| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
TRANSLATIONAL PHYSIOLOGY
1Institute of Clinical Physiology, National Council for Research; 2Department of Medicine, University of Pisa; 3Scuola Superiore Sant'Anna, Pisa, Italy; and 4Department of Physiology, New York Medical College, Valhalla, New York
Submitted 28 July 2007 ; accepted in final form 1 October 2007
Under resting conditions, the failing heart shifts fuel use toward greater glucose and lower free fatty acid (FFA) oxidation. We hypothesized that chronic metabolic abnormalities in patients with dilated cardiomyopathy (DCM) are associated with the absence of the normal increase in myocardial glucose uptake and maintenance of cardiac mechanical efficiency in response to pacing stress. In 10 DCM patients and 6 control subjects, we measured coronary flow by intravascular ultrasonometry and sampled arterial and coronary sinus blood. Myocardial metabolism was determined at baseline, during atrial pacing at 130 beats/min, and at 15 min of recovery by infusion of [3H]oleate and [13C]lactate and measurement of transmyocardial arteriovenous differences of oxygen and metabolites. At baseline, DCM patients showed depressed coronary flow, reduced uptake and oxidation of FFA, and preferential utilization of carbohydrates. During pacing, glucose uptake increased by 106% in control subjects but did not change from baseline in DCM patients. Lactate release increased by 122% in DCM patients but not in control subjects. Cardiac mechanical efficiency in DCM patients was not different compared with control subjects at baseline but was 34% lower during stress. Fatty acid uptake and oxidation did not change with pacing in either group. Our results show that in DCM there is preferential utilization of carbohydrates, which is associated with reduced flow and oxygen consumption at rest and an impaired ability to increase glucose uptake during stress. These metabolic abnormalities might contribute to progressive cardiac deterioration and represent a target for therapeutic strategies aimed at modulating cardiac substrate utilization.
microcirculation
This article has been cited by other articles:
|
|
 |
|
  B. C. Bergman, T. Tsvetkova, B. Lowes, and E. E. Wolfel Myocardial glucose and lactate metabolism during rest and atrial pacing in humans J. Physiol., May 1, 2009; 587(9): 2087 - 2099. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. van Bilsen, F. A. van Nieuwenhoven, and G. J. van der Vusse Metabolic remodelling of the failing heart: beneficial or detrimental? Cardiovasc Res, February 15, 2009; 81(3): 420 - 428. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Ingwall Energy metabolism in heart failure and remodelling Cardiovasc Res, February 15, 2009; 81(3): 412 - 419. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Neglia and A. L'Abbate Myocardial Perfusion Reserve in Ischemic Heart Disease J. Nucl. Med., February 1, 2009; 50(2): 175 - 177. [Full Text] [PDF]
|
|
|
|
 |
|
 B. C. Bergman, T. Tsvetkova, B. Lowes, and E. E. Wolfel Myocardial FFA metabolism during rest and atrial pacing in humans Am J Physiol Endocrinol Metab, February 1, 2009; 296(2): E358 - E366. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Qanud, M. Mamdani, M. Pepe, R. J. Khairallah, J. Gravel, B. Lei, S. A. Gupte, V. G. Sharov, H. N. Sabbah, W. C. Stanley, et al. Reverse changes in cardiac substrate oxidation in dogs recovering from heart failure Am J Physiol Heart Circ Physiol, November 1, 2008; 295(5): H2098 - H2105. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
