Copyright © 1990 by the European Society of Cardiology.
© 1990 The European Society of Cardiology
Myocardial and coronary effects of captopril during pacing-induced ischaemia in patients with coronary artery disease
Medical Clinic, University of Tuebingen F.R.G.
Address for correspondence: Karl R. Karsch, Assoc. Prof. of Medicine/Cardiology, Medical Clinic, University of Tuebingen, Otfried-Mueller-Str. 10 7400 Tuebingen, F.R.G.
It has been speculated that ACE inhibitors may have beneficial effects in patients with coronary artery disease not only by their vasodilator properties but also by an effect on an assumed local renin-angiotensin system in atherosclerotic coronary arteries. Thus, the aim of the present study was to evaluate the effect of a single intravenous infusion of captopril on haemodynamics and coronary diameter at rest and during myocardial ischaemia induced by rapid atrial pacing. The study was performed in 12 patients with coronary artery disease and exertional angina pectoris despite medical therapy. Central haemodynamics (PAO, PAP) and left ventricular end-diartolic pressure were measured. Biplane cineventriculography and coronary arteriography were performed during control pacing (10% above the normal heart rate) before and after 15 min of captopril infusion, as well as during angina pectoris induced by rapid atrial pacing before and after captopril (six patients 0·15mg kg–1, six patients 0·3 mg kg–1).
Mean aortic pressure was not significantly decreased by either 0·15 mg kg–1 or 0·3mg kg–1, whereas mean pulmonary pressure was significantly reduced by captopril by 28% at rest and 34% during rapid atrial pacing. Neither the endsystolic volume index nor left ventricular ejection fraction was significantly affected by captopril. Left ventricular end-diastolic volume index was reduced by 9% at rest and 7% during pacing-induced angina. Left ventricular end-diastolic pressure decreased from 11 ± 9 mmHg to 4·8 ± 4·1 mmHg at rest after captopril, and from 10 ± 11 mmHg to 5·1 ± 5·0 mmHg during pacing-induced angina after captopril. Quantitative coronary analysis revealed an increase of 0·1 mm at rest after captopril and an increase from 0·9 ± 0·1 to 1·1 ± 0·2 mm during ischaemia after captopril. This increase was even more pronounced by measurernenf of the minimal diameter ratio which increased at rest from 0·4 ± 0·2 to 0·54 ± 0·1 mmHg after captopril and during pacing-induced ischaemia from 0·4 ± 0·1 to 0·6 ± 0·1 mmHg after captopril.
The results are compatible to patients with chronic heart failure and substantiate the predominant effect of ACE inhibitors as vasodilators by reducing preload significantly. If the mild vasodilation seen at the site of the atherosclerotic lesion is indeed due to a local effect of ACE inhibitors during myocardial ischaemia remains still open to question. Thus, therapy with ACE inhibitors for coronary artery disease requires validation in further clinical studies.
Key Words: Medical Clinic • i.v. captopril • pacing-induced angina