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Do beta-adrenergic blocking agents increase coronary flow reserve?

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
卷 38, 期 7, 页码 1866-1871

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ELSEVIER SCIENCE INC
DOI: 10.1016/S0735-1097(01)01664-3

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Background Beta-adrenergic blocking agents are the cornerstone in the treatment of coronary artery disease (CAD). The exact pathophysiologic mechanism is not clear but depends largely on the oxygen-sparing effect of the drug, thus, the effect of metoprolol on coronary flow reserve and coronary flow velocity reserve (CFVR) was determined in patients with CAD. Methods Corona blood flow velocity was measured with the Doppler Row wire in 23 patients (age: 56 +/- 10) undergoing percutaneous transluminal coronary, angioplasty for therapeutic reasons. Measurements were carried out at rest, after 1-min vessel occlusion (postischemic CFVR) as well as after intracoronary adenosine (pharmacologic CFVR) before and after 5 mg intravenous metoprolol. In a subgroup (n=15), absolute flow was measured from coronary flow velocity multiplied by coronary cross-sectional area. Results Rate-pressure product decreased after metoprolol from 9.1 to 8.0 x 10(3) mm Hg/min (p<0.001). Pharmacologic CFVR was 2.1 at rest and increased after metoprolol to 2.7 (p=0.002). Likewise, postischemic CFVR increased from 2.6 to 3.3 (p<0.001). Postischemic CFVR was significantly higher than pharmacologic CFVR before as well as after metoprolol. Coronary vascular resistance decreased after metoprolol from 3.4 +/-2.0 to 2.3 +/-0.7 mm Hg x s/cm (p<0.02). Conclusions The following conclusions were drawn from this study. Metoprolol is associated with a significant increase in postischemic and pharmacologic MIR. However, postischemic CFVR is significantly higher than pharmacologic CFVR. The increase in CFVR by metoprolol can be explained by a reduction in vascular resistance. The increase in CFVR (=increased supply) and the reduction in oxygen consumption (= decreased demand) after metoprolol explain the beneficial effect of this beta-blocker in patients with CAD. (J Am Coll Cardiol 2001;38:1866-71) (C) 2001 by the American College of Cardiology.

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