[Statins and antiplatelet agents: complementary mechanisms of action at the coronary artery level].
Atherothrombotic lesions associate atherosclerosis with a thrombotic reaction; they result from a complex inflammatory response to multifactorial stress. Endothelial dysfunction, lipid accumulation in the arterial intima, the recruitment of circulating monocytes and differentiation into macrophages and then foam cells, and an inflammatory reaction, all participate in the genesis of atheromatous plaque. The lipid core and fibrous parts of the plaque then contribute to its progression towards stenosis as a result of lipid infiltration, an accumulation of foam cells and the proliferation of smooth muscle cells with the synthesis of extracellular matrix. Atheromatous plaque is likely to rupture. The inflammatory components and an accumulation of cholesterol are two important characteristics found in the event of plaque rupture. The importance of the incorporation of thrombotic material formed during a silent rupture should also be emphasised. Among the factors favouring plaque rupture, a distinction can be made between extrinsic factors such as hypertension, and intrinsic factors which reflect the vulnerability of the plaque in terms of its quantitative aspects (relative composition in lipids and fibrous tissues) and qualitative characteristics (solidity of the fibrous cap and proteins in the extracellular matrix, the degradation of which is controlled by metalloproteinases). In the prevention of atherothrombosis-related complications, statins and platelet inhibitors have complementary mechanisms of action. Statins reduce inflammation, modify the composition of atheromatous plaque and promote stabilisation, while acetylsalicylic acid reduces the formation of thrombin, exerts an anti-thrombotic action, reduces endothelial dysfunction and the proliferation of vascular smooth muscle cells, and, like statins, has an anti-inflammatory effect. As a result, in the context of the B.A.S.I.C. strategy recommended by 2002-2003 ESC guidelines, the fixed statin-acetylsalicylic acid combination appears to constitute a logical combination in coronary patients in order to prevent the clinical complications linked to atherothrombosis.
INSERM UMR S 551, Université Pierre et Marie Curie, Hôpital de la Pitié-Salpêtrière, 75651 Paris, France.
John
J
Chapman
D050197:Atherosclerosis / Q000473:pathology / Q000517:prevention & control; D003327:Coronary Disease / Q000188:drug therapy* / Q000473:pathology; D003331:Coronary Vessels / Q000187:drug effects* / Q000473:pathology; D050171:Dyslipidemias / Q000097:blood / Q000188:drug therapy; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008055:Lipids / Q000097:blood; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D013927:Thrombosis / Q000473:pathology / Q000517:prevention & control
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D010975:Platelet Aggregation Inhibitors