Grand Rounds Series - Northwestern Cardiology Fellows

Unstable Angina and Non-ST elevation

Myocardial Infarction

John Blair, MD

Unstable Angina / Non ST-Elevation Myocardial

Infarction (UA/NSTEMI)

• Pathophysiology

• Diagnosis

• Initial Therapy

• Risk-Stratification

• Invasive vs Conservative

• Post AMI Care www.

Clinical trial results.org

UA / NSTEMI

• Pathophysiology

• Diagnosis

• Initial Therapy





Sudden Thrombus or Thromboembolism

Superficial

Erosion

Ruptured

Fibrous Cap

Modified from Libby P

Circ 104:365,2001 www.


Hamm Lancet 358:1533,2001

Presentation

Working Dx

Ischemic Discomfort

Acute Coronary Syndrome

Davies MJ

Heart 83:361, 2000

ECG

No ST Elevation

NSTEMI

Biochem.

Marker

Final Dx Unstable Angina www.


ST Elevation

Myocardial Infarction

NQMI Qw MI

Causes of UA/NSTEMI

• Thrombus or thromboembolism , usually arising on disrupted or eroded plaque – Most Common Cause.

• Dynamic obstruction – coronary spasm or vasoconstriction

• Progressive mechanical obstruction to coronary flow – ie restenosis after PCI

• Coronary arterial inflammation

• Coronary artery dissection

• Secondary UA – Increasing oxygen demands in the setting of a fixed lesion. www.


Acute Coronary Syndromes

• Pathophysiology

• Diagnosis

• Initial Therapy





Likelihood that Signs and Symptoms Represent ACS

Feature High Likelihood Intermediate

Likelihood

History Chest/L arm pain similar to prior angina, known

CAD

Exam

Chest/L arm pain, >70 y/o,

Male, DM,

MR murmur, hypotension, diaphoresis, pulm edema, rales

Extracardiac vascular disease

ECG

Cardiac

Markers

New transient ST deviation (>1mm) or TWI in multiple leads

Elevated TnI,

TnT, CK-MB

Fixed Q waves,

ST depression

0.5-1mm, TWI

>1mm

Normal www.


Low

Likelihood

Probable ischemia, recent cocaine use

CP on palpation

TWI <1mm in leads with dominant R waves

Normal

Algorithm for Evaluation and Management of Patients

Suspected of Having ACS www.


Timing of Release of Various Biomarkers After Acute

Myocardial Infarction www.



• Pathophysiology

• Diagnosis

• Initial Therapy





Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs

• IIb/IIIa inhibitors

• Plavix

• ACE/ARB

• Aldosterone Blockade

• Statins www.


• Increases oxygen supply to ischemic tissue

• Start at 4L/min

• Use caution in COPD patients

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• Blocks formation of thromboxane A

2 and thus prevents platelet aggregation

• Reduces mortality, reinfarction, and stroke in patients with MIs

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• Blocks catecholamines from binding to β-adrenergic receptors

• Reduces myocardial demand by reducing HR, BP, contractility

• Decreases incidence of primary VF

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• Dilates coronary arteries

• Increases venous dilation and therefore decreases venous return

• Decreases myocardial demand by decreasing preload

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• Reduces pain of ischemia and anxiety  indirect effect on catecholamines

• May dilate coronary arteries and reduce preload  decreases myocardial oxygen demand

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• Heparins - Indirect thrombin inhibitors including LMWH

• DTI - Direct thrombin inhibitors

• Reduce further coagulation

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• Blocks platelet receptor so platelets cannot bind fibrinogen and form clots

• caution in renal disease (tirofiban, ebtifbatide) and with thrombocytopenia

(abciximab)

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• Blocks the ADP receptor on platelets which also prevents fibrinogen binding and clot formation

• Bleeding risks during CABG have limited its immediate use until coronary anatomy defined

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• reduces peripheral vasoconstriction and blood pressure

• Alters post-MI LV remodeling

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• reduces fibrosis, hypokalemia, and arrhythmias

• beneficial in high-risk post-AMI LV dysfunction

Treatment

• Oxygen

• Aspirin

• Beta-blocker

• Nitroglycerin

• Morphine

• Heparins, DTIs


• Plavix

• ACE/ARB




• reduce LDL

• may decrease inflammation

Initial Therapy

• Anti-ischemic and Analgesic therapy

• Anti-platelet therapy

• Anti-coagulant therapy www.


ACC/AHA Guidelines – Updated in 2007 from 2002 www.


Anti-ischemic and Analgesic Therapy

•

Bed/chair rest

– Class I, C

•

O2

for SaO2 < 90%, respiratory distress, or hypoxemia – Class I, B

•

NTG

0.4 mg sl q 5 min x 3 doses, then gtt for ongoing ischemic discomfort – Class I, C

•

NTG

iv within 48h for persistent ischemia, HF, or

HTN. Should not preclude use of BB – Class I, B

•

Oral BB

therapy within 24h without 1) HF, 2) low output, 3) risk of shock, 4) relative contraindications

– Class I, B www.


Anti-ischemic and Analgesic Therapy

•

CCB

(nondihydropyridine) if contraindication for BB in the absence of contraindications – Class I, B

•

ACE inhibitor

for LVEF <0.40 and no hypotension

(SBP <100 or <30 below baseline) – Class I, A

•

ARB

if intolerant to ACE inhibitor – Class I, A

• NSAIDS should be discontinued – Class I, C www.


Anti-Platelet Therapy

•

ASA

– started immediately and continued indefinitely – Class I, A

•

Plavix

– loading dose (300-600mg)* plus maintenance 75 mg if ASA intolerant – Class I, A

• If h/o GIB, PPI plus anti-platelet therapy – Class I, B

•

GP IIB/IIIA

therapy depends on strategy chosen

(more on this later)

* Risk/benefit to higher loading dose regimens is yet to be determined www.


Anti-Coagulant Therapy

•

Anticoagulant

Therapy should be added to antiplatelet therapy as soon as possible after presentation

• Choice of anticoagulant depends on the strategy chosen (more on this later) www.


There is an Incremental Benefit to ASA, UFH/LMWH, and

GPIIb/IIIa Therapy www.



• Pathophysiology

• Diagnosis

• Initial Therapy





Kaplan-Meier Estimates of Probability of Death Based on Admission Electrocardiogram www.


–13 (127)

Troponin I Levels to Predict the Risk of Mortality in


Antman EM, Tanasijevic MJ, Thompson B, et al. N Engl J Med 1996;335:1342 –9 (201) www.


TIMI Risk Score – Cardiac Events by 14 Days

(TIMI 11B, ESSENCE) www.


GRACE Prediction Score – All-cause Mortality Within 6

Months of Discharge

Eagle KA, Lim MJ, Dabbous OH, et al. JAMA 2004;291:2727-33(168) www.


What is Elevated Risk?

www.



• Pathophysiology

• Diagnosis

• Initial Therapy





Choose A Strategy

• Initial Conservative – Angiography only if patient

fails medical management

(refractory or resting angina) or has

objective evidence of ischemia

(stress testing)

• Initial Invasive – Angiography before failure of medical management or stress testing

– Immediate angiography (ISAR-COOL) or

– Deferred Angiography (all other trials – 12-48h) www.


Choose A Strategy - Rationale

• Initial Conservative

– Early trials demonstrate similar efficacy (TIMI IIIB,

MATE, VANQWISH, RITA-2)

– Aggressive antiplatelet and anticoagulant therapy has reduced events

• Initial Invasive

– Rapidly identify the 10-20% with nonocclusive CAD and the 20% with 3v CAD www.


Less Events in Early Invasive Strategy www.


Choose A Strategy – Guidelines

• Initial invasive

– Refractory angina or hemodynamic/electrical instability (Class I, B)

– Initially stabilized patients without contraindications and with elevated risk for events (Class I, A)

• Initial Conservative

– May be considered in patients with elevated risk (Class IIb,B)

– May consider physician or patient preference

(Class IIb,C)

– Women with low-risk features (Class I, B) www.


Anticoagulants and Antiplatelets – Initial Invasive

Strategy

Recommendation Evidence

Enoxaparin, UFH (I, A), bivalirudin, or fondaparinux (I,

B) ASAP

Plavix or IIb/IIIa inhibitor prior to angiography* (I, A)

*Abciximab only if no delay to cath and PCI likely (I, B)

Enoxaparin: ESSENCE,

TIMI IIB, SYNERGY,

OASIS 5, ACUTE II,

INTERACT, A to Z

Fondaparinux: OASIS 5

Bivalirudin: ACUITY

Plavix: CURE

GPIIb/IIIa Inhibitor: ISAR-

REACT-2 (abciximab),

PURSUIT (ebtifbatide),

PRISM PLUS (tirofiban) www.


Anticoagulants and Antiplatelets – Initial Conservative

Strategy

Recommendation Evidence

Enoxaparin, UFH, (I, A) or

Fondaparinux (I, B) ASAP

Fondaparinux if increased bleeding risk (I, B)

Plavix (loading dose plus maintainence) ASAP, continued for 1 month, ideally up to 1 year (I, A) etifibatide or tirofiban in addition to Plavix (IIb, B), but not abciximab (IIIA) www.


Enoxaparin: ESSENCE,

TIMI 11B, A to Z,

INTERACT

Fondaparinux: OASIS 5

CURE

ARMYDA 2

Important Points in Hospital Care

• Stress test before discharge for assessment of ischemia in initial conservative strategy. Must be free of resting ischemia or HF for 12-24h – Class I, C

• If not classified as low risk, angiography should be performed – Class I, A

• Fasting lipid panel within 24 hours – Class I, C

• Statin regardless of baseline LDL-C pre-discharge

• Echo or MUGA must be done if no plan for left ventriculography by angiogram – Class I, B www.



• Pathophysiology

• Diagnosis

• Triage

• Initial Therapy




Post-AMI Care

• Similar to care after STEMI

• Focus on secondary prevention of coronary events…

– ASA

– Statin

– BB

– BP control

– Smoking Cessation

– Healthy Lifestyle

• …And treatment of LV systolic Dysfunction (EF<40)

– ACE inhibitor

– ARB if ACE inhibitor intolerant

– Eplerenone if HF or DM, and eGFR > 30, and K < 5 www.


When to Stop Plavix www.


Thank You

Grand Rounds Series - Northwestern Cardiology Fellows

Unstable Angina and Non-ST elevation

Myocardial Infarction

John Blair, MD

Ischemic Discomfort

Acute Coronary Syndrome

No ST Elevation

NSTEMI

ST Elevation

Bed/chair rest

O2

NTG

NTG

Oral BB

CCB

ACE inhibitor

ARB

ASA

Plavix

GP IIB/IIIA

Anticoagulant

fails medical management

objective evidence of ischemia

Thank You

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Grand Rounds Series - Northwestern Cardiology Fellows

Unstable Angina and Non-ST elevation

Myocardial Infarction

John Blair, MD

Ischemic Discomfort

Acute Coronary Syndrome

No ST Elevation

NSTEMI

ST Elevation

Bed/chair rest

O2

NTG

NTG

Oral BB

CCB

ACE inhibitor

ARB

ASA

Plavix

GP IIB/IIIA

Anticoagulant

fails medical management

objective evidence of ischemia

Thank You

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