Defective fibrinolytic states as triggers of myocardial infarction: the cardiologist's view.
Disclosure of a specific prothrombotic/antifibrinolytic state by determination of plasminogen activator inhibitor type 1 (PAI-1), tissue-type plasminogen activator (t-PA), and t-PA/PAI-1 complex levels in plasma may help to define patients at high risk of developing acute coronary syndromes. According to the mechanisms of PAI-1 up-regulation, i.e. genetic factors, an activated renin-angiotensin-aldosterone system, and other atherosclerotic risk factors (hypertriglyceridemia, insulin resistance), PAI-1 plasma levels might be reduced by the action of antidiabetic drugs, fibrates, statins, as well as by inhibitors of the renin-angiotensin-aldosterone system, and this effect might contribute to the anti-atherosclerotic and antithrombotic actions of these drugs. Moreover, PAI-1 resistant fibrinolytic agents may be beneficial in thrombolytic therapy of acute myocardial infarction.
Huber
K
K
Department of Cardiology, University of Vienna, Austria. kurt.huber@univie.ac.at
D001778:Blood Coagulation Disorders / Q000150:complications*; D005342:Fibrinolysis; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy / Q000209:etiology*