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.