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Coronary collateral perfusion in patients with coronary artery disease: effect of metoprolol

Billinger, Michael ; Raeber, Lorenz ; Seiler, Christian ; Windecker, Stephan ; Meier, Bernhard ; Hess, Otto M.

In: European Heart Journal, 2004, vol. 25, no. 7, p. 565-570

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    Title
    • Coronary collateral perfusion in patients with coronary artery disease: effect of metoprolol
    Author
    • Billinger, Michael. Cardiology, Swiss Cardiovascular Centre, University Hospital, CH-3010 Bern, Switzerland
    • Raeber, Lorenz. Cardiology, Swiss Cardiovascular Centre, University Hospital, CH-3010 Bern, Switzerland
    • Seiler, Christian. Cardiology, Swiss Cardiovascular Centre, University Hospital, CH-3010 Bern, Switzerland
    • Windecker, Stephan. Cardiology, Swiss Cardiovascular Centre, University Hospital, CH-3010 Bern, Switzerland
    • Meier, Bernhard. Cardiology, Swiss Cardiovascular Centre, University Hospital, CH-3010 Bern, Switzerland
    • Hess, Otto M.. Cardiology, Swiss Cardiovascular Centre, University Hospital, CH-3010 Bern, Switzerland
    Document Type
    • Postprint
    OAI-PMH Identifier
    • oai:doc.rero.ch:303207
    Summary
    Background The use of ultrathin Doppler angioplasty guidewires has made it possible to measure collateral flow quantitatively. Pharmacologic interventions have been shown to influence collateral flow and, thus, to affect myocardial ischaemia. Methods Twenty-five patients with coronary artery disease undergoing PTCA were included in the present analysis. Coronary flow velocities were measured in the ipsilateral (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(n=25\) \end{document}) and contralateral (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(n=6\) \end{document}; two Doppler wires) vessels during PTCA with and without i.v. adenosine (140 μg/kg.min) before and 3 min after 5 mg metoprolol i.v., respectively. The ipsilateral Doppler wire was positioned distal to the stenosis, whereas the distal end of the contralateral wire was in an angiographically normal vessel. The flow signals of the ipsilateral wire were used to calculate the collateral flow index (CFI). CFI was defined as the ratio of flow velocity during balloon inflation divided by resting flow. Results Heart rate and mean aortic pressure decreased slightly (ns) after i.v. metoprolol. The collateral flow index was 0.25±0.12 (one fourth of the resting coronary flow) during the first PTCA and 0.27±0.14 (ns versus first PTCA) during the second PTCA, but decreased with metoprolol to 0.16±0.08 (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(p{<}0.0001\) \end{document} vs. baseline) during the third PTCA. Conclusions Coronary collateral flow increased slightly but not significantly during maximal vasodilatation with adenosine but decreased in 23 of 25 patients after i.v. metoprolol. Thus, there is a reduction in coronary collateral flow with metoprolol, probably due to an increase in coronary collateral resistance or a reduction in oxygen demand