Exercise capacity in heart transplant recipients: Relation to impaired endothelium-dependent vasodilation of the peripheral microcirculation - 09/09/11
Abstract |
Objectives The aim of this study was to examine the responses to endothelium-dependent and -independent vasodilators on the peripheral microcirculation in heart transplant recipients in relation to exercise capacity compared with that in healthy controls.
Background Impaired endothelium-dependent vasodilation of the microcirculation may play an important role in the limitation of exercise capacity after heart transplantation.
Methods Microvascular perfusion responses to four graded levels of iontophoretically applied 1% acetylcholine (endothelium-dependent vasodilator) and 1% sodium nitroprusside (SNP) (endothelium-independent) in the forearm skin of 42 transplant recipients and 16 age-matched controls were determined by laser Doppler perfusion measurements. Maximal exercise capacity was assessed by peak oxygen uptake (peak Vo 2) during progressive, symptom-limited, upright bicycle exercise.
Results With similar baseline perfusion levels in transplant recipients and controls (4.2 ± 0.4 vs 4.6 ± 0.6 arbitrary units [AU]), the increases in perfusion to acetylcholine, but not to SNP, were significantly attenuated in the transplant recipients:7.0 ± 1.0 vs 11.0 ± 2.0, 12.7 ± 1.5 vs 21.0 ± 2.8, 21.0 ± 1.9 vs 32.7 ± 2.4, and 28.0 ± 1.6 vs 39.2 ± 2.4 AU, respectively(all p < 0.01). Peak Vo 2 was significantly lower in the transplant recipients (22.4 ± 1.0 vs 38.0 ± 2.9 ml/kg/min; p < 0.01).Furthermore, acetylcholine responses of the transplant recipients correlated closely to their peak Vo 2, irrespective of level of application (r = 0.63; p < 0.001, all four acetylcholine responses taken together), whereas no such correlation was found for SNP responses. In the control group, no relation was observed in acetylcholine/SNP responses to peak Vo 2.
Conclusions Exercise limitation in transplant recipients appears strongly associated with attenuated endothelium-dependent vasodilation of the peripheral microcirculation. (Am Heart J 1998;136:320-8.)
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From the aDepartment of Cardiology, Rikshospitalet, and the bDepartment of Surgery, Ullevå l Hospital, University of Oslo. |
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Reprint requests: Arne K. Andreassen, MD, Medical Department B, Rikshospitalet, 0027 Oslo, Norway. |
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4/1/89731 |
Vol 136 - N° 2
P. 320-328 - août 1998 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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