[The pathogenesis of the evolution of the atheroma plaque]

The different theories on the pathogenesis of the atherosclerotic plaque may be integrated into a single multifactorial one. According to this, the atherosclerotic risk factors produce impairement of the endothelial cell function as well as the release of growing factors leading to smooth muscle cells and macrophage activation and subsequent collagen synthesis and foam cells formation, the two main components of the atheroma plaque. The arterial thrombosis is another important factor for the atherosclerotic plaque growth and for the occlusive complications that leads to acute ischemic syndromes. The same etiologic risk factor that initiate the atherosclerotic process are implicated in its progression. Most coronary acute syndromes show the same pathologic syndrome of a fissured atherosclerotic plaque with a superimposed thrombus. The lipid rich plaques with a thin fibrous cap and the presence of monocyte/macrophages are unstable and prone to fissuring more than the old fibrous plaques. The arterial stress can be an important precipitating factor for the plaque disruption. The possibility of slowing human atherosclerosis and even inducing its regression is one of the present therapeutic goals. One of the most useful approaches is the lipid lowering therapy in hyperlipidemic patients with atherosclerosis. These treatments have demonstrated its efficacy in decreasing the arterial occlusive complications even before showing the atherosclerotic plaque regression. Another approach would be the use of aspirin and other antiplatelet and antithrombotic agents that may partially prevent the progression of the atherosclerotic process.