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Acute Coronary Syndromes

Rabeea Aboufakher, MD, FACC, FSCAI

Section Chief of Cardiology

Altru Health System

Grand Forks, ND

Overview

� Epidemiology

� Pathophysiology

� Clinical features and diagnosis

� STEMI management

� NSTEMI/UA management

Introduction/Epidemiology

� CAD is a major cause of death and disability worldwide

� Responsible for one third of all deaths in

individuals over age 35

� 17.6 million persons in the US have CAD

Introduction/Epidemiology

� ACS will strike 935,000 people a year in the US, an estimated 250,000 of those will be STEMIs

� In ND 43% of adults have 3 or more risk factors

for Cardiovascular disease

� CV disease is the #1 leading cause of death in ND

Age adjusted death rates for coronary heart disease by race/ethnicity and sex, US, 1999 to 2008

Prevalence of CAD

and CAD mortality have declined over the

past 4 decades in the

US

Deaths from cardiovascular disease, US, 1900 to 2008

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PATHOPHYSIOLOGY

CAD

� Spectrum of presentation

� silent ischemia

� exertion-induced angina

� unstable angina

� acute myocardial infarction

� STEMI

� NSTEMI

Acute coronary syndromes

Stable Vs. Unstable

� Slowly accruing high-grade stenoses of epicardial coronary arteries may progress to complete occlusion but do not usually precipitate ACS� Stable angina

� Silent ischemia

� Abrupt and catastrophic transition may occur characterized by plaque disruption by rupture of the fibrous cap or erosion of the surface� ACS

Pathophysiology of ACS

The shift in our understanding of ACSs Pathophysiology of ACSThe Vulnerable Plaque

Most lesions that cause ACSs are not severely stenotic

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CLINICAL FEATURES

Chest Pain

Atypical presentations are common in women,

diabetics and the elderly

ECG

� Septal: V1 and V2

� Anterior: V3 and V4

� Lateral: V5 and V6

� Anteroseptal: V1-V4

� Anterolateral: V3-V6

� Extensive anterior: V1-V6

� Inferior: II, III, aVF

� High Lateral: I, aVL

� Posterior: R wave and ST depression in V1-V2

Always look for the reciprocal changes

Extensive Anterior STEMI

Inferior STEMI with Posterior and

Lateral InvolvementIsolated Posterior STEMI

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LBBB ST Depression

T Wave Inversion Cardiac Enzymes

Coronary Angiography

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STEMI MANAGEMENTACC/AHA GUIDELINES

STEMI: Time is muscle!!

STEMI

What is

1/5/2015 ©2010, American Heart Association

Improving the System of Care for STEMI Patients

Mission: Lifeline

• Mission: Lifeline will:

– Promote ideal STEMI systems of care

– Help STEMI patients get the life-saving care they need in time

– Bring together healthcare resources into an efficient, synergistic system

– Improve overall quality of care

• The initiative is unique in that it:

– Addresses the continuum of care for STEMI patients

– Preserves a role for the local STEMI-referral hospital

– Understands the issues specific to rural communities

– Promotes different solutions/protocols for rural vs. urban/suburban areas

– Recognizes there is no “one-size-fits-all” solution

– Knows the issues of implementing national recommendations on a community level

ND Hospitals

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Pre-hospital Care (EMS)

� Non-enteric-coated aspirin (162-325 mg chewed) Class I

� Pre-hospital ECG Class IIa

� Oxygen Class I

� IV access

� Morphine as needed for pain control Class I

� Sublingual nitroglycerine Class I

Initial Recognition and Management in the ED

� Hospitals should develop guideline-based, institution-specific written protocols for triaging and managing pts with symptoms suggestive of STEMI Class I

� Door to needle time should be < 30 minutes Class I

� Door to balloon time should be < 90 minutes Class I

� Focused history and physical to make sure other important diagnoses are not missed

ECG

� 12 lead ECG should be performed and shown to the ED physician within 10 minutes of arrival

Class I

� If the ECG is not diagnostic but symptoms continue repeat ECG in 5-10 minutes Class I

� If inferior ST elevation a right sided ECG should

be done to assess for RV infarction Class I

Beta Blockers

Class IOral beta-blocker therapy should be administered

promptly to those patients without a contraindication

Class IIa

It is reasonable to administer IV beta-blockerspromptly to patients without contraindications, especially if a tachyarrhythmia or hypertension is

present

Reperfusion Therapy: Primary PCI vs. Fibrinolysis Reperfusion Therapy

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Relative Risk of In-Hospital Death with Each Additional 15 Minute Interval in Door to Balloon Time As Compared to Less Than 90 Minutes

Nallamothu B et al. N Engl J Med 2007;357:1631-1638

Reperfusion Therapy

Heparin

� UFH bolus of 60 U/kg (maximum 4000 U) followed by an initial

infusion of 12 U/kg per hour (maximum 1000 U/hr) adjusted to maintain aPTT at 1.5 to 2.0 times

� Should be given with fibrinolysis Class I

� Should also be given to pts treated with primary PCI Class I

� LMWH especially enoxaparin is an acceptable alternative to UFH in

pts who undergo PCI or fibrinolysis but is contraindicated in

� Patients older than 75 years

� Patients with renal dysfunction (Cr >2.5 in men and >2.0 in women)

Class IIb

Glycoprotein IIb/IIIa Inhibitors

� It is reasonable to start treatment with abciximab or other GP IIb/IIIa inhibitors before PCI Class IIa

� Have fallen out of favor due to increased bleeding and use of better antiplatelet and anticoagulant agents

� May have a role in the high risk patient with large burden of thrombus and low risk of bleeding

Direct Thrombin Inhibitors: Bivalirudin

� The most significant advance in antithrombotic agents during PCI

� Has several advantages over heparin

� Specific thrombin inhibitor so activity is predictable (no need for ACT testing

� Short half-life (25-30 minutes)

� No risk of heparin-induced thrombocytopenia

� Lower risk of bleeding

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Bivalirudin in Primary PCI Antiplatelet Therapy

� Aspirin should be continued indefinitely after STEMI Class I

� A loading dose of P2Y12 antagonist is recommended when PCI is planned Class I

� Clopidogrel 300 or 600 mg

� Prasugrel 60 mg

� Ticagrelor 180 mg

� The duration of treatment should be at least 12

months after stenting Class I

� Should be discontinued 5 days before CABG

ACE-I and ARB

� An ACE-I or an ARB should be given orally within the first 24 hours of STEMI

� In pts with anterior infarct, pulmonary congestion or with EF<40% Class I

� In all patient with STEMI Class IIa

� IV ACE-I or ARB should not be given in the first 24 hours to avoid hypotension Class III

Summary of Initial Treatment in ED

� MONA

� ECG with interpretation within 10 minutes

� Decision on reperfusion therapy (fibrinolysis or primary PCI)

� Activate cath lab if PCI center

� Decision on transfer if non-PCI center

� Load with a P2Y12 antagonist (confirm with cardiologist)

� UFH or LMWH

� Consider glycoprotein IIb/IIIa inhibitor (only after discussion with cardiologist)

� BB if no contraindication

UA/NSTEMI MANAGEMENTACC/AHA GUIDELINES

NSTEMI and Unstable Angina

� The only difference is cardiac enzyme elevation due to more severe ischemia

� Same symptoms, pathophysiology and

management guidelines

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Unstable Angina

� Angina occurring at rest and prolonged, usually greater than 20 min

� New-onset angina of at least CCS class III severity

� Previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (i.e., increased by 1 or more CCS class to at least CCS class III severity)

TIMI Risk Score

� Age > 65 yrs

� > 3 risk factors for CAD

� Prior coronary stenosis > 50%

� ST segment deviation on admission ECG

� > 2 anginal episodes in prior 24 hrs

� Elevated serum cardiac biomarkers

� Use of ASA in prior 7 days

TIMI Risk Score for Non-ST Elevation ACS High-Risk Patients

Pt. Characteristics– Older age (>75 yrs)

– Hemodynamic instability– Signs and symptoms of CHF– Ventricular arrhythmias

Disease severity– Crescendo, recurrent or refractory angina

– Positive serum cardiac biomarkers– ST-segment deviation

Initial Medical Treatment

� Similar to STEMI management with MONA, beta blockers and ACE-I inhibitors

� No beta blockers if

� Signs of HF

� Patient is at risk of cardiogenic shock (bradycardia or hypotension)

� Severe asthma or reactive airway disease

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Nitroglycerine

� Give if ongoing ischemic discomfort

� Do not give if:

� SBP < 90

� HR < 50

� Tachycardia

� Suspected RV infarct

� Treatment with PDE inhibitors

Antiplatelet Therapy

� Aspirin

� Clopidogrel (300-600 mg loading dose followed by 75 mg daily)

� Prasugrel (60 mg loading dose followed by

10 mg daily) (only for patients undergoing PCI in the cath lab)

� Ticagrelor (180 mg loading dose followed by

90 mg BID)

Aspirin in UA/NSTEMI Clopidogrel in UA/NSTEMI

Prasugrel in ACS

� Prasugrel

� Less MI

� Less stent

thrombosis

� More bleeding

� Not useful/ harmful

� History of CVA or TIA

� Age > 75 years

� Weight < 60 kg

Ticagrelor in ACS

� Ticagrelor

� Less vascular

death and MI

� Less stent

thrombosis

� No major difference in

bleeding

� STEMI and

NSTEMI/UA

� Aspirin < 100 mg

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GP IIb/IIIa Inhibitors

� Selective rather than routine use is advised due to high risk of bleeding in certain groups of patients with triple antiplatelet therapy

� Do not use if no plans for PCI

� Abciximab is preferred for STEMI

� Eptifibitide and tirofiban are associated with less thrombocytopenia and shorter half lives

Anticoagulation

� Initial invasive strategy

� UFH

� Enoxaparin

� Bivalirudin (direct thrombin inhibitor)

� Fondaparinux (Factor X inhibitor)

� Initial conservative strategy

� UFH

� Enoxaparin

� Fondaparinux

Bivalirudin in Acuity

� Similar

ischemic events

� Less bleeding events

� Superior net

clinical outcome

Initial Invasive Vs. Initial Conservative Strategy

Initial Invasive Vs. Initial Conservative Strategy

� Most patients with UA/NSTEMI should undergo initial invasive strategy with angiography and intention to revascularize

� Initial conservative strategy

� Patients with multiple co-morbidities

� Patients with chest pain unlikely to be cardiac

� Low risk ACS especially in older underweight women if stress

testing is low risk

QUESTIONS?

Thank you for your attention