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INTRODUCTION

  • Acute coronary syndrome (ACS) involves acute myocardial ischemia resulting from imbalance between myocardial oxygen demand and supply. Classification based on electrocardiographic (ECG) changes includes: (1) ST-segment-elevation myocardial infarction (STEMI) or (2) non–ST-segment-elevation ACS (NSTE-ACS), which includes non–ST-segment-elevation MI (NSTEMI) and unstable angina (UA).

PATHOPHYSIOLOGY

  • Endothelial dysfunction, inflammation, and formation of fatty streaks contribute to development of atherosclerotic coronary artery plaques. Eventual plaque rupture and subsequent thrombus formation abruptly decreases myocardial blood flow and oxygen supply, leading to ischemia and potentially infarction.

  • Atherosclerotic plaques that rupture typically have thin fibrous caps and tend to be nonobstructive, occluding <70% of the luminal diameter; thus, patients may not experience angina prior to plaque rupture due to adequate autoregulation that maintains blood flow and oxygen supply during increased myocardial oxygen demand. Increased catecholamine release during physical or emotional stress may enhance the likelihood of rupture of a thinning fibrous cap.

  • Plaque rupture breaches the barrier between the necrotic plaque core and blood components; circulating platelets are attracted and adhere to the area of injury. Platelet adhesion occurs via platelet glycoprotein (GP) VI receptors binding to collagen within the damaged fibrotic cap, as well as platelet GP Ib-IX receptors and von Willebrand factor. Platelets are then activated by collagen, thrombin, thromboxane A2, adenosine diphosphate (ADP), epinephrine, and serotonin. Binding of these activators to their specific receptors on the platelet surface (eg, P2Y12 receptor for ADP, protease-activated receptor [PAR]-1 for thrombin) results in increased platelet surface area and release of further platelet activators from granules within platelets. Assembly of tenase and prothrombinase complexes within activated platelets produces most of the activated factor Xa and IIa (thrombin) in the coagulation cascade. A change in the conformation of the GP IIb/IIIa surface receptors of platelets cross-links platelets to each other through fibrinogen bridges, resulting in platelet aggregation and formation of a platelet plug in the area of plaque rupture.

  • Activation of the clotting cascade forms a fibrin meshwork (thrombus) around the platelet plug that traps cellular components such as red blood cells and causes abrupt reduction in myocardial blood flow and oxygen supply. If ischemia is left untreated, myocyte necrosis and cell death may ensue.

  • Subtypes of MI are based on etiology: (1) rupture, fissure, or erosion of an atherosclerotic plaque (90% of cases); (2) reduced myocardial oxygen supply or increased demand in the absence of a coronary artery process; (3) MI resulting in death without the possibility of measuring biomarkers; (4) MI associated with percutaneous coronary intervention (PCI; Type 4a) or stent thrombosis (Type 4b); and (5) MI associated with coronary artery bypass graft (CABG) surgery.

  • After MI, acute and chronic adaptations occur to prevent hemodynamic collapse but may also lead to ventricular remodeling and post-MI complications. Stimulation of the sympathetic nervous system (SNS) and renin–angiotensin–aldosterone system (RAAS) compensates for decreased cardiac output. However, chronic hyperactivation of these systems can lead to ventricular hypertrophy and further impairment ...

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