Why the study?
Do ACE inhibitors (captopril or enalapril) affect tissue plasminogen activator (tPA) antigen and plasminogen activator inhibitor (PAI) activity levels in congestive heart failure patients?
Do ACE inhibitors (captopril or enalapril) affect tissue plasminogen activator (tPA) antigen and plasminogen activator inhibitor (PAI) activity levels in congestive heart failure patients?
ACE inhibitors do not appear to affect tPA antigen or PAI activity in CHF patients, suggesting other mechanisms are responsible for their observed antithrombotic effects.
ACE inhibitor initiation does not alter tPA or PAI in CHF; leaves open alternative antithrombotic mechanisms.
Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce the incidence of future coronary artery thromboses in postmyocardial infarction patients. A possible prothrombotic role for the angiotensin system has been postulated, and support for this has been provided by a recent study that demonstrated that an infusion of angiotensin increases levels of the prothrombotic plasminogen activator inhibitor (PAI). In the current study the authors have investigated the effect of two ACE inhibitors, captopril and enalapril, on tissue plasminogen activator (tPA) and PAI in 33 congestive heart failure (CHF) patients. Blood samples were obtained pretreatment and then at weeks 1, 12, and 24 after initiation of ACE inhibitor therapy for measurement of tPA antigen and PAI activity levels. The results of the study indicated that the initiation of ACE inhibitors had no significant effects on tPA antigen or PAI activity levels at the time points studied, and no significant differences were demonstrated between captopril and enalapril. The results suggest, therefore, that ACE inhibitors do not affect tPA antigen or PAI activity in CHF patients, and thus another mechanism is probably responsible for the observed decrease in coronary artery thromboses in post-MI patients treated with ACE inhibitors.
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Bridges et al. (1995) studied this question.
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