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Myocardial Substrate Utilization and Left Ventricular Function in Adriamycin Cardiomyopathy

Division of Nuclear Medicine of the Department of Radiology, Massachusetts General Hospital and the Department of Radiology, Harvard Medical School, Boston, Massachusetts

Correspondence: For correspondence or reprints contact: Dr. Alan J. Fischman, Div. of Nuclear Medicine, Dept. of Radiology, Massachusetts General Hospital, 32 Fruit St., Boston, MA 02114.

ABSTRACT

We evaluated alterations of substrate utilization in a rat model of adriamycin cardiomyopathy with deteriorating left ventricular function. Rats were treated with adriamycin (2 mg/kg), once a week for 6, 8, 9 and 10 wk. Fluorine-18-F-deoxyglucose (¹⁸F-FDG) and ¹²⁵I-beta-methyl-branched fatty acid (¹²⁵I-BMIPP) were used as tracers of glucose and fatty acid metabolism and ^99mTc-hexakis (2-methoxyisobutyl-isonitrile) (^99mTc-MlBl) was used as a myocardial blood flow tracer. Left ventricular ejection fraction (LVEF) calculated from gated blood pool images was used as an indicator of cardiac function. LVEF was normal in the 6-wk group (78.0 ±4.8%), abruptly decreased in the 8-wk group (43.1% ± 10.1%) and further deteriorated in the 9-wk group (27.6% ± 13.4%). Accumulation of ¹⁸F-FDG (%kgID/g) in the hearts of adriamycin treated animals progressively decreased compared to controls (2.19% ± 0.38%); 1.47% ± 0.42% (p < 0.01) at 6 wk, 1.22% ± 0.27% (p < 0.001) at 8 wk, 0.69% ± 0.56% (p < 0.001) at 9 wk and 0.50% ± 0.08% (p < 0.001) at 10 wk. This decrease occurred earlier than the deterioration in LVEF. Myocardial accumulation of ¹²⁵I-BMIPP decreased in the advanced stages of adriamycin cardiomyopathy and was well correlated with the decrease in ¹⁸F-FDG accumulation. However, the decrease was less profound than for ¹⁸F-FDG; 53.7% ± 9.8% versus 31.6% ± 25.4% of control at 9 wk (p = NS), 49.5% ± 15.3% versus 22.6% ± 3.5% of control at 10 wk (p < 0.05). Accumulation of ^99mTc-MIBI did not differ between controls and the adriamycin treated groups. There were no differences in blood glucose levels between controls and adriamycin treatment groups. Both glucose and fatty acid utilization are decreased in adriamycin-induced cardiomyopathy and these critical impairments in energy metabolism are associated with heart failure. Impaired myocardial glucose utilization measured with ¹⁸F-FDG may be a particularly sensitive marker of adriamycin cardiomyopathy.

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