410

Point of ViewResearch on Unstable Coronary Syndromes

Unstable AnginaA Classification

Eugene Braunwald, MD

T he establishment of a prognosis and theapproach to the treatment of many diseasesis aided greatly by a logical classification.

For example, classification of a wide variety ofneoplasms by anatomic extent, microscopic appear-ance, and the presence of special markers nowforms the basis for selecting appropriate therapy. Incardiology, the classification of patients with acutemyocardial infarction and congestive heart failurehas been of enormous value in following the prog-ress and in selecting therapy of individual patientsand in comparing the outcome of similar patientstreated at different locations and at different times.The purpose of this article is to provide a classifi-cation of unstable angina. This classification isdesigned to facilitate communication about thesepatients, to aid in the decision regarding diagnosticmeasures and therapy of individual patients, and toprovide a more precise basis for including patientsin and for evaluating the outcome of clinical trials.Unstable angina is a complex condition. Early in

this century, the clinical-pathologic features of twoof the principal manifestations of ischemic heartdisease-acute myocardial infarction and chronicstable angina-had already been well described. Ithas taken much longer to define a syndrome that isintermediate in severity between these two condi-tions. In 1923, Wearn' described, in a group of 19patients with acute myocardial infarction confirmedat necropsy, attacks of angina pectoris that mayprecede myocardial infarction and serve as warn-ings of the presence of coronary artery disease. In1937, Sampson and Eliaser2 and Feil3 separatelydescribed a syndrome consisting of severe, pro-longed anginal pain that often led to acute myocar-dial infarction, and they termed it "impending acutemyocardial infarction." Other terms that have beenused for this condition include "preinfarction angina,""crescendo angina," "status anginosus,'" "accel-erated angina," "acute coronary insufficiency," and

The opinions expressed in this point of view are not necessar-ily those of the editors or of the American Heart Association.From the Department of Medicine, Harvard Medical School,

Brigham and Women's and Beth Israel Hospitals, Boston,Massachusetts.Address for correspondence: Eugene Braunwald, MD, Brigham

and Women's Hospital, 75 Francis Street, Boston, MA 02115.

"intermediate coronary syndrome"4-7; the term mostfrequently used now, "unstable angina," was used byFowler8 and Conti et a19 in 1971. This large number ofdesignations, as well as the lack of a clear, agreed-upon definition, reflects the ambiguity that has con-tinued to be associated with this "catch-all" syn-drome. Unstable angina probably consists of a numberof conditions, all characterized by severe transientmyocardial ischemia.10-13

Unstable angina is very common and often quiteserious; it is responsible for more than 750,000hospitalizations annually in the United States14 andthus ranks among the most frequent causes of hos-pitalization in this country. More than 70,000 ofthese hospitalized patients develop myocardialinfarction,13 and some die suddenly.15 An unknown,but probably large, number of patients with unstableangina are not hospitalized but are treated at home.Many patients with unstable angina do not developserious complications, but after recovery from theacute episode, they are left with chronic stableangina of varying severity. A minority of patientsrecover without developing either complications orchronic angina. In addition, a substantial percentageof patients who develop acute myocardial infarction,ranging from 30% to 60% in most series,16 experiencea prodrome of unstable angina before reaching thehospital. A significant percentage of patients withacute myocardial infarction develop unstable anginain the early postinfarction period.There is currently intense interest in elucidating

the pathogenesis of unstable angina.10'17 Maseri18 hasemphasized that both increased myocardial oxygendemand in the presence of severly restricted coro-nary reserve and dynamic stenosis caused by coro-nary vasoconstriction may be responsible. Coronaryarteriographic examinations have revealed that rapidprogression of coronary stenosis often precedes thedevelopment of unstable angina19 and that this ste-nosis is frequently caused by eccentric, irregularlesions20 often associated with filling defects thoughtto be caused by coronary thrombi.21-24 Angioscopicstudies at operation have revealed that many patientswith unstable angina have disrupted, fissured plaquesoften associated with mural thrombi25; the latterfinding has been confirmed by pathologic exami-nation.26 Also, evidence exists that abnormal coro-

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Braunwald Classification of Unstable Angina 411

TABLE 1. Classification of Unstable Angina

Clinical circumstances

A. Develops in presence ofextracardiac condition that B. Develops in absence of C. Develops within 2 wk

intensifies myocardial extracardiac condition after AMISeverity ischemia (secondary UA) (primary UA) (postinfarction UA)

I. New onset of severe anginaor accelerated angina; norest pain IA IB IC

IT. Angina at rest within pastmonth but not withinpreceding 48 hr (Angina atrest, subacute) IIA IIB IIC

ITT. Angina at rest within 48 hr(Angina at rest, acute) IIIA IIIB IIIC

Patients with UA may also be divided into three groups depending on whether UA occurs 1) in the absence of treatment for chronicstable angina, 2) during treatment for chronic stable angina, or 3) despite maximal anti-ischemic drug therapy. These three groups maybe designated by subscripts 1, 2, or 3, respectively.

Patients with UA may be further divided into those with and without transient ST-T wave changes during pain.UA, unstable angina; AMI, acute myocardial infarction.

nary vasoconstriction18 and activation of platelets27and of the clotting system10 may occur during and beof pathogenetic importance in unstable angina. Cor-onary thrombi causing variable degrees of coronaryobstruction may develop and regress rapidly,reflecting the opposing actions of the hemostatic andfibrinolytic systems. Platelet emboli may causearrhythmias and sudden death in these patients.28Unstable angina occurring soon after acute myocar-dial infarction is particularly dangerous, often her-alds infarct extension, and is associated with a highincidence of recurrent events29-32; the latter alsooccur more frequently in patients whose episodes ofchest pain are accompanied by transient electrocar-diographic changes of ischemia.33-38

Considerable efforts are also underway to improvethe treatment of unstable angina, and a variety oftherapeutic approaches are being actively used andinvestigated. In addition to anti-ischemic pharma-cologic agents (nitrates, ,3-adrenergic blockers, andcalcium antagonists), therapeutic options includeanticoagulants, antiplatelet aggregating agents,thromboxane synthesis inhibitors, thromboxanereceptor blockers, thrombolytic agents, percutane-ous transluminal angioplasty, and coronary arterybypass surgery.1"'39-48 New methods of revascular-ization, such as coronary atherectomy, balloon angio-plasty with stents, and laser angioplasty, are beingactively investigated. These modes of therapy arebeing tested in various combinations and sequences,and a major challenge will be to select individualpatients with unstable angina for various treatmentoptions.One impediment to obtaining a clearer understand-

ing of the natural history of unstable angina and toevaluating therapeutic strategies is the heteroge-neous nature of the syndrome and the lack ofgeneral agreement about its precise definition. Cur-rently, a broad spectrum of patients with ischemicepisodes varying widely in cause, severity, progno-sis, and responsiveness to therapy are lumped

together under the broad umbrella of unstable anginapectoris. These patients can be described by usinginformation obtained not only from the clinicalexamination and routine electrocardiogram but alsofrom a variety of specialized tests, including coro-nary arteriography, left ventriculography, continu-ously recorded (Holter) electrocardiography, andperfusion scintigraphy. Characterization of patientsby all of these methods can lead to the classificationof unstable angina into an almost infinite number ofsubgroups. Such fine classification is almost asuseless to the clinician as is the lumping of allpatients into a single category.To separate patients with unstable angina into a

manageable number of meaningful and easily under-stood subgroups based on the severity, the pre-sumed precipitating cause, and the presence ofelectrocardiographic changes, a clinical classifica-tion of this condition is proposed (Table 1). Thisclassification focuses on three important aspects ofunstable angina: 1) the severity of the clinical man-ifestations, 2) the clinical circumstances in whichunstable angina occurs, and 3) whether or not thesymptomatic ischemic episodes are accompaniedby transient electrocardiographic changes. The clas-sification can be made before obtaining the above-mentioned specialized laboratory tests, and oncethe tests are performed, the results may then beused to supplement the clinical information and thestandard electrocardiogram. This classification ofunstable angina is based on two premises: 1) thepatient's symptoms are actually caused by myocar-dial ischemia, and 2) in patients with prolongedischemia, the diagnosis of acute myocardial infarc-tion is excluded by electrocardiography or serumenzyme determinations. Often, this exclusion mustbe retrospective.

ClassificationSeverity

Class L New onset severe or accelerated angina.Patients with new onset (<2 months in duration)

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412 Circulation Vol 80, No 2, August 1989

exertional angina pectoris that is severe or frequent(>3 episodes/day) or patients with chronic stableangina who develop accelerated angina (that is,angina distinctly more frequent, severe, longer induration, or precipitated by distinctly less exertionthan previously) but who have not experienced painat rest during the preceding 2 months.

Class I. Angina at rest, subacute. Patients withone or more episodes of angina at rest during thepreceding month but not within the preceding 48hours.

Class III. Angina at rest, acute. Patients with oneor more episodes of angina at rest within the pre-ceding 48 hours.

In classes II and III, manifestations described inclass I may also occur. Unstable angina is no longerconsidered to be present when a patient has beenasymptomatic or suffers angina that has been stablefor more than 2 months.

Clinical Circumstances in Which UnstableAngina Occurs

Class A. Secondary unstable angina. Patients inwhom unstable angina develops secondary to aclearly identified condition extrinsic to the coronaryvascular bed that has intensified myocardial isch-emia. Such conditions reduce myocardial oxygensupply or increase myocardial oxygen demand andinclude anemia, fever, infection, hypotension, uncon-trolled hypertension, tachyarrhythmia, unusual emo-tional stress, thyrotoxicosis, and hypoxemia sec-ondary to respiratory failure.

Class B. Primary unstable angina. Patients whodevelop unstable angina pectoris in the absence ofan extracardiac condition that has intensified isch-emia, as in class A.

Class C. Postinfarction unstable angina. Patientswho develop unstable angina within the first 2 weeksafter a documented acute myocardial infarction.

Electrocardiographic ChangesIf an electrocardiogram has been recorded during

an episode of chest pain, the presence or absence oftransient ST-T abnormalities is noted. (The pres-ence of such abnormalities is associated with moresevere underlying disease.33-38)

Intensity of TreatmentFor research purposes, especially clinical trials, it

may be helpful also to classify patients by the inten-sity of treatment as follows: 1) unstable anginaoccurring in the absence of or with minimal antiangi-nal therapy; 2) unstable angina occurring in thepresence of appropriate therapy for chronic stableangina (the administration of conventional oral dosesof antianginal drugs, i.e., ,3-adrenergic blockers, long-acting nitrates, and calcium antagonists); and 3)unstable angina occurring in the presence of maxi-mally tolerated doses of all three categories of anti-ischemic drugs, including intravenous nitroglycerin.49

These three levels of treatment may be desig-nated by the subscripts 1, 2, and 3.

DiscussionThis classification of unstable angina, which should

be tested prospectively, permits the grading ofpatients with unstable angina from the mildest tothe most severe condition. An example of themildest form would be a patient with chronic stableangina who develops marked intensification ofexertion-induced angina pectoris after blood lossand who has no ST segment or T wave changesduring angina. This patient would be in class IAwithout transient electrocardiographic changes (I,accelerated angina; A, secondary unstable angina).At the other end of the spectrum is the patient whoexperiences recurrent angina at rest with transientST segment depressions several days after an acutemyocardial infarction. This patient would be inclass IIIC with transient electrocardiographicchanges (class III, angina at rest, acute; C, postin-farction unstable angina).

Unstable angina is a dynamic condition, andpatients may initially be in one class and move toanother as the underlying disease changes or asresponse to treatment occurs. For example, a patientwith the new onset of severe and frequent exer-tional angina without an apparent provocative ex-tracardiac condition is in class IB. If that patientthen developed an episode of angina at rest, hewould be in class IIIB. If no pain recurred for 48hours, he would be in class IIB.The classification of the intensity of treatment

may be used as follows. A patient with a history ofprimary unstable angina at rest during convales-cence from a myocardial infarction who is receivingno anti-ischemia therapy is in class 111C1. If epi-sodes of pain persist despite treatment with usualdoses of antianginal agents, the patient wouldadvance to 111C2; if during treatment with intrave-nous nitroglycerin the episodes disappeared formore than 48 hours, the patient would be classifiedas IGC3.Although the proposed classification of unstable

angina is clinical, it can be related to the underlyingdisease. Angioscopic observations performed dur-ing operation suggest a good correlation betweenthe presence of nonocclusive thrombi and the recentoccurrence of angina at rest.25 Such thrombi usuallyundergo rapid spontaneous lysis and thereforebecome less prevalent with the passage of time.Thrombolytic or anticoagulant therapy may there-fore be of great value in patients in class III, of lessvalue in class II, and of little value in class I. Theprecipitation of unstable angina by changes in con-ditions extrinsic to the coronary artery bed thathave intensified ischemia (class A) is compatiblewith fixed, severe coronary obstruction, and thepresence of a fissured plaque or thrombus need notbe presumed (but cannot, of course, be excluded).Unstable angina secondary to an increase in myo-

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Braunwald Classification of Unstable Angina 413

cardial oxygen needs or abnormal coronary vaso-constriction generally responds to bed rest, mildsedation, and vigorous treatment with multiple anti-ischemic drugs; failure to respond to such vigoroustherapy suggests total or subtotal coronary occlu-sion, sometimes by a thrombus.

It is hoped that this classification will aid in theclear description of and communication aboutpatients with unstable angina, in the elucidation ofthe natural history and prognosis of the varioussubgroups, in the precise definition of patientsselected for clinical trials so that therapy can beevaluated in comparable patients, and ultimately inthe development of treatment regimens that areappropriate for each subgroup.

AcknowledgmentsThe aid of a number of colleagues who reviewed

this manuscript is gratefully acknowledged. Partic-ularly valuable suggestions were made by Drs. C.R.Conti, S. Epstein, V. Fuster, L. Goldman, R.Gorlin, S. Gottlieb, R. Helfant, A. Maseri, R. Ross,and T. Ryan.

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Circulation 1989;80:410-414

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E BraunwaldUnstable angina. A classification.

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1989 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.80.2.410

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