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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.

Angiology
|September 1, 1995
PubMed

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.

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