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  • Title: Paradoxical increase in coronary flow velocity after termination of acetylcholine infusion is a marker of the impaired vasodilatation at coronary microvessels in patients with angina and normal coronary arteries.
    Author: Takeuchi M, Nohtomi Y, Kuroiwa A.
    Journal: Catheter Cardiovasc Interv; 1999 Oct; 48(2):170-7. PubMed ID: 10506773.
    Abstract:
    Some patients with anginal chest pain and normal coronary arteries exhibit a paradoxical increase in coronary flow velocity after termination of acetylcholine infusion. The aim of this study was to investigate whether this paradoxical increase in the flow velocity is associated with the impaired microvascular dilatation to pharmacological stimuli. We infused graded doses of endothelium-dependent vasodilator acetylcholine (10, 50, and 100 microg/min for 2 min) and the endothelium-independent vasodilators, papaverine and nitroglycerin, into the left coronary artery in 15 patients with chest pain and normal coronary arteries. Coronary blood flow responses were evaluated by Doppler guidewire and quantitative angiography in the proximal left anterior descending coronary artery. Seven patients showed a paradoxical increase in coronary flow velocity after termination of acetylcholine infusion with the highest dose (100 microg/min), whereas eight showed no change or a decrease in the flow velocity. This was also observed in 50 microg/min of acetylcholine infusion. In patients with a paradoxical increase in the flow velocity, coronary flow velocity responses to acetylcholine during three graded doses were significantly blunted in comparison to those without a paradoxical increase. In contrast, coronary flow reserve to papaverine and nitroglycerin was similar in the two groups. Epicardial artery vasoreactivity to acetylcholine did not differ between the two groups. Papaverine and nitroglycerin also caused a similar degree of coronary dilatation in both groups. These results suggest that the paradoxical increase in coronary flow velocity observed immediately after termination of the intracoronary acetylcholine infusion is a marker of impaired nitric oxide-dependent dilatation of the coronary microvessels in patients with normal coronary arteries. Cathet. Cardiovasc. Intervent. 48:170-177, 1999.
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