Smith E B
Department of Clinical Biochemistry, University of Aberdeen, Scotland.
Cardiologia. 1994 Dec;39(12 Suppl 1):169-72.
Raised levels of plasma low density lipoprotein, lipoprotein (a), and fibrinogen have emerged as major risk factors for myocardial infarction and atherosclerosis. In this brief review some of their interactions with arterial intima are discussed. All the plasma macro-molecules appear to be present even in normal intima, and to cross the endothelium in healthy, young experimental animals by vesicular transport. The precursor of large fibrous plaques appears to be the gelatinous lesion, which is characterized by oedema, accumulation of large amounts of low density lipoproteins and fibrinogen in the expanded interstitial fluid space, deposition of fibrin, and smooth muscle cell proliferation. It is postulated that deposition of fibrin may be a key event, stimulating smooth muscle cell proliferation by providing a scaffold for migration, a source of fibrin degradation products which are mitogenic, and binding thrombin. Fibrin may also be a factor in lipid accumulation because it binds lipoprotein (a) with high affinity, and may also bind low density lipoprotein.
