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J Am Coll Cardiol, 2005; 46:1085-1092, doi:10.1016/j.jacc.2005.05.075
(Published online 20 September 2005). © 2005 by the American College of Cardiology Foundation |
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* Division of Internal Medicine-Section of Nutrition/Metabolism
Unit of Clinical Spectroscopy, Universitá Vita e Salute San Raffaele, Milan, Italy
Internal Medicine-Section of Organ Transplantation, Universitá Vita e Salute San Raffaele, Milan, Italy
Division of Diagnostic Radiology, Universitá Vita e Salute San Raffaele, Milan, Italy
|| Division of Nuclear Medicine, Universitá Vita e Salute San Raffaele, Milan, Italy
¶ Faculty of Exercise Sciences, Universitá degli Studi di Milano, Milan, Italy.
Manuscript received January 10, 2005; revised manuscript received May 23, 2005, accepted May 24, 2005.
* Reprint requests and correspondence: Dr. Gianluca Perseghin, Section of Nutrition/Metabolism & Unit of Clinical Spectroscopy, Istituto Scientifico H San Raffaele Internal Medicine, via Olgettina 60, 20132 Milan, Italy. (Email: perseghin.gianluca{at}hsr.it).
OBJECTIVES: To test whether left ventricular (LV) dysfunction affecting type 1 diabetic-uremic patients was associated with abnormal heart high-energy phosphates (HEPs) and to ascertain whether these alterations were also present in recipients of kidney or kidney-pancreas transplantation.
BACKGROUND: Heart failure is the major determinant of mortality in patients with diabetic uremia. Both uremia and diabetes induce alterations of cardiac HEPs metabolism.
METHODS: Magnetic resonance imaging and phosphorous magnetic resonance spectroscopy of the LV were performed in the resting state by means of a 1.5-T clinical scanner. Eleven diabetic-uremic patients, 5 nondiabetic patients with uremia, 11 diabetic recipients of kidney transplantation, and 16 diabetic recipients of combined kidney-pancreas transplantation were studied in a cross-sectional fashion. Eleven nondiabetic recipients of kidney-only transplant and 13 healthy subjects served as control groups.
RESULTS: Uremic patients had higher LV mass, diastolic dysfunction, and lower phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio in comparison with recipients of kidney-pancreas or nondiabetic recipients of kidney transplant. In diabetic recipients of kidney transplant the PCr/ATP ratio was higher than in uremic patients but was lower than in the controls. Recipients of combined kidney-pancreas transplant had a higher ratio than uremic patients but no difference was found in comparison with controls.
CONCLUSIONS: Altered resting myocardial HEPs metabolism may contribute to LV dysfunction in diabetic-uremic patients. In diabetic recipients of kidney transplantation, a certain degree of LV metabolic and functional impairment was found. In combined kidney-pancreas recipients the resting LV metabolism and function were not different than in controls.
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