V. E. Wendt, M.D.; S. Gudbjarnason, M.D.; T. B. Stock, M.D.; R. O. Hayden, M.D., F.A.C.P.; M. Rothlin, M.D.; R. J. Bing, M.D., F.A.C.P.
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Metabolism of the heart was studied in 31 patients with cardiac myopathy caused by progressive muscular dystrophy (PMD), thyrotoxicosis, and unknown causes. Arteriosclerotic, hypertensive, and rheumatic heart diseases were excluded. Several of the patients suffered from congestive heart failure. The coronary sinus was intubated and lactate, pyruvate, glucose, MDH, aldolase, and inorganic phosphate were determined in arterial and coronary vein blood. The oxidation-reduction potential (redox potential) differences between arterial and coronary vein blood were calculated from the ratio of lactate/pyruvate to determine the presence of myocardial anoxia. In PMD the cardiac output was elevated, and there was a rise in
Wendt VE, Gudbjarnason S, Stock TB, et al. Cardiac Metabolism in Cardiomyopathies.. Ann Intern Med. 1962;56:672. doi: https://doi.org/10.7326/0003-4819-56-4-672_1
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Published: Ann Intern Med. 1962;56(4):672.
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