Pathophysiology of acute coronary syndromes

Acute coronary syndromes (ACS) comprise a spectrum of clinical conditions, initiated by rupture of an atherosclerotic coronary plaque with overlying acute thrombosis. The consequences of thrombosis include direct obstruction of blood flow to the coronary beds, as well as distal embolization of the platelet-rich thrombus. Both of these processes may lead to myocardial ischemia and may progress to myocyte necrosis and myocardial infarction. The coronary thrombus may be completely occlusive, as is frequently seen in ST-segment-elevation myocardial infarction (STEMI), or nonocclusive, as can be observed in unstable angina or non-ST-elevation myocardial infarction (UA/NSTEMI). The latter two entities are also known collectively as non-STelevation acute coronary syndromes (NSTEACS). This chapter discusses the basic pathophysiology underlying ACS. Braunwald has described five processes contributing to development of ACS, or any atherothrombotic event (Figure 1.1). These processes include: (1) thrombus on preexisting plaque, (2) dynamic obstruction from coronary spasm or Prinzmetal’s angina, (3) progressive mechanical obstruction, (4) inflammation and/or infection, and (5) secondary unstable angina due to global myocardial oxygen supply and demand mismatch.