Author + information
- Received May 18, 1988
- Revision received September 19, 1988
- Accepted October 13, 1988
- Published online March 1, 1989.
- Russell C. Reeves, MD, FACC∗,
- William T. Evanochko, PhD,
- Robert C. Canby, MEE,
- Jeanie B. McMillin, PhD and
- Gerald M. Pohost, MD, FACC
- ↵∗Address for reprints:Russell C. Reeves, MD, The University of Alabama at Birmingham, Department of Medicine, Division of Cardiovascular Disease, Birmingham, Alabama 35294.
Histopathologic studies have demonstrated accumulation of lipid droplets in myocardium subjected to ≥6 h of ischemic insult. Proton nuclear magnetic resonance (NMR) spectroscopy can provide a noninvasive means to evaluate changes in tissue lipid and, potentially, to characterize the ischemic insult. To determine whether lipids accumulate with a brief ischemic insult, myocardial lipid content was evaluated by 1H NMR spectroscopy of ex-vivo samples from seven dogs in a model of postischemic dysfunction created by 15 min of left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Regional myocardial function was assessed by measuring segment length shortening with use of a pair of ultrasonic crystals placed in the ischemic zone and in the control zone.
During the occlusion, all dogs had significant ischemia of the occlusion zone as measured by radiolabeled microspheres (0.08 ± 0.08 versus 0.88 ± 0.09 ml/g per min for the control zone), and all dogs developed systolic stretching of the ischemic zone segment. Myocardial lipid content was significantly elevated in the samples from the coronary occlusion zone (p < 0.02). The increase in lipid signal may result from the ischemia-induced decrease in beta oxidation and resultant accumulation of fatty acyl esters (for example, fatty acids, triglycerides and acylcarnitines).
In conclusion, this study shows that myocardium subjected to a brief (approximately 15 min) coronary occlusion followed by 3 h of reperfusion demonstrates a significant increase in NMR-detectable lipid content.
☆ This study was supported in part by Grants HL-17667 and HL-38863 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
☆☆ We gratefully acknowledge the important contributions of Kathy Kirk, PhD in the statistical analyses of Margaret A. Burchfield in secretarial assistance.
- Received May 18, 1988.
- Revision received September 19, 1988.
- Accepted October 13, 1988.