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[Long-term hemodynamic function of the transplanted heart].

The aim of this study was to identify the long-term haemodynamic changes of the transplanted heart. Between 1987 and 1997, 136 patients required cardiac transplantation at Dijon hospital. During follow-up, 76 patients aged 51.2 +/- 9.46 years underwent catheter studies (12 women, 15.8%; and 64 men, 84.2%). Right and left heart catheterisation was performed at 3 months, 1, 2, 3 and 5 years after transplantation. Right heart catheterisation included measurement of mean pulmonary artery and pulmonary capillary pressures and pulmonary arteriolar resistances. During left heart catheterisation, cardiac output, mean aortic pressure, the ejection fraction, the dp/dt max of the left ventricular wall, systemic arterial resistances and left ventricular end diastolic pressures were measured. At each catheter study, the indexed myocardial mass, indexed end systolic and end diastolic left ventricular volumes, the mass/volume ratio, the residual serum cyclosporine concentrations and the serum creatinine were analysed. In addition, an endomyocardial biopsy was also performed. Initially raised, the mean pulmonary artery and pulmonary capillary pressures decrease from the 3rd month to the 2nd year. From the 3rd year onwards, they readjust to the upper limits of normal. The pulmonary artery resistances underwent the same changes. The left heart parameters remained constant over the period of follow-up but with a heart rate, mean aortic pressure and left ventricular end diastolic pressure higher than normal. The indexed myocardial mass was increased at all periods. The indexed left ventricular end systolic and diastolic volumes decreased with a M/V ratio which increased. Cyclosporine concentrations decreased whereas serum creatinine increased. The frequency of severe rejection and of coronary atherosclerosis was low. Significant correlations were observed between different parameters at different periods. In the long-term, the function of the transplanted heart is not normal in the strict sense of the term. The apparent normality is obtained by anti-hypertensive treatment. The transplanted heart adapts to the increase in cyclosporine-induced afterload by permanent myocardial hypertrophy, and increased diastolic pressure probably relates to diastolic dysfunction without noticeable intracardiac fibrosis.