Information de reference pour ce titreAccession Number: | 00003017-199404000-00020.
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Author: | Stratton, John R.; Kemp, Graham J.; Daly, Richard C.; Yacoub, Sir Magdi; Rajagopalan, Bheeshma.
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Institution: | Received November 23, 1993; revision accepted December 14, 1993. From the Division of Cardiology, Department of Medicine, Seattle VA Medical Center and University of Washington (J.R.S.); the MRC Biochemical and Clinical Magnetic Resonance Unit, John Radcliffe Hospital, Headington, Oxford, UK (G.J.K., B.R.); the Division of Thoracic and Cardiovascular Surgery, Mayo Clinic, Rochester, Minn (R.C.D.); and the National Heart and Lung Institute, Harefield Hospital, Middlesex, UK (M.Y.). Correspondence to John R. Stratton, MD, Cardiology (111-C), Seattle VA Medical Center, 1660 South Columbian Way, Seattle, WA 98108.
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Title: | Heart Failure/Cardiac Transplantation: Effects of Cardiac Transplantation on Bioenergetic Abnormalities of Skeletal Muscle in Congestive Heart Failure.[Report]
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Source: | Circulation. 89(4):1624-1631, April 1994.
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Abstract: | Background Patients with advanced heart failure have bioenergetic abnormalities of skeletal muscle metabolism during exercise. Using Phosphorus-31 magnetic resonance spectroscopy, we sought to determine whether skeletal metabolic responses to exercise are normalized by orthotopic cardiac transplantation.
Methods and Results Four groups were studied: healthy normal volunteers (n=9), subjects awaiting heart transplantation (n=10), subjects <6 months (mean, 4 months) after transplant (n=9), and subjects >6 months (mean, 15 months) after transplant (n=8). None of the posttransplant patients had biopsy evidence of rejection at the time of study. There were no significant differences in age, preoperative functional class, or symptom duration among the three patient groups. Metabolic responses were monitored in the dominant arm during incremental weight pull exercise and 10 minutes of recovery by Phosphorus-31 magnetic resonance spectroscopy, with measurement of pH and the phosphocreatine (PCr)/(PCr+inorganic phosphate (Pi)) ratio, an index of PCr concentration. In addition, based on recovery data, the rate of PCr resynthesis was calculated as a measure of oxidative metabolism that is independent of work level, recruitment, or muscle mass, and the effective maximal rate of mitochondrial ATP synthesis (Vmax) was determined. Analysis was by ANOVA. There were no differences between groups in pH or PCr/(PCr+Pi) at rest. Compared with the normal control group, the pretransplant group had a decreased exercise duration (11.3+-2.5 versus 15.0+-1.3 minutes, P=.02), a lower submaximal exercise PCr/(PCr+Pi) ratio (0.58+-0.11 versus 0.76+-0.08, P<.05), a reduced PCr resynthesis rate (13+-6 versus 22+-9 mmol/L per minute, P<.05), and a lower calculated Vmax (26+-14 versus 53+-26 mmol/L per minute, P<.05). In the group studied early after transplantation, all the changes noted in the pretransplant group persisted and were if anything somewhat worse. In the group studied late after transplantation, there was a significant improvement in the PCr resynthesis rate compared with the early-posttransplant group (27+-6 late versus 15+-6 mmol/L per minute early, P<.05) and statistically nonsignificant trends toward improvements in submaximal exercise pH (6.86+-0.24 late versus 6.72+-0.24 early) and submaximal PCr/(PCr+Pi) ratio (0.56+-0.14 late versus 0.44+-0.15 early) and Vmax (45+-21 late versus 33+-15 mmol/L per minute early). However, compared with normal subjects, exercise duration and submaximal PCr/(PCr+Pi) were still reduced in the late-posttransplant group.
Conclusions Despite successful heart transplantation, skeletal muscle abnormalities of advanced heart failure persist for indefinite periods, although partial improvement occurred at late times. The persistent abnormalities may contribute to the reduced exercise capacity that is present in most patients after transplantation. (Circulation. 1994;89:1624-1631.)
(C) 1994 American Heart Association, Inc.
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References: | 1. Drexler H. Skeletal muscle failure in heart failure. Circulation. 1992;85:1621-1623.
2. Marie PY, Escanye JM, Brunotte F, Robin B, Walker P, Zannad F, Robert J, Gilgenkrantz JM. Skeletal muscle metabolism in the leg during exercise in patients with congestive heart failure. Clin Sci. 1990;78:515-519.
3. Mancini DM, Ferraro N, Tuchler M, Chance B, Wilson JR. Detection of abnormal calf muscle metabolism in patients with heart failure using phosphorus-31 nuclear magnetic resonance. Am J Cardiol. 1988;62:1234-1240.
4. Massie BM, Conway M, Yonge R, Frostick S, Sleight P, Ledingham J, Radda G, Rajagopalan B. 31P nuclear magnetic resonance evidence of abnormal skeletal muscle metabolism in patients with congestive heart failure. Am J Cardiol. 1987;60: 309-315.
5. Massie B, Conway M, Yonge R, Frostick S, Ledingham J, Sleight P, Radda G, Rajagopalan B. Skeletal muscle metabolism in patients with congestive heart failure: relation to clinical severity and blood flow. Circulation. 1987;76:1009-1019.
6. Massie BM, Conway M, Rajagopalan B, Yonge R, Frostick S, Ledingham J, Sleight P, Radda G. Skeletal muscle metabolism during exercise under ischemic conditions in congestive heart failure: evidence for abnormalities unrelated to blood flow. Circulation. 1988;78:320-326.
7. Wilson JR, Fink L, Maris J, Ferraro N, Power VJ, Eleff S, Chance B. Evaluation of energy metabolism in skeletal muscle of patients with heart failure with gated phosphorus-31 nuclear magnetic resonance. Circulation. 1985;71:57-62.
8. Rajagopalan B, Conway MA, Massie B, Radda GK. Alterations of skeletal muscle metabolism in humans studied by phosphorus 31 magnetic resonance spectroscopy in congestive heart failure. Am J Cardiol. 1988;62:53E-57E.
9. Massie BM. Exercise tolerance in congestive heart failure: role of cardiac function, peripheral blood flow, and muscle metabolism and effect of treatment. Am J Med. 1988;84:75-82.
10. Szlachic J, Massie B, Kramer B, Topic N, Tubau J. Correlates and prognostic implication of exercise capacity in chronic congestive heart failure. Am J Cardiol. 1985;51:1037-1042.
11. Wiener DH, Fink LI, Maris J, Jones RA, Chance B, Wilson JR. Abnormal skeletal muscle bioenergetics during exercise in patients with heart failure: role of reduced muscle blood flow. Circulation. 1986;73:1127-1136.
12. Mancini DM, Walter G, Reichek N, Lenkinski R, McCully KK, Mullen JL, Wilson JR. Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. Circulation. 1992;85:1364-1373.
13. Mancini DM, Coyle E, Coggan A, Beltz J, Ferraro N, Montain S, Wilson JR. Contribution of intrinsic skeletal muscle changes to 31P NMR skeletal muscle metabolic abnormalities in patients with chronic heart failure. Circulation. 1989;80:1338-1346.
14. Sullivan M, Green H, Cobb F. Skeletal muscle biochemistry in ambulatory patients with long-term heart failure. Circulation. 1990; 81:518-527.
15. Minotti JR, Johnson EC, Hudson TL, Zuroske G, Murata G, Fukushima E, Cagle TG, Chick TW, Massie BM, Icenogle MV. Skeletal muscle response to exercise training in congestive heart failure. J Clin Invest. 1990;86:751-758.
16. Adamopoulos S, Coats A, Brunotte F, Arnolda L, Meyer T, Thompson C, Dunn J, Stratton J, Kemp G, Radda G, Rajagopalan B. Physical training improves skeletal muscle metabolism in patients with chronic heart failure. J Am Coll Cardiol. 1993;21: 1101-1106.
17. Stratton J, Dunn J, Adamopoulous S, Radda G, Rajagopolan B. Forearm training partially reverses abnormal skeletal muscle metabolism responses during exercise in heart failure. J Am Coll Cardiol. 1992;19:161A. Abstract.
18. Kavanaugh T, Yacoub M, Mertens D, Kennedy J, Campbell R, Sawyer P. Cardiorespiratory responses to exercise training after orthotopic cardiac transplantation. Circulation. 1988;77:162-168.
19. Pope S, Stinson E, Daughters G, Schroeder J, Ingels N, Alderman E. Exercise response of the denervated heart in long term cardiac transplant recipients. Am J Cardiol. 1980;46:213-218.
20. Bussieres-Chafe L, Pflugfelder P, Menkis A, Novick R, McKenzie F, Taylor A, Kostuk W. Basis for the aerobic impairment during exercise in patients late post cardiac transplantation. J Am Coll Cardiol. 1993;21:433A. Abstract.
21. Stevenson L, Sietsma K, Tillisch J, Lem V, Walden J, Kobashigawa J, Moriguchi J. Exercise capacity for survivors of cardiac transplantation or sustained medical therapy for stable heart failure. Circulation. 1990;81:78-85.
22. Arnold DL, Matthews PM, Radda GK. Metabolic recovery after exercise and the assessment of mitochondrial function in vivo in human skeletal muscle by means of 31P NMR. Magn Reson Med. 1984;1:307-315.
23. Taylor DJ, Bore PJ, Styles P, Gadian DG, Radda GK. Bioenergetics of intact human muscle: a 31P nuclear magnetic resonance study. Mol Biol Med. 1983;1:77-94.
24. Taylor DJ, Styles P, Matthews PM, Arnold DA, Gadian DG, Bore P, Radda GK. Energetics of human muscle: exercise-induced ATP depletion. Magn Reson Med. 1986;3:44-54.
25. Arnold DL, Taylor DJ, Radda GK. Investigation of human mitochondrial myopathies by phosphorus magnetic resonance spectroscopy. Ann Neurol. 1985;18:189-196.
26. Taylor DJ, Bore PJ, Styles P, Gadian DG, Radda GK. Bioenergetics of intact human muscle: a 31P nuclear magnetic resonance study. Mol Biol Med. 1983;1:77-94.
27. Veech RL, Lawson JWR, Cornell NW, Krebs HA. Cytosolic phosphorylation potential. J Biol Chem. 1979;254:6538-6547.
28. Harris RC, Hultman E, Nordesjo LO. Glycogen, glycolytic intermediates and high energy phosphates determined in biopsy samples of musculus quadriceps femoris of man at rest: methods and variance of values. Scand J Clin Lab Invest. 1974;33:109-120.
29. Kemp GJ, Taylor DJ, Radda GK. Control of phosphocreatine resynthesis during recovery from exercise in human skeletal muscle. NMR Biomed. 1993;6:66-72.
30. Chance B, Leigh JS, Clark BJ, Maris J, Kent J, Nioka S, Smith D. Control of oxidative metabolism and oxygen delivery in human skeletal muscle: a steady state analysis of the work/energy cost transfer function. Proc Natl Acad Sci U S A. 1985;82:8384-8388.
31. Chance B, Williams GR. Respiratory enzymes in oxidative phosphorylation: the steady state. J Biol Chem. 1955;217:409-427.
32. Barnes P, Taylor D, Kemp G, Radda G. Skeletal muscle bioenergetics in the chronic fatigue syndrome. J Neurol Neurosurg Psychiatry. 1993;56:679-683.
33. Wiener DH, Maris J, Chance B, Wilson JR. Detection of skeletal muscle hypoperfusion during exercise using phosphorus-31 nuclear magnetic resonance spectroscopy. J Am Coll Cardiol. 1986;7: 793-799.
34. Sinoway L, Minotti J, Davis D, Pennock J, Burg J, Musch T, Zelis R. Delayed reversal of impaired vasodilation in congestive heart failure after heart transplantation. Am J Cardiol. 1988;61: 1076-1079.
35. Teo K, Yusuf S, Wittes J, Theodoropoulos S, Dhalla N, Aikenhead J, Yacoub M. Preserved left ventricular function during supine exercise in patients after orthotopic cardiac transplantation. Eur Heart J. 1992;12:321-329.
36. Fernandez-Sola J, Campistol J, Casademount J, Grau J, Urbano-Marquez A. Reversible cyclosporin myopathy. Lancet. 1990;335: 362-363. Letter.
37. Goy J, Stauffer S, Deruaz J. Myopathy as a possible side effect of cyclosporin. Lancet. 1989;1:446-447.
38. Arellano F, Krupp P. Muscular disorders associated with cyclosporin. Lancet. 1991;337:915. Letter.
39. Smith PF, Eydelloth RS, Grossman SJ, Stubbs RJ, Schwartz MS, Germershausen JI, Vyas KP, Kari PH, MacDonald JS. HMG-CoA reductase inhibitor-induced myopathy in the rat: cyclosporine A interaction and mechanism studies. J Pharmacol Exp Ther. 1991; 257:1225-1235.
40. Luscher TF, Yang Z, Diederich D, Buhler FR. Endothelium- dependent vascular responses: effect of hypertension and cyclosporin A. Z Kardiol. 1989;6:132-136.
41. Diederich D, Yang Z, Luscher T. Chronic cyclosporine therapy impairs endothelium-dependent relaxation in the renal artery of the rat. J Am Soc Nephrol. 1992;2:1291-1297.
42. Karch SB, Billingham ME. Cyclosporine induced myocardial fibrosis: a unique controlled case report. J Heart Transplant. 1985; 4:210-212.
43. Nayler WG, Gu XH, Casley DJ, Panagiotopoulos S, Liu J, Mottram PL. Cyclosporine increases endothelin-1 binding site density in cardiac cell membranes. Biochem Biophys Res Commun. 1989;163:1270-1274.
44. Paul L, ter Keurs M, Kingma I, ter Keurs H. Inotropic effects of cyclosporin in rat heart muscle. J Heart Lung Transplant. 1992;11: 336-341.
45. Ikeuchi M, Kida K, Goto Y, Matsuda H. In vivo and in vitro effects of cyclosporin A on glucose transport. Biochem Pharmacol. 1992; 43:1459-1463.
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Language: | English.
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Document Type: | Clinical Investigation and Reports.
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Journal Subset: | Clinical Medicine.
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ISSN: | 0009-7322
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NLM Journal Code: | daw, 0147763
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