TY - JOUR
T1 - Dipyridamole-induced increased glucose uptake in patients with single-vessel coronary artery disease assessed with PET
AU - Araujo, Luis I.
AU - McFalls, Edward O.
AU - Lammertsma, Adriaan A.
AU - Jones, Terry
AU - Maseri, Attilio
PY - 2001
Y1 - 2001
N2 - Background. The aim of this study was to determine the relationship between vasodilatation-induced ischemia and poststress glucose uptake. Coronary vasodilators may induce myocardial ischemia due to coronary steal through collateral circulation or transmural blood flow redistribution with diminished subendocardial perfusion. Myocardial ischemia can be demonstrated by increased glucose uptake as previously shown in patients with exercise-induced ischemia. Methods and Results. We studied 11 patients with single-vessel disease and no history of myocardial infarction. Five patients had no collateral circulation, and 6 had angiographic evidence of collateral vessels. We measured myocardial blood flow (MBF) and glucose uptake at baseline and after the administration of dipyridamole (0.56 mg/kg) with positron emission tomography, using O-15 water and fluorine 18 deoxyglucose (FDG) as perfusion and glucose tracers. MBF at baseline was 0.82 ± 0.13 mL/g/min in normal areas and 0.80 ± 0.15 mL/g/min in areas supplied by stenotic arteries. MBF during dipyridamole was 2.05 ± 0.66 and 1.19 ± 0.66 mL/g/min in normal areas and areas with stenotic arteries, respectively (P ≤ .001). FDG uptake at baseline was 1.36 ± 0.55 in normal areas and 1.57 ± 0.62 in areas supplied by stenotic arteries. FDG uptake after dipyridamole infusion was 1.79 ± 1.1 and 4.04 ± 0.84 in normal areas and areas with stenotic arteries, respectively (P ≤ .001). MBF and FDG uptake were not different between patients with collateral circulation and those without collateral circulation. Conclusions. Increased myocardial glucose uptake was consistently observed after dipyridamole administration in those areas with diminished coronary vasodilatory capacity. The similar MBF and FDG findings in patients with and without collateral circulation may indicate that transmural blood flow redistribution appears to be a possible mechanism of dipyridamole-induced myocardial ischemia.
AB - Background. The aim of this study was to determine the relationship between vasodilatation-induced ischemia and poststress glucose uptake. Coronary vasodilators may induce myocardial ischemia due to coronary steal through collateral circulation or transmural blood flow redistribution with diminished subendocardial perfusion. Myocardial ischemia can be demonstrated by increased glucose uptake as previously shown in patients with exercise-induced ischemia. Methods and Results. We studied 11 patients with single-vessel disease and no history of myocardial infarction. Five patients had no collateral circulation, and 6 had angiographic evidence of collateral vessels. We measured myocardial blood flow (MBF) and glucose uptake at baseline and after the administration of dipyridamole (0.56 mg/kg) with positron emission tomography, using O-15 water and fluorine 18 deoxyglucose (FDG) as perfusion and glucose tracers. MBF at baseline was 0.82 ± 0.13 mL/g/min in normal areas and 0.80 ± 0.15 mL/g/min in areas supplied by stenotic arteries. MBF during dipyridamole was 2.05 ± 0.66 and 1.19 ± 0.66 mL/g/min in normal areas and areas with stenotic arteries, respectively (P ≤ .001). FDG uptake at baseline was 1.36 ± 0.55 in normal areas and 1.57 ± 0.62 in areas supplied by stenotic arteries. FDG uptake after dipyridamole infusion was 1.79 ± 1.1 and 4.04 ± 0.84 in normal areas and areas with stenotic arteries, respectively (P ≤ .001). MBF and FDG uptake were not different between patients with collateral circulation and those without collateral circulation. Conclusions. Increased myocardial glucose uptake was consistently observed after dipyridamole administration in those areas with diminished coronary vasodilatory capacity. The similar MBF and FDG findings in patients with and without collateral circulation may indicate that transmural blood flow redistribution appears to be a possible mechanism of dipyridamole-induced myocardial ischemia.
KW - Coronary vasodilators
KW - Myocardial blood flow
KW - Myocardial ischemia
KW - Myocardial metabolism
KW - Positron emission tomography
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U2 - 10.1067/mnc.2001.113615
DO - 10.1067/mnc.2001.113615
M3 - Article
C2 - 11391304
AN - SCOPUS:0034969326
SN - 1071-3581
VL - 8
SP - 339
EP - 346
JO - Journal of Nuclear Cardiology
JF - Journal of Nuclear Cardiology
IS - 3
ER -
