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Inhibition of angiotensin converting enzyme cannot prevent increases in angiotensin II production in coronary

Y Hojo1, U Ikeda, T Katsuki

  • 1Department of Cardiology, Jichi Medical School, Minamikawachi-machi Tochigi 329-0498, Japan.

Heart (British Cardiac Society)
|April 18, 2000
PubMed

Insights

Angiotensin converting enzyme (ACE) inhibitors did not prevent increased angiotensin II production in the coronary circulation after percutaneous transluminal coronary angioplasty (PTCA). This finding is crucial for understanding cardiovascular responses to PTCA in patients with myocardial ischemia.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Interventional Cardiology

Background:

  • Percutaneous transluminal coronary angioplasty (PTCA) can induce local angiotensin II production in the coronary circulation.
  • Angiotensin II plays a role in myocardial ischemia and cardiovascular remodeling.
  • The efficacy of angiotensin converting enzyme (ACE) inhibitors in mitigating this response is not well-established.

Purpose of the Study:

  • To investigate whether ACE inhibition can prevent angiotensin II production in the coronary circulation following PTCA.
  • To assess the impact of chronic ACE inhibitor therapy on angiotensin II levels during and after PTCA in patients with myocardial ischemia.

Main Methods:

  • A study involving 41 patients undergoing elective PTCA and 6 control subjects.
  • Patients were categorized into two groups: those on chronic ACE inhibitor therapy (Group A) and those not (Group B).
  • Blood samples were collected from the aorta and coronary sinus before and 24 hours after PTCA to measure ACE activity and angiotensin II concentrations.

Main Results:

  • Patients on ACE inhibitors (Group A) had significantly lower aortic ACE activity compared to Group B.
  • No significant differences in aortic angiotensin II concentrations were observed between the groups.
  • Coronary sinus-to-aorta differences in angiotensin II, indicating local production, were not significantly different at baseline across all groups.
  • PTCA significantly increased coronary angiotensin II production in both Group A and Group B patients to a similar extent.

Conclusions:

  • Chronic ACE inhibition does not prevent the increase in coronary angiotensin II production induced by PTCA.
  • These findings suggest that alternative or additional therapeutic strategies may be needed to manage angiotensin II-mediated effects post-PTCA.
Abstract

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