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Definitions (Circulation 2004;110:e82; Circulation 2007;116:e148; Circulation 2008;117:296)
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- Acute coronary syndrome (ACS): umbrella term, includes all clinical syndromes compatible with acute myocardial ischemia arising from an imbalance in myocardial oxygen supply & demand
- Classified based on ECG results into ST-segment elevation ACS (STE myocardial infarction STEMI) & non-STE ACS (NSTEACS)
- NSTEACS classified based on cardiac biomarkers (troponins) into NSTEMI or unstable angina (UA)
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Etiology (Circulation 2004;110:e82; Circulation 2007;116:e148; Circulation 2008;117:296)
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- Most common cause is reduced myocardial perfusion due to coronary artery narrowing caused by thrombus formation on a disrupted atherosclerotic plaque
- In NSTEACS, coronary artery is partially occluded by thrombus; in STEMI, thrombus typically totally occlusive
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(N Engl J Med 2009;360:2237; Lancet 2008;372:570; N Engl J Med 2004;350:277; N Engl J Med 2007;357:2482)
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- Atherosclerotic plaque rupture exposes thrombogenic components of the plaque
- Vulnerable plaques contain numerous inflammatory cells, large lipid core, & a thin fibrous cap
- Platelets arrive & adhere to the site of rupture → platelets release mediators such as epinephrine, adenosine diphosphate (ADP), thromboxane A2 (TXA2), & thrombin → activate & maintain platelet response
- Activated platelets are also source of inflammatory mediators: CD40 ligand, P-selectin, & IL-1β
- Tissue factor initiates extrinsic clotting cascade → enzymatic conversion of fibrinogen to fibrin by thrombin; further stabilizes the thrombus (now cross-linked platelets & fibrin)
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Risk Stratification (Am Heart J 2009;158:193; JAMA 2000;284:835) guides ACS pharmacotherapy & management
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- STEMI patients have the highest risk of in-hospital & short-term major adverse cardiac events (MACE) & should treat emergently without regard to cardiac biomarkers
- NSTEACS patients have variable risk profiles classified using one of several risk assessment tools (ex: TIMI risk score → estimates risk of MACE by 14d)
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Treatment Goals: early restoration of blood flow to infarct-related artery to prevent infarct expansion (MI) or prevent complete occlusion & MI (in UA); prevention of death & complications; prevention of coronary artery reocclusion; relief of ischemic chest discomfort (Circulation 2004;110:e82; Circulation 2007;116:e148; Circulation 2008;117:296)
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