This chapter discusses the pathophysiology of coronary thrombus formation (see accompanying Hurst’s Central Illustration), which constitutes the basis of acute coronary events. The luminal thrombus in up to three fourths of cases may be secondary to plaque rupture, and in the remaining cases it may result from plaque erosion; very infrequently calcific nodules may induce luminal thrombosis. Upon plaque rupture, components of deeper layers of the plaque are exposed to the circulating blood, which leads to marked platelet aggregation. The nature of the substrate exposed after plaque rupture likely determines whether a nonocclusive mural thrombus persists or whether the thrombus progresses to become occlusive. Indeed, the atheromatous core of a plaque is substantially more active than other substrates at triggering thrombosis and, therefore, ruptured plaques with large atheromatous core are at high risk of leading to acute coronary syndromes. The local geometry at the site of damage (degree of stenosis) and local hemodynamic conditions, as well as the presence of circulating systemic factors, also influence the mechanisms of thrombus formation.
Hurst's Central Illustration: Quantifying the physiological severity of coronary artery disease for clinical decision making.
Quantifying the physiological severity of coronary artery disease for clinical decision making. Coronary flow reserve and stress perfusion are complimentary quantifiers of physiological severity of coronary artery disease that should be used together to provide a complete and definitive depiction of disease severity.
Low coronary blood flow causes acute coronary syndromes (ACS), angina pectoris, myocardial infarction, impaired left ventricular (LV) function, heart failure, arrhythmia, and death. High coronary blood flow capacity associates with cardiovascular health; its variations, reflecting our emotional states, lifestyles, and food, even the postprandial lipid surge of the last meal, are all documented to alter coronary blood flow and risk factors, symptoms, and outcomes of coronary artery disease. Evolving from 200 million years ago, concepts regarding the mammalian heart—coronary blood flow, human gender evolution, fluid dynamic equations, coronary pressure flow measurements, quantitative perfusion imaging, diagnostic tests, coronary artery disease in women versus men, and how poor coronary flow is optimally treated—constitute a highly integrated continuum, a syncytium of knowledge immediately relevant to current cardiovascular medicine and patient well-being.
Resurgent interest in coronary blood flow related to myocardial “ischemia” derives, in part, from substantial disconnects in cardiovascular medicine. Immediate percutaneous coronary intervention (PCI) in ACS reduces myocardial infarction and cardiovascular mortality.1 However, all elective revascularization trials driven by “ischemia” on diagnostic testing fail to reduce myocardial infarction or cardiovascular deaths despite relief of angina2,3,4,5,6,7,8,9 (Fig. 34–1).
Outcomes in (A) patients with non-ST-segment elevation acute coronary syndromes in the FRISC-II, RITA-3, and ICTUS trials, (B) patients with stable coronary artery disease at 12-year follow-up ...