Fibrinogen and plasminogen activator inhibitor-1 levels in hypertension and coronary heart disease. Potential effects of beta-blockade

Abstract

The roles of fibrinolysis, fibrinogen, and plasminogen activator inhibitor-1 in the development of coronary heart disease are reviewed, and possible effects of long-term treatment with beta-blockade are discussed. Decreased fibrinolysis is associated with coronary artery disease, and coronary thrombus formation is the most frequent event precipitating myocardial infarction. Recently, it has also been shown that high levels of fibrinogen and plasminogen activator inhibitor-1 are predictors for myocardial infarction. Because beta-blockers are used to treat hypertension, angina, and myocardial infarction, it is important to determine the impact of beta-blockers on fibrinolysis. Several factors influence fibrinolysis. Some forms of stress and epinephrine infusions increase fibrinolysis, probably by stimulating beta 2-adrenoceptors. Nonselective beta-blockers may adversely affect this process, whereas beta 1-selective antagonists and those with intrinsic sympathomimetic activity may not. Since prostacyclin synthesis is correlated to increased fibrinolytic activity and since beta-blockers may moderate stress-induced reductions in prostacyclin formation, beta-blockers may have the potential to exert a beneficial effect on fibrinolysis in chronic stress situations. The net effect of beta-blockade is not easily predicted and probably depends on the nature of the stress (whether it is acute or chronic), the status of the patient, and the selectivity of the beta-blocker. Nevertheless, it remains a possibility that beta-blockers may exert a positive therapeutic effect in relation to coronary thrombosis by an action on fibrinolytic mechanisms.