedure.

PseudoaneurysmIndicator

� Yes� No


CardiovascularCatheterization—RetroperitonealHemorrhage

Development of newbleeding into theretroperitoneal spaceoriginating at a vascularaccess site andoccurring within 72 h ofa procedure.

RetroperitonealHemorrhage Indicator

� Yes� No






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CABG CABG surgery is aprocedure performedto bypass partially orcompletely occludedcoronary arteries withveins and/or arteriesharvested fromelsewhere in the body,thereby improving theblood supply to thecoronary circulationsupplying themyocardium (heartmuscle).

Coronary Artery BypassGraft Surgery Indicator

� Yes� No

CABG—Status Classification of theurgency of a CABGsurgical procedure,based on the patient’sclinical status beforeentering the operatingroom

Coronary Artery BypassGraft Surgery Status

� Elective� Urgent� Emergency� Salvage

Elective Patient cardiac statushas been stable in thedays or weeks beforethe operation. Theprocedure can bedeferred withoutincreased risk ofcompromised cardiacoutcome.

Urgent Procedure requiredduring the samehospitalization tominimize chances ofclinical deterioration oradverse outcome.Clinical conditionsinclude (but are notlimited to) acute orworsening chest pain,acute or worsening HF,acute MI, criticalcoronary stenosis, IABPsupport, UA withintravenousnitroglycerin, and restangina.

Emergency Procedure requiredbecause of ongoing,refractory (difficult,complicated, and/orunmanageable),unrelenting cardiaccompromise, with orwithout hemodynamicinstability, and notresponsive to any formof therapy exceptcardiac surgery. Anemergency operation isone in which thereshould be no delay inproviding operativeintervention. The clinicalstatus of the patient caninclude any of thefollowing:




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a) Ischemic dysfunc-tion (any of thefollowing): 1)ongoing ischemia,including restangina despitemaximal medicaltherapy (medicaland/or IABP); 2)acute evolving MIwithin 24 h beforesurgery; or 3) pul-monary edemarequiringintubation.

b) Mechanicaldysfunction (eitherof the following): 1)shock with circula-tory support or 2)shock without cir-culatory support.

Salvage The patient isundergoing CPR or isbeing managed withextracorporealmembrane oxygenationen route to theoperating room orbefore induction ofanesthesia. The clinicalacuity of the patient is adying state.

Cardiothoracic Surgery—Inoperable/ExtremeRisk

Heart Team assessmentthat a patient isinappropriate forcardiothoracic surgery,based on predictedoperative mortality,comorbidities, frailty/debilitation, previousprocedures, technicalinoperability, and/orother extenuatingcircumstances.

Cardiothoracic SurgeryInoperable-Extreme RiskIndicator

� Yes� No

Adapted from STS/ACCTVT Registry v2.0 Coder’sData Dictionary. Availableat: https://www.ncdr.com/TVT/Libraries/TVT_Library/2_0_CoderDataDictionary.sflb.ashx. Accessed December12, 2014 (59).

CABG—Type Type of CABG conduit. Coronary Artery GraftType

� Saphenous vein graft� Arterial graft, in situ� Arterial graft, free

Saphenous vein graft CABG composed ofsaphenous vein.

Arterial graft, in situ CABG composed ofarterial conduit, wherethe origin of the graftremains intact.

Arterial graft, free CABG composed ofan artery that hasbeen completelyfreed from its originallocation.

PCI—Bypass Graft LesionLocation

Location of a lesionwithin a CABGwhere PCI wasperformed.

Coronary Artery GraftLesion Location

� Graft origin� Graft body� Graft anastomosis






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Graft origin The section of a graftfrom the connection(anastomosis) of thegraft with the aorta (orfrom the origin if in situ),inclusive of the first 3mm of the graft.

Graft body The section of a graftbetween the origin andthe anastomosis.

Graft anastomosis The section of a graftfrom the connection(anastomosis) of thegraft with the coronaryartery, inclusive of theretrograde 3 mm of thegraft.

CABG—Anastomosis The coronary arterysegment to which aCABG is connected.

Coronary Artery GraftAnastomosis

� Coronary arterysegment (seeAppendix 10)

ACCF indicates American College of Cardiology Foundation; AHA, American Heart Association; ARC, Academic Research Consortium; CABG, coronary artery bypass graft; CEC, ClinicalEvents Committee; CFR, coronary flow reserve; CPR, cardiopulmonary resuscitation; ECG, electrocardiogram; ED, emergency department; FFR, fractional flow reserve; IABP, intra-aortic balloon bump; LAD, left anterior descending; MI, myocardial infarction; mm, millimeter; NCDR, National Cardiovascular Data Registry; NHLBI, National Heart, Lung, andBlood Institute; PCI, percutaneous coronary intervention; PTCA, percutaneous transluminal coronary angioplasty; QCA, quantitative coronary angiography; SCAI, Society for CardiacAngiography and Interventions; SNOMED-CT, Systemized Nomenclature of Medicine–Clinical Terms; TIMI, Thrombolysis in Myocardial Infarction; TLF, target lesion failure; TLR, targetlesion revascularization; TVF, target vessel failure; TVR, target lesion revascularization; and UA, unstable angina.



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Coronary ArteryDominance

Pattern of thecoronary arteries thatsupply blood to theinferior wall of the leftventricle, classifiedinto 1 of 3 mutuallyexclusive categories(right, left, co-dominant).

Coronary ArteryDominance

� Left� Right� Co-dominant

Revised from AustenWG, Edwards JE, FryeRL, et al. A reportingsystem on patientsevaluated for coronaryartery disease. Reportof the Ad HocCommittee for Gradingof Coronary ArteryDisease, Council onCardiovascular Surgery,American HeartAssociation. Circulation.1975;51:5–40 (41).Alderman EL, Stadius M.Angiographic definitionsof the BypassAngioplastyRevascularizationInvestigation. CoronaryArtery Disease.1992;3:1189–207 (42).Medina A, Suarez deLezo J, Pan M. [A newclassification ofcoronary bifurcationlesions]. Rev EspCardiol. 2006;59:183(44).

Left The PDA and PLA arisefrom the left circumflexartery.

Right The PDA and PLA arisefrom the right coronaryartery.

Co-dominant The right coronaryartery supplies the PDA,and the circumflexartery supplies the PLA.Thus, both the rightcoronary and leftcircumflex arteriescontribute to the bloodsupply of the inferiorwall of the leftventricle.

Coronary ArterySegments

[value set] � Right coronaryartery ostium

� Proximal rightcoronary artery

� Mid right coronaryartery

� Distal right coronaryartery

� Right PDA� Posterolateral

segmental artery� First right postero-

lateral branch� Second right

posterolateralbranch

� Third right postero-lateral branch

� Posterior descend-ing septal perforator

� Right ventricularbranch

� Left main coronaryartery ostium

Revised from AustenWG, Edwards JE, FryeRL, et al. A reportingsystem on patientsevaluated for coronaryartery disease. Reportof the Ad HocCommittee for Gradingof Coronary ArteryDisease, Council onCardiovascular Surgery,American HeartAssociation. Circulation.1975;51:5–40 (41).Alderman EL, Stadius M.Angiographic definitionsof the BypassAngioplastyRevascularizationInvestigation. CoronaryArtery Disease.1992;3:1189–207 (42).Medina A, Suarez deLezo J, Pan M.


APPENDIX 10. CARDIOVASCULAR ANATOMY



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� Left main coronaryartery body

� Left main coronaryartery bifurcation

� LAD artery ostium� Proximal LAD� Mid LAD� Distal LAD� First diagonal

branch� First diagonal lateral

branch� Second diagonal

branch� Second diagonal

lateral branch� Third diagonal

branch� Third diagonal

lateral branch� Anterior descending

septal perforator� Left circumflex ar-

tery ostium� Proximal left

circumflex artery� Mid left circumflex

artery� Distal left circum-

flex artery� First obtuse mar-

ginal branch� First obtuse mar-

ginal lateral branch� Second obtuse mar-

ginal branch� Second obtuse mar-

ginal lateral branch� Third obtuse mar-

ginal branch� Third obtuse mar-

ginal lateral branch� Left atrioventricular

artery� Left PDA� First left postero-

lateral branch� Second left

posterolateralbranch

� Third left postero-lateral branch

� Ramus intermediusbranch

� Ramus intermediuslateral branch

[A new classificationof coronary bifurcationlesions]. Rev EspCardiol. 2006;59:183(44).

Right coronary arteryostium

Origin of the rightcoronary artery,including the first 3 mmof the artery

Draft code: 1aSNOMED-CT: 56789007Draft code: 1a

Proximal right coronaryartery

Proximal portion of theright coronary artery,from the ostium of theright coronary artery tothe origin of the firstright ventricular branch

Draft code: 1BARI: 1NCI: C102337SNOMED-CT: 91083009

Mid right coronary artery Middle portion of theright coronary artery,from the origin of thefirst right ventricularbranch to the acutemargin

Draft code: 2BARI: 2NCI: C102329SNOMED-CT:13647002þ255562008




457



PermissibleValues



Distal right coronaryartery

Distal portion of theright coronary artery,from the acute marginto the origin of theposterior descendingartery


Right PDA In right dominant andmixed circulations, thevessel that runs inthe posteriorinterventricular grooveand supplies septalperforator branches


Posterolateral segmentalartery

In right-dominantcirculations, the distalcontinuation of theright coronary arteryin the posterioratrioventricular grooveafter the origin of theright PDA


First right posterolateralbranch

In right-dominantcirculations, the firstposterolateral branchoriginating from theright posterioratrioventricular artery

Draft code: 6BARI: 6SNOMED-CT: 91761002

Second rightposterolateral branch

In right-dominantcirculations, the secondposterolateral branchoriginating from theright posterioratrioventricular artery


Third right posterolateralbranch

In right-dominantcirculations, the thirdposterolateral branchoriginating from theright posterioratrioventricular artery


Posterior descendingseptal perforator

Septal perforatorvessel originating fromthe PDA

Draft code: 9BARI: 9

Right ventricular branch Branch arising from theright coronary artery tosupply the rightventricular wall


Left main coronaryartery ostium

Origin of the leftcoronary artery,including the first 3 mmof the artery

Draft code: 11aSNOMED-CT: 76862008

Left main coronaryartery body

Body of the left maincoronary artery, fromthe ostium to thebifurcation

Draft code: 11bBARI: 11SNOMED-CT: 3227004

Left main coronaryartery bifurcation

Distal end of the leftmain coronary artery,including the terminal3 mm through thebifurcation of the leftmain into the LAD andleft circumflex arteries

Draft code: 11c

LAD artery ostium Origin of the LADcoronary artery,including the first 3 mmof the artery

Draft code: 12a





458



PermissibleValues



Proximal LAD artery Proximal portion of theLAD coronary artery,from the ostium to theorigin of the first septal


Mid LAD artery Middle portion of theLAD coronary artery,from the origin of thefirst septal artery to theorigin of the third septalartery


Distal LAD artery Distal portion of theLAD coronary artery,from the origin of thethird septal artery tothe terminus


First diagonal branch First of the 3 longestbranches originatingfrom the LAD artery tosupply the anterolateralwall of the left ventricle


First diagonal lateralbranch

Branch of the firstdiagonal branch

Draft code: 15dBARI: 15a

Second diagonal branch Second of the 3 longestbranches originatingfrom the LAD artery tosupply the anterolateralwall of the left ventricle


Second diagonal lateralbranch

Branch of the seconddiagonal branch


Third diagonal branch Third of the 3 longestbranches originatingfrom the LAD artery tosupply the anterolateralwall of the left ventricle


Third diagonal lateralbranch

Branch of the thirddiagonal branch


Anterior descendingseptal perforator

Septal perforator vesseloriginating from theLAD artery to supplythe interventricularseptum


Left circumflex arteryostium

Origin of the leftcircumflex coronaryartery, including thefirst 3 mm of the artery

Draft code: 19a

Proximal left circumflexartery

Proximal portion of theleft circumflex coronaryartery, from the ostiumto the origin (or thenominal location of) thefirst marginal branch


Mid left circumflex artery Middle portion of theleft circumflex coronaryartery, from the originsof (or nominal locationsof) the first marginal tothe second marginal


Distal left circumflexartery

Distal portion of the leftcircumflex coronaryartery, from the originof (or the nominallocation of) the secondmarginal to theterminus (in right-dominant systems), or

Draft code: 21BARI: 19aSNOMED-CT: 6511003




459



PermissibleValues



to the origin of the firstleft posterolateral in allother dominant systems

First obtuse marginalbranch

First of the 3 longestbranches originatingfrom the left circumflexartery to supply thelateral wall of the leftventricle


First obtuse marginallateral branch

Branch of the firstmarginal branch


Second obtuse marginalbranch

Second of the 3 longestbranches originatingfrom the left circumflexartery to supply thelateral wall of the leftventricle


Second obtuse marginallateral branch

Branch of the secondmarginal branch


Third obtuse marginalbranch

Third of the 3 longestbranches originatingfrom the left circumflexartery to supply thelateral wall of the leftventricle


Third obtuse marginallateral branch

Branch of the thirdmarginal branch


Left atrioventricularartery

In left-dominant andmixed circulations, thedistal continuation ofthe left circumflexcoronary artery in theposterioratrioventricular groove


Left posteriordescending artery

In left-dominantcirculations, the vesselthat arises from thedistal continuation ofthe left atrioventricularartery, travels in theposteriorinterventricular grooveand supplies septalperforator branches


First left posterolateralbranch

In left-dominant andmixed circulations, thefirst posterolateralbranch originating fromthe posterioratrioventricular leftcircumflex artery


Second leftposterolateral branch

In left-dominant andmixed circulations, thesecond posterolateralbranch originating fromthe posterioratrioventricular leftcircumflex artery


Third left posterolateralbranch

In left-dominant andmixed circulations, thethird posterolateralbranch originating fromthe posterioratrioventricular leftcircumflex artery






460



PermissibleValues



Ramus intermediusbranch

Branch vessel whoseorigin bisects theorigins of the LAD andcircumflex arteries


Ramus intermediuslateral branch

Branch of the ramusintermedius branch


Peripheral ArterySegments

[value set] � Infrarenal aorta� Left renal artery� Right renal artery� Left common iliac

artery� Right common iliac

artery� Left external iliac

artery� Right external iliac

artery� Left internal iliac

artery� Right internal iliac

artery� Left common

femoral artery� Right common

femoral artery� Left superficial

femoral artery� Right superficial

femoral artery� Left profunda

femoris artery� Right profunda

femoris artery� Left popliteal

artery—above knee� Right popliteal

artery—above knee� Left popliteal

artery—below knee� Right popliteal

artery—below knee� Left anterior tibial

artery� Right anterior tibial

artery� Left tibio-peroneal

trunk� Right tibio-peroneal

trunk� Left peroneal artery� Right peroneal

artery� Left posterior tibial

artery� Right posterior tibial

artery� Left accessory renal

artery� Right accessory

renal artery

Diehm N, Pattynama PM,Jaff MR, et al. Clinicalendpoints in peripheralendovascularrevascularization trials: acase for standardizeddefinitions. Eur J VascEndovasc Surg.2008;36:409–19 (60).

Infrarenal aorta Draft code: 400

Left renal artery Draft code: 501

Right renal artery Draft code: 401

Left common iliac artery Draft code: 502

Right common iliacartery

Draft code: 402




461



PermissibleValues



Left external iliac artery Draft code: 503

Right external iliac artery Draft code: 403

Left internal iliac artery Draft code: 504

Right internal iliac artery Draft code: 404

Left common femoralartery

Draft code: 505

Right common femoralartery

Draft code: 405

Left superficial femoralartery

Draft code: 506

Right superficial femoralartery

Draft code: 406

Left profunda femorisartery

Draft code: 507

Right profunda femorisartery

Draft code: 407

Left popliteal artery—above knee

Draft code: 508

Right popliteal artery—above knee

Draft code: 408

Left popliteal artery—below knee

Draft code: 509

Right popliteal artery—below knee

Draft code: 409

Left anterior tibial artery Draft code: 510

Right anterior tibialartery

Draft code: 410

Left tibio-peroneal trunk Draft code: 511

Right tibio-peronealtrunk

Draft code: 411

Left peroneal artery Draft code: 512

Right peroneal artery Draft code: 412

Left posterior tibialartery

Draft code: 513

Right posterior tibialartery

Draft code: 413

Left accessory renalartery

Draft code: 514

Right accessory renalartery

Draft code: 414

This table describes coronary artery dominance, coronary artery segments, and lower abdominal, pelvic, and lower extremity artery segment concepts. The bulleted lists are the permissiblevalues for the terminology concept; the following rows provide more detail about the individual permissible values. The table includes a draft simple numbering code for the coronary andperipheral artery segments, as well as references to existing coding systems describing the specific segments where available. The numbering code schema uses the letter “a” to designatethe ostium, “b” to designate the body, “c” to designate the bifurcation terminus, and “d” to identify a lateral branch of a branch.

BARI indicates Bypass Angioplasty Revascularization Investigators; LAD, left anterior descending; NCI, National Cancer Institute; PDA, posterior descending artery; PLA, postero-lateral artery; and SNOMED-CT, Systemized Nomenclature of Medicine–Clinical Terms.




462


PermissibleValues



PVI A PVI is a catheter-based oropen surgical proceduredesigned to improve arterialor venous blood flow orotherwise modify or revisevascular conduits.Procedures may include, butare not limited to,percutaneous transluminalballoon angioplasty, stentplacement, thrombectomy,embolectomy, atherectomy,dissection repair, aneurysmexclusion, treatment ofdialysis conduits, placementof various devices,intravascular thrombolysisor other pharmacotherapies,and open surgical bypass orrevision. In general, theintention to performpercutaneous vascularintervention is denoted bythe insertion of a guidewireinto an artery or vein. Forthe sake of simplicity, thisdefinition applies to theextracranial carotid arteryand other noncardiacarteries and excludes theintracranial vessels, veins,and lymphatics.

Peripheral VascularIntervention Indicator

� Yes http://www.cdisc.org/therapeutic (49)

PVI—Status Classification of the urgencyof a PVI procedure at thetime the operator decides toperform the PVI.Nonelective proceduresinclude urgent andemergency procedures.

Peripheral VascularIntervention Status

� Elective� Urgent� Emergency

http://www.cdisc.org/therapeutic (49),modeled on the similarcoronary PCI concept.

Elective A procedure that isscheduled andperformed on a patientwith stable disease or inwhom there is nourgency and/orincreased morbidity ormortality associatedwith a plannedprocedure.

Urgent A procedure that is notan emergency but isrequired to beperformed on a timelybasis (#24 h) (e.g., apatient who has beenstabilized followinginitial treatment ofacute limb ischemia andthere is clinicalconsensus that adefinitive procedureshould occur within thenext 24 h).

Emergency A procedure that isrequired to beperformed immediatelybecause of the acutenature of the medicalcondition (e.g., acute


APPENDIX 11. PERIPHERAL VASCULAR INTERVENTION


463



http://www.cdisc.org/%20therapeutic

http://www.cdisc.org/%20therapeutic


PermissibleValues



limb ischemia, acuteaortic dissection) andthe increased morbidityor mortality associatedwith a temporal delay intreatment.

PVI—Target LesionSegment

Name of the peripheralartery segment where PVIwas performed that is thesubject of clinicalinvestigation. In the contextof clinical investigation, anylesion treated or for whichtreatment was attemptedwith a device or techniquebeing studied. The length ofthe target lesion is inclusiveof the section of vesseltreated with the studydevice (e.g., a stent) and the10 mm proximal and 10 mmdistal to the treated section.

Peripheral VascularIntervention TargetLesion Segment Name

� Peripheral arterysegment (seeAppendix 10)

PVI—Procedure Success Achievement of asatisfactory final residualdiameter stenosis byangiography at the end ofthe procedure (and withoutflow-limiting dissection orhemodynamically significanttranslesional pressuregradient). The specificparameter for final percentresidual stenosis is typicallybetween <30% and <50%;selection of the appropriatepercentage may varydepending on the specificintervention applied, thevascular territory, andanticipated or desiredtherapeutic response.Procedural success alsoimplies absence of in-hospital major adverseevents (e.g., death, stroke,MI, acute onset of limbischemia, need for urgent/emergency vascular surgery,and other procedure-specific major adverseevents).In the context of clinicalinvestigation, ideally theassessment of the residualstenosis at the end of theprocedure should beperformed by anangiographic corelaboratory.The balloon inflation, stentplacement, or othertherapeutic interventionmay be preceded by use ofadjunctive devices (e.g.,percutaneous mechanicalthrombectomy, directionalor rotational atherectomy,laser, and chronic totalocclusion crossing device),as predefined in theprotocol.

Peripheral VascularIntervention ProcedureSuccess Indicator

� Yes� No

Adapted from Diehm N,Pattynama PM, Jaff MR,et al. Clinical endpoints inperipheral endovascularrevascularization trials: acase for standardizeddefinitions. Eur J VascEndovasc Surg.2008;36:409–19 (60).





464


PermissibleValues



PVI—Stent Restenosis Renarrowing of a stentimplanted at a lesion site totreat a prior stenosis, to adiameter stenosis of >50%within the stent, inclusive ofthe original treated site plusthe adjacent vascularsegments 10 mm proximaland 10 mm distal to thestent.

Peripheral VascularInterventionRestenosis, In-Stent—Angiographic BinaryIndicator

� Yes� No

Adapted from Diehm N,Pattynama PM, Jaff MR,et al. Clinical endpoints inperipheral endovas-cularrevascularization trials: acase for standardizeddefinitions. Eur J VascEndovasc Surg.2008;36:409–19 (60).

PVI—Lesion Restenosis Renarrowing of a lesion sitefollowing treatment of aprior stenosis, to a diameterstenosis of >50% at thepreviously treated lesionsite, inclusive of the originaltreated site plus theadjacent vascular segments10 mm proximal and 10 mmdistal to the treatedsegment.

Peripheral VascularInterventionRestenosis, Lesion—Angiographic BinaryIndicator

� Yes� No

Adapted from Diehm N,Pattynama PM, JaffMR, et al. Clinicalendpoints in peripheralendovascularrevascularization trials: acase for standardizeddefinitions. Eur J VascEndovasc Surg.2008;36:409–19 (60).

PVI—TLR Repeat PVI of a target lesion(including 10 mm proximaland 10 mm distal to theindex device) or surgicalintervention/bypass of atarget vessel, performedfor restenosis or othercomplication involvingthe target lesion.In the assessment of TLR,angiograms should beassessed by an angiographiccore laboratory (ifdesignated). Angiograms(and core laboratoryassessment thereof) andother source documentationshould be made available tothe CEC for review onrequest.

Peripheral VascularIntervention TargetLesionRevascularizationIndicator

� Yes� No


PVI—Ischemia Before TLR Criteria for clinical orfunctional ischemia includeany of the following:a) Recurrent/progressive

intermittentclaudication

b) Critical limb ischemiac) Recurrence of the clin-

ical syndrome for whichthe initial procedurewas performed.

Percutaneous CoronaryIntervention TargetLesionRevascularizationIschemia Indicator

� Yes� No


PVI—Clinically Driven TLR TLR is clinically driven if thetarget lesion diameterstenosis is >50% AND thesubject has either clinical orfunctional ischemia (e.g.,recurrent/progressiveintermittent claudication,critical limb ischemia) ORrecurrence of the clinicalsyndrome for which theinitial procedure wasperformed. Clinically drivenTLR occurs in the absenceof protocol-directedsurveillanceultrasonography orangiography.

Percutaneous CoronaryIntervention TargetLesionRevascularizationClinically DrivenIndicator

� Yes� No





465




PermissibleValues



PVI—TLF The composite of ischemia-driven TLR AND eitherevidence of clinical orfunctional ischemia (e.g.,recurrent/progressiveintermittent claudication,critical limb ischemia) ORrecurrence of the clinicalsyndrome for which theinitial procedure wasperformed. If it cannot bedetermined with certaintywhether clinical/functionalischemia or the clinicalsyndrome was related to thetarget vessel, it isconsidered a TLF.

Peripheral VascularIntervention TargetLesion Failure Indicator

� Yes� No


PVI—Target Vessel Name of the peripheralartery level containing aPVI target lesion that isthe subject of clinicalinvestigation. In the contextof clinical investigation, atarget vessel is anynoncardiac ornonintracranial blood vesselthat contains the targetlesion treated with the studydevice. The target vesselincludes the target lesion aswell as the entire length ofnative vessel upstream anddownstream from the targetlesion, including sidebranches.For the arteries of the leg,the vasculature is dividedinto 3 vessel “levels”: aorto-iliac, femoral-popliteal, andtibial-crural.

Peripheral VascularIntervention TargetVessel Name

� Aorto-iliac� Femoro-popliteal� Tibial-crural


Aorto-iliac Infrarenal aorta and iliacarteries (to the bottomof the pelvic rim/inguinal ligament),including branches ofthese vessels.

Femoro-popliteal Femoral and poplitealarteries (to the origin ofthe anterior tibialartery), includingbranches of thesevessels.

Tibial-crural Anterior tibial andbelow, including thearteries of the foot.

PVI—TVR Repeat intervention orsurgical bypass of anysegment of a target vessel.In the assessment of TVR,angiograms should beassessed by an angiographiccore laboratory (ifdesignated). Angiograms(and core laboratoryassessment thereof) andother source documentationshould be made available tothe CEC for review onrequest.

Peripheral VascularIntervention TargetVesselRevascularizationIndicator

� Yes� No






466




PermissibleValues



PVI—Vessel Patency The absence of clinicallydriven TLR and/or absenceof recurrent target lesiondiameter stenosis >50% byimaging (e.g., invasiveangiography or, mostcommonly, duplexultrasonography).If patency data areincorporated within theprimary endpoint of aclinical trial, theangiographic images orduplex ultrasonographicimages should be assessedby appropriate corelaboratories and madeavailable to the CEC forreview on request.

Vessel PatencyIndicator

� Yes� No


PVI—Target Limb The target limb is theextremity that contains thetarget lesion and all thenative vessels upstream anddownstream from it,including side branches.

Peripheral VascularIntervention TargetLimb Name

� Right leg� Left leg


PVI—Target Limb Failure TLF is the composite ofischemia-drivenrevascularization of thetarget limb and majoradverse ischemic eventsaffecting the target limb. Ifit cannot be determinedwith certainty whether anevent was related to thetarget limb, it is considereda TLF.

Peripheral VascularIntervention TargetLimb Failure Indicator

� Yes� No


PVI—Nontarget LesionSegment

Name of a peripheral arterysegment where PVI wasperformed that is NOT thesubject of clinicalinvestigation. In the contextof clinical investigation, anylesion not treated or forwhich treatment was notattempted with the deviceor technique being studied.This includes lesions treatedwith (nonstudy) PVI andlesions managed medically.

Peripheral VascularIntervention Non-Target Lesion SegmentName


PVI—Nontarget LesionRevascularization

Any (de novo or repeat)vascular intervention of anontarget lesion or bypasssurgery of a nontargetvessel. This includesrevascularization at the timeof an index (study) vascularintervention of a separatetarget lesion andsubsequentrevascularization after theindex (study) vascularintervention.

Peripheral VascularIntervention Non-Target LesionRevascularizationIndicator

� Yes� No


PVI—Nontarget Vessel In the context of clinicalinvestigation, any vessel orbypass graft not treated orfor which treatment was notattempted with a device ortechnique being studied.

Peripheral VascularIntervention Non-Target Vessel Name

� Aorto-iliac� Femoro-popliteal� Tibial-crural

Adapted from Diehm N,Pattynama PM, Jaff MR,et al. Clinical endpoints inperipheral endovascularrevascularization trials: acase for standardized




467


PermissibleValues



This includes vessels treatedwith (nonstudy) vascularintervention and vesselsmanaged medically. For thearteries of the leg, thevasculature is divided into 3vessel “levels”: aorto-iliac,femoral-popliteal, andtibial-crural.

definitions. Eur J VascEndovasc Surg.2008;36:409–19 (60).

Aorto-iliac Infrarenal aorta and iliacarteries (to the bottomof the pelvic rim/inguinal ligament),including branches ofthese vessels.

Femoro-popliteal Femoral and poplitealarteries (to the origin ofthe anterior tibialartery), includingbranches of thesevessels.

Tibial-crural Anterior tibial andbelow, including thearteries of the foot.

PVI—Nontarget VesselRevascularization

Any (de novo or repeat)vascular intervention orsurgical bypass of anysegment of a nontargetvessel. This includesrevascularization of anontarget lesion at the timeof an index (study) vascularintervention or subsequentto the index vascularintervention.

Peripheral VascularIntervention Non-Target VesselRevascularizationIndicator

� Yes� No


Peripheral Artery BypassGraft—Lesion Location

Location of a lesion within aperipheral artery bypassgraft where PVI wasperformed.

Peripheral Artery GraftLesion Location

� Graft anastomosis—proximal

� Graft body� Graft anastomosis—

distal


Graft anastomosis—proximal

The section of a graftfrom the connection(anastomosis) of thegraft with the proximalartery, inclusive of thefirst 3 mm of the graft.

Graft body The section of a graftbetween the proximaland distal anastomoses.

Graft anastomosis—distal The section of a graftfrom the connection(anastomosis) of thegraft with the distalartery, inclusive of theretrograde 3 mm of thegraft.

Peripheral Artery BypassGraft—Type

Type of peripheral arterybypass graft conduit.

Peripheral Artery GraftType

� Autologous veingraft

� Synthetic graft� Composite graft� Cadaveric graft—

arterial� Cadaveric graft—

venous� Other graft





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PermissibleValues



Autologous vein graft Bypass graft composedof autologous vein(harvested from thepatient).

Synthetic graft Bypass graft composedof nonbiological conduitmaterial.

Composite graft Bypass graft composedof a composite ofmaterials.

Cadaveric graft—arterial Bypass graft composedof artery harvestedfrom a cadaver.

Cadaveric graft—venous Bypass graft composedof vein harvested from acadaver.

Other graft Bypass graft notcomposed ofautologous vein,synthetic conduit,composite construction,or of cadaveric origin.

Peripheral Artery BypassGraft—SyntheticMaterial

Type of material used in asynthetic peripheral arterybypass graft conduit.

Peripheral Artery Graft,Synthetic Material

� Gortex� PTFE� Polyester� Dacron� Polyurethane

Peripheral Artery BypassGraft—Anastomosis

The peripheral arterysegment to which aperipheral artery bypassgraft is connected.

Peripheral Artery GraftAnastomosis



CEC indicates Clinical Events Committee; PTFE, polytetrafluoroethylene; PVI, peripheral vascular intervention; TLF, target lesion failure; TLR, target lesion revascularization; and TVR,target vessel revascularization.



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