New insights into atherosclerotic plaque rupture
- Box 110, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK
- Dr Bennettmrb{at}mole.bio.cam.ac.uk
- Received 1 June 2000
- Accepted 4 July 2000
Coronary artery atherosclerosis is the major cause of mortality and morbidity in the industrialised world. Progressive narrowing of coronary arteries causes angina. However, it is rupture of the plaque that causes the catastrophic consequences of atherosclerosis, such as myocardial infarction. Recent work has identified that the stability of the plaque rather than its absolute size determines the likelihood of rupture, making a change in plaque composition rather than plaque regression a worthwhile clinical goal. This review summarises recent advances in the understanding of plaque rupture, and identifies areas in which new therapies may be directed.
Key points
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Myocardial infarction is caused mostly by plaques that cause <50% stenosis
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Statins cause profound changes in plaque composition and reduce clinical events, with little change in plaque size
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Statins reduce inflammatory cell content and lipid content of experimental atherosclerotic plaques
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Statins increase vascular smooth muscle cell and collagen content of experimental atherosclerotic plaques
The vulnerable plaque
Myocardial infarction and unstable angina are caused by rupture or erosion of an atherosclerotic plaque, with subsequent thrombus formation and occlusion of the artery. The plaque that causes a patient's heart attack is not necessarily the one that is identified at angiography. Cardiologists conventionally describe coronary artery stenoses as significant when they occupy >50% of the arterial lumen, that is when they become flow limiting. However, a series of postmortem and angiographic studies has identified that nearly 70% of myocardial infarctions are caused by rupture of plaques that cause <50% stenosis, and that <20% are caused by lesions that are >70% stenotic (reviewed by Falk et al 1). Thus, the quality of the plaque rather than the quantity determines the clinical consequences of atherosclerosis.
The atherosclerotic plaque consists of a collection of vascular smooth muscle cells (VSMCs) and inflammatory cells (macrophages and T lymphocytes), with both intracellular and extracellular lipid. …
