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A comparative study of captopril and enalapril on endothelial cell function in congestive heart failure patients
A B Bridges1, M McLaren, J J Belch
1University Department of Medicine, Ninewells Hospital and Medical School, Dundee, Scotland.
Insights
Angiotensin-converting enzyme (ACE) inhibitors did not alter levels of tissue plasminogen activator (tPA) or plasminogen activator inhibitor (PAI) in patients with heart failure. This suggests another mechanism is responsible for ACE inhibitors' protective effects against coronary artery thrombosis.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hemostasis and Thrombosis
Background:
- Angiotensin-converting enzyme (ACE) inhibitors reduce coronary artery thrombosis in post-myocardial infarction patients.
- The angiotensin system may have a prothrombotic role, as angiotensin infusion increases plasminogen activator inhibitor (PAI) levels.
- The direct effect of ACE inhibitors on key hemostatic factors like tissue plasminogen activator (tPA) and PAI in heart failure is not well understood.
Purpose of the Study:
- To investigate the impact of ACE inhibitors (captopril and enalapril) on tPA antigen and PAI activity levels in patients with congestive heart failure (CHF).
Main Methods:
- 33 patients with CHF were enrolled.
- Blood samples were collected pre-treatment and at 1, 12, and 24 weeks after initiating ACE inhibitor therapy.
- Levels of tPA antigen and PAI activity were measured.
Main Results:
- ACE inhibitor therapy did not significantly affect tPA antigen levels at any time point.
- ACE inhibitor therapy did not significantly affect PAI activity levels at any time point.
- No significant differences in tPA or PAI levels were observed between captopril and enalapril treatments.
Conclusions:
- ACE inhibitors do not appear to influence tPA antigen or PAI activity in patients with CHF.
- The cardioprotective effects of ACE inhibitors against coronary thrombosis in post-MI patients are likely mediated by mechanisms other than modulation of tPA and PAI levels.
Abstract:
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.