Acute coronary syndromes

Classification based upon

  • Clinical presentation
  • Electrocardiogram
  • Serum markers
    • Troponin is preferred marker
    • CK-MB is acceptable but less specific

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ACS and the Unstable plaque
  • Endothelial damage induces adhesion molecules & endothelial leakage
    • Leucocytes and oxidized LDL cholesterol enter vessel wall
    • Leucocytes ingest oxidized LDL cholesterol, become trapped, lyse and form an inflamation-inducing liquid-containing lipid core
    • Fibrous cap shields blood stream from contact with tissue factor and other pro-coagulants in lipid core
    • Breakdown of fibrous cap leads to plaque rupture
  • Plaque rupture leads to ACS
    • Platelets adhere & aggregate
    • Clotting cascade initiated
    • Regional m yocardial blood supply is reduced or interrupted

Arch Intern Med. 2000;160:25 Image is on publisher's web site and may require subscription to view

ACC/AHA Classification of benefit

Class I

Benefit >>> Risk

 

Indicated

Class IIa

Benefit >> Risk

Additional studies with focused objectives are needed.

Reasonable

Class IIb

Benefit >= Risk

Additional studies with broad objectives or more registry data needed.

May be considered

Class III

Risk >= Benefit

No additional studies needed

Not indicated, should not be performed
Circulation. 2008;117:296
Circulation.2007;116:803

Unstable coronary plaque

Acute coronary syndromes

Estimate patient's risk

Low-risk, pain-free patients

Guideline classification scheme
Examples
 #1
#2
Click on bullets to change slides
 

Estimate short-term risk of death or MI

High risk

Intermediate risk

History & Physical

  • Age over 75
  • Accelerated angina within 48 hours
  • Prolonged (more than 20 minutes) or ongoing chest pain
  • Homodynamic compromise: hypotension, bradycardia, tachycardia, pulmonary edema/worsening rales, S3, new/worsening MR murmur
  • Age greater than 70
  • Prior ASA use
  • Prior MI, CABG, pathologic Q-waves
  • Resolved angina lasting 20 minutes or relieved by rest or GTN
  • Cerebral or peripheral vascular disease

ECG & Laboratory

  • ST segment shift over 0.5 mm during rest pain
  • Bundle branch block not known to be old
  • Sustained ventricular tachycardia
  • Marked elevation of cardiac injury markers (TnT or TnI over 0.1 ng/mL)
  • Pathologic Q-waves
  • T wave inversion more than 0.2 mV
  • Slight troponin elevation (0.01 to 0.1 ng/mL)
Circulation. 2008;117:296
Circulation.2007;116:803

Low-risk pain-free patient with chest pain

Classify syndrome

  • Noncardiac
  • Chronic stable angina
  • Possible acute coronary syndrome (ACS)
    • Recently resolved, atypical or resting chest descomfort
    • Negative ECG
    • Normal cardiac markers
  • Definite acute coronary syndrome (ACS)
    • Recent, new, sustained, accelerating chest discomfort
    • ECG and/or markers often abnormal

Low risk

  • No high or intermediate risk features
  • Normal cardiac injury markers
  • Pain free at time of examination

Recommendations

  • Definite/possible ACS and normal markers and negative ECG
    • Monitor and repeat ECG and markers in 6 to 12 hours
    • If ECG and markers remain normal, perform treadmill or pharmacological stress test
    • If stress test is negative, low risk patients can be managed as outpatients
  • Admit patients with ACS and any one of
    • Ongoing pain
    • Positive cardiac markers
    • New ST segment deviation
    • New deep T wave inversion
    • Hemodynamic abnormalities
    • Any other intermediate or high risk feature
    • Positive stress test
Circulation. 2007;116:803
Circulation. 2008;117:296

48-year old woman with chest pain and normal troponin

Electrocardiogram

Angiogram one

Angiogram two
BMJ 2003;326:1259 Images above are on publisher's web site and may require subscription to view

Patient with chest pain, elevated troponin and no ST-segment elevation

Angiogram one

Angiogram two
BMJ 2003;326:1259 Images above are on publisher's website and may require subscription to view