Myocardial bioenergetic abnormalities in a canine model of left ventricular dysfunction

Kenneth M. McDonald, Minoru Yoshiyama, Gary S. Francis, Kamil Ugurbil, Jay N. Cohn, Jianyi Zhang

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28 Citations (Scopus)

Abstract

Objectives. The purpose of this study was to assess high energy phosphate compound metabolism in remodeled left ventricular myocardium. Background. The development of heart failure several years after myocardial infarction is often unexplained. Certain abnormalities of remodeled myocardium suggest that structural changes occurring in viable myocardium after discrete myocardial damage may contribute to the later appearance of heart failure. Whether these abnormalities alter metabolism in the surviving muscle and thereby possibly contribute to ventricular dysfunction is unknown. Methods. High energy phosphate compound metabolism was assessed using spatially localized phosphorus-31 nuclear magnetic resonance spectroscopy. Eleven dogs with documented left ventricular dysfunction, resulting from infarction produced by transmyocardial direct current shock, were compared with eight normal dogs. Analyses were performed at baseline and during coronary hyperperfusion induced by intravenous adenosine. Myocardial blood flow was measured with radioactive microspheres. Results. The creatine phosphate/adenosine triphosphate (CP ATP) ratio was significantly reduced in the left ventricular dysfunction group in both the subepicardium ([mean ± SE] 1.94 ± 0.08 vs. 2.32 ± 0.13, p = 0.019) and the subendocardium (1.71 ± 0.07 vs. 2.05 ± 0.07, p = 0.004). Intravenous adenosine produced significant coronary hyperemia in both groups but was less marked in dogs with left ventricular dysfunction. The improvement in myocardial perfusion was accompanied by a significant increase in the subendocardial CP ATP ratio (from 1.71 ± 0.07 to 1.92 ± 0.08, p = 0.01) in dogs with left ventricular dysfunction. Conclusions. An abnormal transmural distribution of high energy phosphate compounds is evident in remodeled myocardium. This abnormality may be related in part to mismatch of oxygen delivery and demand.

Original languageEnglish (US)
Pages (from-to)786-793
Number of pages8
JournalJournal of the American College of Cardiology
Volume23
Issue number3
DOIs
StatePublished - Mar 1 1994

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Left Ventricular Dysfunction
Energy Metabolism
Canidae
Myocardium
Dogs
Phosphocreatine
Phosphates
Adenosine
Heart Failure
Adenosine Triphosphate
Ventricular Dysfunction
Hyperemia
Microspheres
Phosphorus
Infarction
Shock
Magnetic Resonance Spectroscopy
Perfusion
Myocardial Infarction
Oxygen

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Myocardial bioenergetic abnormalities in a canine model of left ventricular dysfunction. / McDonald, Kenneth M.; Yoshiyama, Minoru; Francis, Gary S.; Ugurbil, Kamil; Cohn, Jay N.; Zhang, Jianyi.

In: Journal of the American College of Cardiology, Vol. 23, No. 3, 01.03.1994, p. 786-793.

Research output: Contribution to journalArticle

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abstract = "Objectives. The purpose of this study was to assess high energy phosphate compound metabolism in remodeled left ventricular myocardium. Background. The development of heart failure several years after myocardial infarction is often unexplained. Certain abnormalities of remodeled myocardium suggest that structural changes occurring in viable myocardium after discrete myocardial damage may contribute to the later appearance of heart failure. Whether these abnormalities alter metabolism in the surviving muscle and thereby possibly contribute to ventricular dysfunction is unknown. Methods. High energy phosphate compound metabolism was assessed using spatially localized phosphorus-31 nuclear magnetic resonance spectroscopy. Eleven dogs with documented left ventricular dysfunction, resulting from infarction produced by transmyocardial direct current shock, were compared with eight normal dogs. Analyses were performed at baseline and during coronary hyperperfusion induced by intravenous adenosine. Myocardial blood flow was measured with radioactive microspheres. Results. The creatine phosphate/adenosine triphosphate (CP ATP) ratio was significantly reduced in the left ventricular dysfunction group in both the subepicardium ([mean ± SE] 1.94 ± 0.08 vs. 2.32 ± 0.13, p = 0.019) and the subendocardium (1.71 ± 0.07 vs. 2.05 ± 0.07, p = 0.004). Intravenous adenosine produced significant coronary hyperemia in both groups but was less marked in dogs with left ventricular dysfunction. The improvement in myocardial perfusion was accompanied by a significant increase in the subendocardial CP ATP ratio (from 1.71 ± 0.07 to 1.92 ± 0.08, p = 0.01) in dogs with left ventricular dysfunction. Conclusions. An abnormal transmural distribution of high energy phosphate compounds is evident in remodeled myocardium. This abnormality may be related in part to mismatch of oxygen delivery and demand.",
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N2 - Objectives. The purpose of this study was to assess high energy phosphate compound metabolism in remodeled left ventricular myocardium. Background. The development of heart failure several years after myocardial infarction is often unexplained. Certain abnormalities of remodeled myocardium suggest that structural changes occurring in viable myocardium after discrete myocardial damage may contribute to the later appearance of heart failure. Whether these abnormalities alter metabolism in the surviving muscle and thereby possibly contribute to ventricular dysfunction is unknown. Methods. High energy phosphate compound metabolism was assessed using spatially localized phosphorus-31 nuclear magnetic resonance spectroscopy. Eleven dogs with documented left ventricular dysfunction, resulting from infarction produced by transmyocardial direct current shock, were compared with eight normal dogs. Analyses were performed at baseline and during coronary hyperperfusion induced by intravenous adenosine. Myocardial blood flow was measured with radioactive microspheres. Results. The creatine phosphate/adenosine triphosphate (CP ATP) ratio was significantly reduced in the left ventricular dysfunction group in both the subepicardium ([mean ± SE] 1.94 ± 0.08 vs. 2.32 ± 0.13, p = 0.019) and the subendocardium (1.71 ± 0.07 vs. 2.05 ± 0.07, p = 0.004). Intravenous adenosine produced significant coronary hyperemia in both groups but was less marked in dogs with left ventricular dysfunction. The improvement in myocardial perfusion was accompanied by a significant increase in the subendocardial CP ATP ratio (from 1.71 ± 0.07 to 1.92 ± 0.08, p = 0.01) in dogs with left ventricular dysfunction. Conclusions. An abnormal transmural distribution of high energy phosphate compounds is evident in remodeled myocardium. This abnormality may be related in part to mismatch of oxygen delivery and demand.

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