EFFECT OF DONOR-RECIPIENT SIZE MISMATCH ON LEFT-VENTRICULAR REMODELING AFTER PEDIATRIC ORTHOTOPIC HEART-TRANSPLANTATION

Left ventricular (LV) hypertrophy has been reported after orthotopic h eart transplantation. This study was designed to determine the pattern of LV remodeling in the first year after pediatric orthotopic heart t rans; plantation and to elucidate the mechanism responsible for change s in LV dimensions. Serial echocardiograms of 20 children who underwen t cardiac transplantation were analyzed off-line, and the following LV parameters were measured and indexed to body surface area (BSA): shor t-axis diameters, posterior wall thickness, length, mass, and volume i n systole and diastole. Mass/volume and short-axis diameter/length rat ios and ejection fraction were calculated. In 5 patients, the donor's echocardiogram was also available for analysis. The patient's systemic blood pressure at the time of the echocardiogram, ischemic time of th e donor heart, number of rejection episodes, biopsy scores, and body s ize of the donor and patient were recorded. patients were assigned to 2 groups based on their donor-recipient weight ratio: group 1, less th an or equal to 1.2 (n = 9); and group 2, >1.2 (n = 11). In group 1, LV mass index remained within normal limits throughout the study period. In group 2, mass index was significantly increased 2 weeks after tran splantation (72 +/- 24 vs 133 +/- 37 g/BSA(1.5), p = 0.0008). LV volum e, geometry, ejection fraction, systemic blood pressure, and number of rejection episodes did not differ significantly between groups. The e xcess LV mass index in group 2 regressed significantly during the firs t year after transplantation from 133 +/- 37 to 93 +/- 17 g/BSA(1.5) ( p<0.005). Similarly, LV mass/volume ratio decreased from 2.4 +/- 0.9 t o 1.5 +/- 0.4 (p<0.02). The degree of initial LV hypertrophy in group 2 correlated with the degree of donor-recipient size mismatch (r = 0.8 6, p<0.0001). This correlation persisted at 6 months after transplanta tion (r = 0.72, p = 0.0015), but wets not present at 12 months. The in itial LV mass in group 2 was significantly smaller when indexed to the donor's BSA (Z score = 2.0 +/- 1.8 SD) than when indexed to the recip ient's BSA (Z score = 6.9 +/- 3.3 SD, p = 0.0008). There was no signif icant difference between LV mass measured in the donor before transpla ntation and the mass measured in the recipient 2 weeks after transplan tation. These results indicate that increased LV mass found immediatel y after transplantation can largely be accounted for by donor-recipien t size mismatch. In patients with LV hypertrophy, the left ventricle r emodels during the first year after transplantation, with regression o f excess mass and a decrease in mass/volume ratio toward the normal ra nge.