FOCUS ON CORONARY SYNDROMES Atherosclerotic Plaque Rupture: an Overview

Atherosclerotic luminal narrowing is determined by plaque mass and local change in vessel size (remodeling). Regard-less of its size, a plaque may rupture with high risk of subsequent thrombus-mediated acute clinical events such as myocardial infarction and stroke. The risk of plaque rupture depends more on plaque type than on plaque size or stenosis severity. Major determinants of a plaque’s vulnerability to rupture are: 1) size and consistency of the lipid-rich atheroma-tous core; 2) thickness of the fibrous cap covering the core; and 3) ongoing inflammation and repair within the cap. Plaque disruption tends to occur at points where the plaque surface is weakest and most vulnerable which coincide with points where stresses, resulting from biomechanical and haemodynamic forces acting on plaques, are concentrated. Therefore, both plaque vulnerability (intrinsic disease) and rupture triggers (extrinsic forces) are important for plaque disruption. The former predisposes the plaque to rupture while the latter may precipitate it. The resultant thrombotic response determines the clinical presentation and the outcome. J Clin Basic Cardiol 2000; 3: 81–6. Key words: atherosclerosis, plaque rupture, remodeling, coronary artery disease Atherosclerotic Plaque Rupture C oronary atherosclerosis starts early in life but it takesdecades to develop mature plaques responsible for ischaemic heart disease (IHD). Proliferation of SMC, ma-trix synthesis and lipid accumulation may narrow the arte