The role of plaque fissures in unstable angina: fact or fiction?
Several factors may contribute to the development of unstable angina. These include underlying atherosclerosis, mural platelet thrombosis, dynamic stenosis, occlusive spasm and microvascular dysfunctions. Of these, thrombosis is the most visible event, but its actual causes remain elusive. Plaque fissure is widely assumed to be the cause of unstable angina. However, studies have shown no evidence of plaque fissure in about 40% of patients dying from acute coronary syndromes and, conversely, fissured plaques have been found in 10-25% of individuals dying of non-cardiac causes. An inflammatory process may activate the coronary intima and the haemostatic system to produce a platelet-rich thrombus. Activated inflammatory cells produce cytokines which can activate the endothelium making it prothrombotic and vasoconstrictive; they can also produce metalloproteases that can lyse the interstitial matrix. Thus, inflammatory lysis of thin atherosclerotic plaques may also cause plaque fissure at one or more sites. Waxing and waning inflammatory activity may explain the multi-layered thrombi and multiple simultaneous coronary fissure and thrombi that have been described in patients with acute coronary syndromes.
Maseri
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Catholic University of Rome, Italy.
Sanna
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T
D000789:Angina, Unstable / Q000097:blood / Q000209:etiology*; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications*; D003328:Coronary Thrombosis / Q000097:blood / Q000150:complications*; D005342:Fibrinolysis; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000473:pathology; D010974:Platelet Aggregation