Background We assessed the relation between the severity ofstenosis in a coronary artery and the degree of impairment ofmyocardial blood flow. Studies in laboratory animals have shownthat as the degree of coronary-artery stenosis increases, themaximal coronary flow measured after maximal vasodilatationprogressively decreases, with a concomitant decrease in basalflow. However, this relation has not been carefully documentedin humans through measurement of myocardial blood flow.
Methods We studied 35 patients with single-vessel coronary arterydisease and normal left ventricular function and 21 age-matchedcontrols. Regional myocardial blood flow in the area suppliedby the stenosed artery was measured by positron-emission tomographywith oxygen-15-labeled water while the subject was at rest (basalflow) and during hyperemia induced by the intravenous administrationof the vasodilator adenosine (140 µg per kilogram of bodyweight per minute) or dipyridamole (0.56 mg per kilogram).
Results The mean (±SD) basal myocardial blood flow was1.14 ±0.42 ml per minute per gram of tissue in the patientsand 1.13 ±0.26 ml per minute per gram in the controls;during hyperemia, myocardial flow was 2.10 ±1.16 and3.37 ±1.25 ml per minute per gram (P<0.001), respectively.Basal flow was unchanged regardless of the severity of stenosis,expressed as a percentage of the diameter of the affected vessel(range of degrees of stenosis, 17 to 87 percent). In contrast,flow during hyperemia correlated inversely and significantlywith the degree of stenosis and correlated directly with theminimal luminal diameter. The coronary vasodilator reserve (definedas the ratio of flow during hyperemia to flow at base line)began to decline when the degree of stenosis was about 40 percentand approached unity when stenosis was 80 percent or greater.
Conclusions In humans, basal myocardial blood flow remains constantregardless of the severity of coronary-artery stenosis. However,during hyperemia, flow progressively decreases when the degreeof stenosis is about 40 percent or more and does not differsignificantly from basal flow when stenosis is 80 percent orgreater.
Source Information
From the Cyclotron Unit, Medical Research Council Clinical Sciences Centre and Royal Postgraduate Medical School, Hammersmith Hospital, London (N.G.U., P.G.C.); the University of Louvain Medical School, Brussels, Belgium (J.A.M., W.W., T.B.); and the Cardiovascular Center, Aalst, Belgium (B.D.B.). Presented in part at the 66th Scientific Sessions of the American Heart Association, Atlanta, November 7-11, 1993.Dr. Baudhuin is deceased.
Address reprint requests to Dr. Camici at the MRC Cyclotron Unit, Hammersmith Hospital, Du Cane Rd., London W12 0HS, United Kingdom.
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