ANTIHYPERTENSIVE DRUG-TREATMENT AND FIBRINOLYTIC FUNCTION

Thromboembolic complications such as ischemic stroke and myocardial in farction are significantly more frequent in patients with arterial hyp ertension. From the available intervention studies, it appears that ph armacologic treatment of hypertension-at least with diuretics and beta -blockers-may more effectively protect against cerebrovascular as comp ared to coronary thromboembolic events. Whether other antihypertensive substances provide a more effective protection with respect to cardia c morbidity and mortality is the subject of numerous studies presently underway. These studies will help to answer the question of whether t he extent of protection from coronary events during antihypertensive t reatment depends on factors beyond blood pressure control. The fibrino lytic system is crucially involved in the pathogenesis of thromboembol ic events. One determinant of this system is the balance between plasm inogen activators (tissue-type plasminogen activator [t-PA]) and inhib itors (plasminogen activator inhibitor 1 [PAI-1]). Experimental and cl inical evidence suggests that at least some of the drugs used in the t reatment of hypertension may alter the activity of the fibrinolytic sy stem. Scarce and controversial data with respect to such an interactio n exist with respect to diuretics, beta-blockers, and calcium antagoni sts. In addition, experimental evidence demonstrates that PAI-1 is sti mulated by angiotensin II (A II), whereas t-PA is activated by bradyki nin. Thus, antihypertensive drugs acting within the renin angiotensin system should exert effects also within the fibrinolytic system. Howev er, results from clinical studies with angiotensin converting enzyme ( ACE) inhibitors and A II receptor antagonists do not unequivocally sup port such a concept. The discrepancy in the results may, at least in p art, be explained by studies performed in healthy volunteer subjects s howing that ACE inhibition profoundly affected fibrinolysis only durin g stimulation of the renin angiotensin system by NaCL restriction. (C) 1998 American Journal of Hypertension, Ltd.