[Morphological basis of atherosclerosis]

Abstract

The lesions of atherosclerosis are initiated as a response to some form of injury to arterial endothelium. Increase in plasma levels of low-density lipoproteins or some components of hyperlipidemic serum may increase the rate of penetration into the artery wall. Monocytes adhere to endothelium, emigrate into the intima and transform into lipid-laden macrophages. The second component of atherogenesis is smooth muscle proliferation in the intima. The proliferating cells originate from cells migrating from the media and from myointimal cells. After adhesion to foci of injury, platelets release platelet-derived growth factor, a potent mitogen for intimal smooth muscle cells. The plaque is increasing, the lumen narrowing. A plaque consisting mainly of yellow, grumous fluid is called an atheroma. The oily content of this plaque is covered by a fibrous cap that is often thin and prone to rupture. An occluding thrombus may result. Lipids and crystalline cholesterol initiate a foreign-body reaction, an inflammatory process. Older lesions are calcified. Examples from the daily work in the mortuary demonstrate the pathogenetic relevance of hypertension, thrombocytes and endothelium.