Evolution in the understanding of the pathophysiology of unstable angina

Ustable angina and myocardial infarction represent a continuous nosologic spectrum, with a predominant underlying mechanism the plaque rupture and the induction of intracoronary thrombosis. Lipid-rich plaques are considered the most vulnerable, and macrophages have been implicated in the induction of plaque rupture. Recently, the thrombogenic lipoprotein Lp(a) has been identified in large quantities within the plaque at the site of macrophage infiltration, and might potentially contribute to the development of an unstable syndrome. However, the clinical presentation of unstable angina is heterogeneous, and implies the potential existence of more than one pathogenetic mechanism. Severe unstable angina has been directly correlated with the presence of complex lesions and intracoronary thrombus, whereas these angiographic findings were relatively rare in milder clinical presentations. Recent work has implicated a role of neutrophils and local plaque inflammation in unstable angina. Thus fur, it has not been clearly determined whether this response precedes the clinical syndrome or wether it is a reaction to it. Reduced myocardial blood flow resulting in ischemic symptoms may be due not only to intracoronary thrombosis, but also to vasospasm or to plaque growth because of smooth muscle cell proliferation, without mural thrombus formation. Mechanisms of plaque growth and luminal narrowing which might act independently or in combination with intracoronary thrombosis may be soon identified.