Atherosclerosis Regression

pp 241-250

Abstract

Many clinical trials have shown that reduction of high cholesterol levels -particulary low density lipoprotein (LDL) cholesterol- decreases the number of plaques, slows progression and increases regression of atherosclerotic lesions. Simultaneously, it gets a considerable improvement in symptomatic patients and a significant reduction in acute cardiac events, facts that improve life quality and reduce cardiac mortality. These changes have been observed during primary and secondary prevention trials. Nevertheless, the notorious reduction of clinical events is not related with similar arteriographic regression. There are many hipotesis to explain these facts. Lesions associated with rapid occlusion and acute events have several pathologic characteristics, including an eccentric, rich lipid core, high macrophage density, and a weak fibrous cap, that makes them sensible to chemical, toxic and mechanical agression. Chronic lesions have a central and smaller lipid core, less macrophage density, and a thick fibrous cover. LDL-B cholesterol, specially oxidized particles, isa potent chemoattractant for monocytes and macrophages. It is also a stimulus for platelet aggregation and release of thromboxane A2, and decreases the synthesis of the potent vasodilator nitric oxide, increasing plaque rupture chances. Nowadays it is largely accepted that aggresive treatment of high levels of cholesterol and LDL cholesterol is a medical responsability, not only secondary prevention, where drugs are generally necessary, but also primary prevention through modifications of cardiovascular risk factors.