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Volume 1, Number 4, December 2000
Acute effects of ACE inhibition on coronary endothelial dysfunction
Georg Nickenig, Alexander Stäblein, Sven Wassmann, Christoph Wyen, Cornelius Müller, Michael Böhm The prerequisite of atherosclerosis,
endothelial dysfunction, is characterised by impaired endothelium-dependent
vasodilation caused by the reduced bioavailibility of nitric oxide (NO). In
order to assess the role of acute ACE inhibition in this setting, coronary arterial
endothelial function was quantified following acute intracoronary administration
of the angiotensin-converting enzyme (ACE) inhibitor quinapril.
Twenty-one patients with non-limiting coronary artery disease were studied before and after acute intracoronary
administration of 10 mg quinapril. Nine patients received pre-treatment with the angiotensin AT1-receptor antagonist
losartan (2x50 mg, p.o.). Coronary cross-sectional diameter was measured via quantitative
angiography and microvascular reaction was investigated by intracoronary Doppler
flow measurement during intracoronary infusion of 0.1 to 10 μmol/l acetylcholine.
Quinapril acutely improved endothelial dysfunction on the macro- as well as the
microvascular level. Losartan did not alter macrovascular function but facilitated
microvascular endothelial function. Acute quinapril application led to no further
improvement of endothelial dysfunction in patients pre-treated with losartan.
Acute quinapril infusion improved endothelial function
in patients with coronary heart disease. Treatment with the AT1-receptor
antagonist losartan led to a slight improvement in microvascular endothelial function,
but pre-treatment with losartan blunted the vascular effect of quinapril, suggesting
that the combination of ACE inhibition and AT1-receptor
antagonism may not exert a synergistic benefical impact on the coronary vasculature. JRAAS 2000;1:361-364. View full PDF article (open in new window)
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