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 Dij
on 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 measur
ement of mean pulmonary artery and pulmonary capillary pressures and pulmon
ary arteriolar resistances. During left heart catheterisation, cardiac outp
ut, mean aortic pressure, the ejection fraction, the dp/dt max of the left
ventricular wall, systemic arterial resistances and left ventricular end di
astolic pressures were measured. At each catheter study, the indexed myocar
dial mass, indexed end systolic and end diastolic left ventricular volumes,
the mass/volume ratio, the residual serum ciclosporine concentrations and
the serum creatinine were analysed. In addition, an endomyocardial biopsy w
as also performed.
Initially raised, the mean pulmonary artery and pulmonary capillary pressur
es 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 resistanc
es underwent the same changes.
The left heart parameters remained constant over the period of follow-up bu
t with a heart rate, mean aortic pressure and left ventricular end diastoli
c pressure higher than normal. The indexed myocardial mass was increased at
all periods. The indexed left ventricular end systolic and diastolic volum
es decreased with a M/V ratio which increased. Ciclosporine concentrations
decreased whereas serum creatinine increased. The frequency of severe rejec
tion and of coronary atherosclerosis was low. Significant correlations were
observed between different parameters at different periods. In the long-te
rm, the function of the transplanted heart is not normal in the strict sens
e of the term. The apparent normality is obtained by anti-hypertensive trea
tment. The transplanted heart adapts to the increase in ciclosporine-induce
d afterload by permanent myocardial hypertrophy, and increased diastolic pr
essure probably relates to diastolic dysfunction without noticeable intraca