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. 1989 Apr;78(4):262-70.

[Reduced myocardial fatty acid utilization in coronary heart disease following symptom limited ergometric stress. Detection of pathologic metabolic patterns using iodine-123-phenylpentadecanoic acid and sequential SPECT]

[Article in German]
Affiliations
  • PMID: 2786661

[Reduced myocardial fatty acid utilization in coronary heart disease following symptom limited ergometric stress. Detection of pathologic metabolic patterns using iodine-123-phenylpentadecanoic acid and sequential SPECT]

[Article in German]
S N Reske et al. Z Kardiol. 1989 Apr.

Abstract

Regional cardiac free fatty acid metabolism of 41 patients with coronary artery disease (CAD) and of 10 controls with normal coronary arteries was studied by means of I-123 phenylpentadecanoic acid (IPPA), a radioiodinated palmitic acid analog, and sequential single photon emission tomography (SPECT). All patients and controls underwent symptom--limited bicycle exercise, with the tracer being injected at peak stress. More than 99% of left ventricular segment of controls showed homogeneous tracer uptake and release, indicating homogeneous free fatty acid turnover in normal myocardium. Homogeneous postexercise uptake was followed by decreasing segmental activity in 75.1% of normally perfused segments in patients with CAD. Sixty-five percent and 88.6% of segments, assigned to the perfusion bed of 50%-75% and greater than 75% obstructed vessels had decreased IPPA release and/or reduced IPPA uptake. Patients with exercise induced ischemia had focal metabolic abnormalities in jeopardized myocardium for significantly longer time than clinical or electrocardiographic signs of ischemia (p less than 0.01). All patients with CAD and a negative stress test had metabolic abnormalities, but exhibited, compared to ECG--positive patients, less pronounced segmental metabolic aberrations. These findings indicate reduced cardiac utilization and delayed oxidation of IPPA, associated with exercise-induced ischemia in CAD. The metabolic changes suggest a marked sensitivity to ischemia as well as prolonged postischemic abnormalities of cardiac fatty acid metabolism in jeopardized myocardium.

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