[Unstable angina. Physiopathology, clinical course and therapeutic principles]

The pathogenic mechanism of unstable angina, a clinical expression of coronary heart disease, is similar to that of myocardial infarction. The main event is the instability of the atheromatous plaque adhering to the coronary intima leading to thrombosis and occlusion. Clinical manifestations can be severe since fatal or non-fatal myocardial infarction occurs in 3.9% and 5.4% of the case respectively. Adapted medical treatment can stabilize the situation in most patients, justifying early preventive treatment. Moreover, it has been estimated that a premonitory phase of angina had gone unnoticed or undiagnosed in one-half of all myocardial infarcts. In nearly all patients with unstable angina, coronarography is of major importance for rapidly defining an adapted therapeutic strategy. Myocardial revascularization (especially by angioplasty) is often needed to limit the risk of major cardiac events occurring within a short or moderate delay. Unfortunately, these procedures carry a supplementary risk of thrombosis. Thus the emphasis placed on measures capable of improving the anti-thrombotic risk in unstable angina by using new antiplatelet agents, or for certain patients at high risk of a major cardiac event, antithrombosis agents. Finally, the search for compounds capable of stabilizing the previously formed atheromatous plaque (and thus avoiding rupture) is a prime objective for an overall management strategy for patients with coronary heart disease.