DIAGNOSTIC METHODS POSITRON EMISSION TOMOGRAPHY Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina

Regional myocardial perfusion and exogenous glucose uptake were assessed with rubidium-82 (82Rb) and 18F-2-fluoro-2-deoxyglucose (FDG) in 10 normal volunteers and 12 patients with coronary artery disease and stable angina pectoris by means of positron emission tomography. In patients at rest, the myocardial uptake of 82Rb and FDG did not differ significantly from that measured in normal subjects. The exercise test performed within the positron camera in eight patients produced typical chest pain and ischemic electrocardiographic changes in all. In each of the eight patients a region of reduced cation uptake was demonstrated in the 82Rb scan recorded at peak exercise, after which uptake of 82Rb returned to the control value 5 to 14 min after the end of the exercise. In these patients, FDG was injected in the recovery phase when all the variables that were altered during exercise, including regional myocardial 82Rb uptake, had returned to control values. In all but one patient, FDG accumulation in the regions of reduced 82Rb uptake during exercise was significantly higher than that in the nonischemic regions, i.e., the ones with a normal increment of 82Rb uptake on exercise. In the nonischemic areas, FDG uptake was not significantly different from that found in normal subjects after exercise. In conclusion, myocardial glucose transport and phosphorylation seem to be enhanced in the postischemic myocardium of patients with exercise-induced ischemia. Circulation 74, No. 1, 81-88, 1986. IT HAS LONG been known that myocardial glucose utilization is enhanced as a consequence of faster anaerobic glycolysis during conditions of reduced oxygen availability, as proved by the greater lactate production.' The importance of coronary flow and washout of the interstitial space in maintaining an accelerated glycolytic rate has been emphasized by studies in isolated working rat hearts submitted to anoxia and ischemia.24 Both anoxia and ischemia produce an initial acceleration of the glycolytic rate caused by rapid activation of glycogen breakdown, which lasts less than 10 min. Thereafter, as tissue glycogen is depleted, the glycolytic rate remains accelerated in the anoxic heart because of a greater utilization of exogenous glucose. In contrast, in the ischemic heart, the From the M.R.C. Cyclotron Unit and Cardiovascular Unit, Hammersmith Hospital, London, and C.N.R. Institute of Clinical Physiology and Istituto di Patologia Medica I, University of Pisa, Pisa, Italy. Dr. Shea was a Clinician-Scientist Awardee of the American Heart Association/British Heart Foundation. His present address is Division of Cardiology, University Hospital, Ann Arbor, MI. Address for correspondence: Paolo Camici, M.D., C.N.R. Institute of Clinical Physiology, Via Savi, 8, 56100 Pisa, Italy. Received Sept. 20, 1984; revision accepted Feb. 27, 1986. accumulation of lactate and the reduction in tissue pH cause a subsequent inhibition of glycolysis in proportion to the degree of restriction of coronary flow. Myocardial ischemia in man is usually a regional phenomenon. Little is known about the focal changes of myocardial glucose utilization that might be associated with episodes of transient ischemia in patients with coronary artery disease (CAD). The recent availability of positron emission tomography (PET) makes possible the noninvasive evaluation of regional myocardial perfusion and metabolism in man.' In the present study, we sought to determine by means of PET whether regional changes in glucose utilization could be demonstrated in the myocardium of patients with CAD and stable angina pectoris after an episode of exercise-induced ischemia. Regional myocardial perfusion and glucose uptake were assessed with rubidium-82 (t2Rb) and '5F-2fluoro-2-deoxyglucose (FDG), respectively. Materials and methods Study population. The study population consisted of 10 normal volunteers (all men, ages 29 to 38 years, with no sympVol. 74, No. 1, July 1986 81 by gest on M ay 3, 2017 http://ciajournals.org/ D ow nladed from