Increased uptake of 18F-fluorodeoxyglucose in postischemic myocardium of patients with exercise-induced angina.

Abstract

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.

Differential 18 F-2-Deoxyglucose Uptake in Viable Dysfunctional Myocardium With Normal Resting Perfusion

“…Clinical data regarding fasting FDG uptake in chronically stunned myocardium are limited. Although it was not the primary focus of their report, Camici et al 21 found no regional variations in fasting FDG uptake before exercise (fractional FDG uptake, 0.11Ϯ0.03 in coronary patients with regional dysfunction and normal flow versus 0.07Ϯ0.04 in control subjects, PϭNS). These observations support the notion that viable, chronically dysfunctional myocardium can be associated with normal FDG uptake in the fasting state, as we found in pigs instrumented for 1 month.…”

Reduced 123I-BMIPP uptake implies decreased myocardial flow reserve in patients with chronic stable angina

“…In effort angina, exogenous glucose uptake is increased after exercise-induced ischemia [12]. Repeated ischemia prolongs abnormal wall motion and the substrate shift from LCFA to glucose.…”

“…Reduced LCFA metabolism was reported both experimentally and clinically in ischemic myocardium [4][5][6]. In ischemic myocardium, the main energy substrate shifts from LCFA to glucose [7][8][9][10][11][12][13][14]. 123 I-BMIPP is a radiolabeled LCFA analogue and is commercially available in Japan.…”

Role of molecular imaging with positron emission tomographic in aortic aneurysms

“…After FDG enters the inflammatory cell, it undergoes phosphorylation by the hexokinase enzyme system to FDG-6-phosphate. However, unlike glucose-6-phosphate, FDG-6-phosphate is not metabolized further along the glycolytic pathway (i.e., not dephosphorylated by glucose-6-phosphatase), resulting in metabolic trapping of 18 FDG-6-PO4 in the cell in direct proportion to its overall metabolic state (15).…”