[Pathological-anatomic basis of unstable angina pectoris]

The primary trigger mechanisms leading to coronary artery disease are largely unknown; however, consensus has been reached that unstable angina pectoris is always associated with acute pathological and anatomical changes in a plaque, most commonly in the form of a plaque fissure or rupture involving the fibrous luminal cap with thrombosis, hemorrhage and dissection. Rupture almost always occurs at the weakest part of the fibrous cap and leads to exposition of extracellular lipids and matrix, necrotic tissue and lipid-laden foam cells. The exact mechanisms of plaque rupture are not entirely known; it is possible, however, that they do represent fatigue breaks in the tissue. The clinical consequences of these events are unstable angina pectoris and myocardial infarction.