Coronary Thrombosis

Abstract

The problem of preventing clinical coronary disease includes not only the prevention of the atheroma and its progression but also protection against thrombosis. Thrombosis is initiated by intimal damage followed by platelet adhesion, aggregation and viscous metamorphosis, resulting in a white platelet thrombus. Red coagulation thrombi follow secondarily. It is mainly the red coagulation thrombus which can be blocked therapeutically by anticoagulants. This limits the efficiency of such therapy, and, there has been a search for means of also regarding the formation of the white platelet thrombus. Platelet adhesion-aggregation is triggered by adenosine diphosphate and depends on a.o., a plasma factor which is lacking in von Willebrand''s disease and which may be called the anti-Willebrand factor (anti-bleeding factor). Coronary heart disease, like diabetes, familial hypercholesterolemia, the post-operative state, etc., is associated with an increased adhesion-aggregation tendency of the blood platelets which is caused by an increased activity of the anti-Willebrand factor. There is corollary evidence for assuming that an increased adhesion aggregation tendency of the blood platelets increases the tendency to thrombosis. The increased adhesion-aggregation tendency of the platelets can be reduced to normal by ingestion of linolenic acid. Linoleic acid and the pen-taenoic and hexaenoic unsaturated fatty acids are without effect. Normal adhesion-aggregation tendency (and normal activity of the anti-Willebrand factor) may be maintained for unlimited periods by a daily intake of about 10-15 ml of refined linseed oil. Rats on a saturated fat diet which is deficient in linolenic acid develop increased adhesion-aggregation tendency and an increased incidence of experimental thrombosis in the jugular vein. Supplements of linseed oil reduces adhesiveness and incidence of thrombosis to the same level as observed on a standard normal diet. Calculations based on dietary studies in Norway from 1912 to 1958 have revealed a striking negative correlation between the content of linolenic acid in the fat consumed and the mortality of cardiovascular diseases. The comparison of a rural district in Norway with low mortality from cardiovascular diseases with Oslo showed an association between a higher content of linolenic acid in the fat consumed, a lower activity of the anti-Willebrand factor (as measured by a lower platelet adhesion-aggregation tendency) and a lower mortality of cardiovascular diseases. These studies are consistent with the view that an increased tendency to thrombosis and coronary heart disease in certain population groups may be directly or indirectly related to a relative deficiency of linolenic acid. A possible prophylactic and therapeutic effect of increasing the linolenic acid content of the fat consumed must be determined by controlled clinical trials.