Do beta-adrenergic blocking agents increase coronary flow reserve?

• Published in: Journal of the American College of Cardiology 2001-12, Vol.38 (7), p.1866-1871
• Main Authors: Billinger, Michael, Seiler, Christian, Fleisch, Martin, Eberli, Franz R, Meier, Bernhard, Hess, Otto M
• Format: Article
• Language: English
• Subjects: Adrenergic beta-Antagonists - administration & dosage; Aged; Angioplasty, Balloon, Coronary; Antianginal agents. Coronary vasodilator agents; Biological and medical sciences; Blood Flow Velocity - drug effects; Cardiovascular system; Coronary Circulation - drug effects; Echocardiography, Doppler - drug effects; Female; Hemodynamics - drug effects; Humans; Male; Medical sciences; Metoprolol - administration & dosage; Middle Aged; Myocardial Infarction - diagnostic imaging; Myocardial Infarction - drug therapy; Oxygen Consumption - drug effects; Pharmacology. Drug treatments; Vascular Resistance - drug effects
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(01)01664-3

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 Coronary blood flow velocity was measured with the Doppler flow 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 × 103mm 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 × 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 CFVR. 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.