4.1 Article Proceedings Paper

Cardiovascular effects of successful renal transplantation: A 30-month study on left ventricular morphology, systolic and diastolic functions

Journal

TRANSPLANTATION PROCEEDINGS
Volume 37, Issue 2, Pages 1039-1043

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.transproceed.2004.12.201

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The purpose of this study was to determine the effects of a successful renal transplantation on left ventricular (LV) morphology, systolic and diastolic function. Forty-three renal transplant patients prospectively studied by echocardiography (30 months follow-up) were divided into two groups. The first echocardiographic examination was performed 3.0 +/- 2.8 months after renal transplantation in group 1 (11 men, 12 women); and 34.4 +/- 29.1 months after transplant in group two (9 men, 11 women). We noticed the following changes in blood pressure (BP): group I systolic BP reduction (from 140.5 +/- 23.6 to 126 +/- 6.8 mm Hg; P < .01), and pulse pressure reduction (from 59.5 +/- 14.9 to 47.5 +/- 9.8 P < .05); group 2, diastolic BP acceleration (from 78.4 +/- 8.7 to 84 6.9 mm Hg, P < .05). LV mass index decreased in group I (from 126.4 +/- 18.0 g/m(2) to 104.6 +/- 15.9 g/m(2), p < .05). The incidence of LV hypertrophy (LVH) decreased in group 1 from 70% to 40% (P < .05). Only one parameter of systolic function-end systolic stress-significantly decreased in both groups: group I from 78 +/- 11 to 61 +/- 12 g/cm(2); group 2 from 63.8 +/- 9.0 to 55.1 +/- 9.0 g/cm(2), p < .05). The pattern of mitral inflow changed: in group 1, the normal pattern decreased from 30% to 20% and the restrictive pattern increased from 0% to 10%; in group 2, the normal mitral inflow pattern decreased from 60% to 20% and abnormal relaxation type increased from 40% to 80%. Regression of LVH after renal transplant improved LV geometry and systolic function. Despite better systolic function a progression of LV diastolic dysfunction was noticed, which might be explained by cyclosporine treatment. Renal transplantation exerted a beneficial impact on cardiomyopathy manifested by LVH and systolic dysfunction.

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