Coronary Artery Disease: Pathological Anatomy and Pathogenesis

Abstract

Coronary atherosclerosis is the major anatomic substrate for the diverse clinical syndromes of coronary heart disease. Coronary atherosclerosis is a disease that develops as an inflammatory response of the arterial wall to chronic, multifactorial injury. Acute ischemic heart disease is usually initiated by erosion, rupture, thrombosis and/or spasm superimposed on vulnerable atherosclerotic plaques with active inflammation. The process may be self-limited (angina pectoris), may trigger a lethal ventricular arrhythmia (sudden cardiac death), or result in death of heart muscle, myocardial infarction (MI). MI progresses as a wavefront of necrosis extending from subendocardium into subepicardium with complete evolution in 3--4 h. The pathogenesis of irreversible myocardial cell injury involves metabolic and electrolyte changes, and activation of necroptotic and apopotic mechanisms of cell injury and death. Timely reperfusion has a profound influence resulting in some further loss of critically injured cells (reperfusion injury) and net salvage of a significant amount of myocardium. Preconditioning by repetitive short intervals of coronary occlusion and reperfusion can significantly retard the subsequent development of MI. Reperfusion can be achieved clinically with coronary angioplasty and cardiac bypass surgery, but associated pathologic changes in coronary arteries can influence long-term outcomes. Progress in understanding the pathobiology of myocardial ischemic injury is leading to new therapeutic approaches to combine with established approaches for reperfusion and salvage of myocardium.