Haemostatic function in myocardial infarction.

Abstract

SUMMARY Coagulation factor VIII, von Willebrand factor, antithrombin, fibrinogen, plasminogen activator capacity, and inhibitors of fibrinolysis, including a recently discovered fast inhibitor of tissue plasminogen activator, were measured three to six months after myocardial infarction in 116 male and 32 female patients aged < 45 and in 136 age and sex matched random controls. Plasma concentrations of fibrinogen and the fast inhibitor of tissue plasminogen activator were raised in male patients (with or without correction for orosomucoid levels, blood group distribution, tobacco and alcohol consumption, and weight/height index) and plasminogen activator capacity was reduced. In female patients the concentrations of factor VIII, von Willebrand factor, the fast inhibitor of tissue plasminogen activator, aC2-antiplasmin, and Cl inhibitor were significantly increased. The increase in factor VIII concentrations depended strongly on a persisting inflammatory response. Multivariate analysis indicated that a combination of fibrinogen and tissue plasminogen activator inhibitor concentrations gave the best independent discrimination between male patients and controls. For female patients the best combination was von Willebrand factor and tissue plasminogen activator inhibitor. Male patients with multiple vessel atheromatosis at coronary angiography had higher fibrinogen concentrations than those with atheromatosis of a single vessel. Atheromatosis was defined as sharp-edged, plaque-like, or irregular indentations, often multiple, into the vessel lumen without features suggesting fibromuscular hyperplasia.Several mechanisms have been suggested to explain the pathogenesis of ischaemic heart disease. According to the thrombogenic theory of atherogenesis,l hypercoagulability may be a prerequisite not only for the development of thrombotic complications but also for the pathogenesis of atherosclerosis. Impaired fibrinolysis at the onset and during the course of myocardial infarction is viewed mainly as a reduction in defensive capacity while coronary occlusion and fibrin formation are under way.

Genetic variation at the beta-fibrinogen locus in relation to plasma fibrinogen concentrations and risk of myocardial infarction. The ECTIM Study.

“…The difference was no longer significant when orosomucoid alone was used as a covariate. 21 Therefore, interpretation of high fibrinogen levels in MI remains unclear.…”

Coagulation factors and the increased risk of stroke in nonvalvular atrial fibrillation.

“…Venipuncture technique and preparation of the plasma samples for analysis have been described. 8 The blood tests were chosen to reflect the different parts of the hemostatic system. 8 In the two stroke groups, blood was sampled at least 12 (mean 25, range 12-46) months after the event to avoid the influence of acute-phase reactions.…”

“…8 The blood tests were chosen to reflect the different parts of the hemostatic system. 8 In the two stroke groups, blood was sampled at least 12 (mean 25, range 12-46) months after the event to avoid the influence of acute-phase reactions. Patients receiving acetylsalicylic acid stopped medication 10 days before the blood samples were drawn.…”

Genetic variation at the plasminogen activator inhibitor-1 locus is associated with altered levels of plasma plasminogen activator inhibitor-1 activity.

“…These studies have consistently shown a decreased fibrinolytic activity in patients compared with controls, a decrease that is due mainly to elevated plasma levels of PAI-1. 7 - 11 Strong support for a cause-and-effect relation between PAI-1 elevation and risk of MI has been obtained from a longitudinal cohort study of 109 unselected men who had survived a first MI before the age of 45 years. This study indicated that a high plasma concentration of PAI-1 activity was associated with reinfarction, along with dyslipoproteinemia, poor left ventricular performance, and multiple-vessel coronary artery disease.…”