TY - JOUR
T1 - Lack of progressive 'restrictive' physiology after heart transplantation despite intervening episodes of allograft rejection
T2 - Comparison of serial rest and exercise hemodynamics one and two years after transplantation
AU - Hosenpud, J. D.
AU - Pantely, G. A.
AU - Morton, M. J.
AU - Wilson, R. A.
AU - Norman, D. J.
AU - Cobanoglu, A. M.
AU - Starr, A.
PY - 1990
Y1 - 1990
N2 - It has been suggested that the cardiac allograft becomes less compliant either because of repeated episodes of rejection, chronic hypertension, or as a direct consequence of immunosuppression. A corollary to this hypothesis is that this reduction in compliance should be a progressive, rather than a static, change. To test this hypothesis, rest and exercise filling pressures, cardiac outputs, and radionuclide ventriculographic systolic and diastolic indices were measured in 20 patients at 1 and 2 years after heart transplant by means of identical protocols at both study times. Between studies 10 of 20 patients had no rejection, five of 20 had one rejection episode, and five of 20 had more than one rejection episode. There were no significant differences in resting or exercise heart rates, pulmonary wedge pressures, cardiac outputs, left or right ventricular ejection fractions, left ventricular peak filling rates, or time to peak filling between the studies at 1 and 2 years. Only resting right atrial pressure increased between year 1 and year 2 (6 ± 2 mm Hg vs 8 ± 4 mm Hg, p = 0.035). These data demonstrate that cardiac allograft function is unchanged between 1 and 2 years after transplantation, despite episodes of intervening rejection and continued immunosuppression. The data further suggest that the previously reported decrease in cardiac allograft compliance does not appear to be caused by a progressive intrinsic abnormality in the allograft, and that other mechanisms for 'restrictive' allograft physiology should be sought.
AB - It has been suggested that the cardiac allograft becomes less compliant either because of repeated episodes of rejection, chronic hypertension, or as a direct consequence of immunosuppression. A corollary to this hypothesis is that this reduction in compliance should be a progressive, rather than a static, change. To test this hypothesis, rest and exercise filling pressures, cardiac outputs, and radionuclide ventriculographic systolic and diastolic indices were measured in 20 patients at 1 and 2 years after heart transplant by means of identical protocols at both study times. Between studies 10 of 20 patients had no rejection, five of 20 had one rejection episode, and five of 20 had more than one rejection episode. There were no significant differences in resting or exercise heart rates, pulmonary wedge pressures, cardiac outputs, left or right ventricular ejection fractions, left ventricular peak filling rates, or time to peak filling between the studies at 1 and 2 years. Only resting right atrial pressure increased between year 1 and year 2 (6 ± 2 mm Hg vs 8 ± 4 mm Hg, p = 0.035). These data demonstrate that cardiac allograft function is unchanged between 1 and 2 years after transplantation, despite episodes of intervening rejection and continued immunosuppression. The data further suggest that the previously reported decrease in cardiac allograft compliance does not appear to be caused by a progressive intrinsic abnormality in the allograft, and that other mechanisms for 'restrictive' allograft physiology should be sought.
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M3 - Article
C2 - 2319369
AN - SCOPUS:0025278526
SN - 0887-2570
VL - 9
SP - 119
EP - 123
JO - Journal of Heart Transplantation
JF - Journal of Heart Transplantation
IS - 2
ER -