Blood Changes in Atherosclerosis and Long After Myocardial Infarction and Venous Thrombosis

Abstract

The following clinical groups of volunteers were studied: patients long after recovery from myocardial infarction (MI), others after recovery from deep vein thrombosis (DVT), patients with intermittent claudication, with diabetes, and male and female controls who were well matched. All were subjected to many platelet and clotting tests together with clinical, biochemical and haematological measurements in an attempt to find long term abnormalities in these various diseases. The male Mis differed very significantly from the controls in having much more heparin neutralizing activity (P < 0.001) and less anti-thrombin (P < 0.01). Less significantly, some bleeding time tests indicated less bleeding and the patients’ platelets were larger. The females with MI had in general the same abnormalities but to a lesser degree. The patients with intermittent claudication, none of whom had a history of MI, had almost the same abnormalities and to the same degree. In deep vein thrombosis the heparin neutralizing activity was also clearly increased; the other tests were generally in the same direction but many were not significant. The diabetics had shorter bleeding times but little else abnormal relative to the controls, suggesting a different pathological process. When all male patients and controls were “scored” according to the degree of atherosclerosis there was a close overall correlation between the degree of atherosclerosis and the increase in the HNA level (r = — 0.50, n = 66, P < 0.001) and the decreased anti-thrombin (r = — 0.25, n = 66, P < 0.05). The platelet abnormalities might indicate activated platelets with increased turnover; decreased anti-thrombin not only favours clotting but could suggest that clotting has occurred. Thus it is suggested that all the abnormalities may be accounted for if minor intravascular or mural coagulation occurs more or less permanently in these patients. This activation of the haemostatic mechanism towards coagulation could be related to the cause of atherosclerosis, or it could be the result. The mechanisms predisposing to or following DVT are somewhat different ; some may be shared. The nine diabetics are clearly quite different. The reported abnormalities found consistently in two studies may (1) illuminate pathogenesis; (2) indicate groups or even individuals at risk. (3) Improvement of the tests by appropriate therapy might justify a clinical trial of that therapy. (4) The high HNA in these syndromes may be relevant to any contemplated heparin therapy.