[The aspect and pathophysiology of acute coronary syndromes]

The acute coronary syndromes (ACS) including unstable angina and myocardial infarction are often triggered by rupture of vulnerable plaques. So called vulnerable plaques are characterized by thin fibrous caps overlying a macrophage-rich atheromatous core. Lesional macrophages overexpress matrix-degrading enzymes such as proteinases. Increased degradation of extracellular matrix like interstitial collagen by proteinases may weaken the fibrous cap and promote plaque rupture. In addition to these structural aspects of vulnerable plaques, stresses induced by intraluminal pressure, coronary vasomotor tone, tachycardia (cyclic stretching and compression), and disruption of nutrient vessels combine to produce plaque rupture at the margin of the fibrous cap near an adjacent plaque-free or carcified segment of the coronary artery wall (shoulder region of plaque). The future development of more effective therapies for ACS relies on continuing advancements in our better understanding of the molecular mechanisms of vascular pathophysiology.