TY - JOUR
T1 - Regional coronary blood flow during relief of pacing-induced angina by nitroglycerin. Implications for mechanism of action
AU - Fuchs, Richard M.
AU - Brinker, Jeffrey A.
AU - Guzman, Pablo A.
AU - Kross, Dean E.
AU - Yin, Frank C.P.
N1 - Funding Information:
From the Cardiovascular Division, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland. This study was supported in part by Ischemic Heart Disease SCOR Grant P50 HL 17655_07 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Dr. Fuchs held a research fellowship from the American Heart Association-Maryland Affiliate, Baltimore, Maryland.M anuscript received June 14, 1982, accepted July 30, 1982. Address for reprints: Frank C. P. Yin, PhD, MD, The Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, Maryland 21205.
PY - 1983/1/1
Y1 - 1983/1/1
N2 - The mechanism for the therapeutic effect of nitroglycerin in stress-induced angina remains controversial; it has been attributed to both increased hlood supply to the ischemic myocardium and decreased myocardial oxygen demand. To investigate the contribution of each of these mechanisms, systemic pressures and great cardiac vein flow were measured in 14 patients with single-vessel disease involving the left anterior descending (LAD) coronary artery during the development of pacing-induced angina and after the administration of nitroglycerin while continuing pacing at the angina-provoking rate. Great cardiac vein flow, measured by thermodilution, represents the venous efflux from the LAD territory and therefore provided an index of flow to the poststenotic myocardium. In 11 patients, nitroglycerin was administered systemically (400 to 800 μg sublingually or 200 μg intravenously); angina was relieved in 10, concomitant with a decrease in both great cardiac vein flow (from 123 ± 29 to 98 ± 29 ml/min, p < 0.001) and mean aortic pressure (from 118 ± 22 to 104 ± 22 mm Hg, p < 0.001). In contrast, when 75 μg of nitroglycerin was administered directly into the left main coronary artery of 7 patients, it produced a small increase in great cardiac vein flow (from 108 ± 32 to 125 ± 31 ml/min, p = 0.059), no change in aortic pressure, and no relief of angina. This study suggests that nitroglycerin's major beneficial action in pacing-induced angina is unrelated to direct effects on the coronary circulation and is likely related to its cardiac unloading effect.
AB - The mechanism for the therapeutic effect of nitroglycerin in stress-induced angina remains controversial; it has been attributed to both increased hlood supply to the ischemic myocardium and decreased myocardial oxygen demand. To investigate the contribution of each of these mechanisms, systemic pressures and great cardiac vein flow were measured in 14 patients with single-vessel disease involving the left anterior descending (LAD) coronary artery during the development of pacing-induced angina and after the administration of nitroglycerin while continuing pacing at the angina-provoking rate. Great cardiac vein flow, measured by thermodilution, represents the venous efflux from the LAD territory and therefore provided an index of flow to the poststenotic myocardium. In 11 patients, nitroglycerin was administered systemically (400 to 800 μg sublingually or 200 μg intravenously); angina was relieved in 10, concomitant with a decrease in both great cardiac vein flow (from 123 ± 29 to 98 ± 29 ml/min, p < 0.001) and mean aortic pressure (from 118 ± 22 to 104 ± 22 mm Hg, p < 0.001). In contrast, when 75 μg of nitroglycerin was administered directly into the left main coronary artery of 7 patients, it produced a small increase in great cardiac vein flow (from 108 ± 32 to 125 ± 31 ml/min, p = 0.059), no change in aortic pressure, and no relief of angina. This study suggests that nitroglycerin's major beneficial action in pacing-induced angina is unrelated to direct effects on the coronary circulation and is likely related to its cardiac unloading effect.
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U2 - 10.1016/S0002-9149(83)80005-8
DO - 10.1016/S0002-9149(83)80005-8
M3 - Article
C2 - 6401374
AN - SCOPUS:0020682556
SN - 0002-9149
VL - 51
SP - 19
EP - 23
JO - The American journal of cardiology
JF - The American journal of cardiology
IS - 1
ER -