Effect of donor-recipient size mismatch on left ventricular remodeling after pediatric orthotopic heart transplantation

Left ventricular (LV) hypertrophy has been reported after orthotopic heart transplantation. This study was designed to determine the pattern of LV remodeling in the first year after pediatric orthotopic heart transplantation and to elucidate the mechanism responsible for changes in LV dimensions. Serial echocardiograms of 20 children who underwent cardiac transplantation were analyzed off-line, and the following LV parameters were measured and indexed to body surface area (BSA): short-axis diameters, posterior wall thickness, length, mass, and volume in systole and diastole. Mass/ volume and short-axis diameter/length ratios and ejection fraction were calculated. In 5 patients, the donorʹs echocardiogram was also available for analysis. The patientʹs systemic blood pressure at the time of the echocardiogram, ischemic time of the donor heart, number of rejection episodes, biopsy scores, and body size of the donor and patient were recorded. Patients were assigned to 2 groups based on their donor-recipient weight ratio: group 1, ≤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 transplantation (72 ± 24 vs 133 ± 37 g/BSA1.5, p = 0.0008). LV volume, geometry, ejection fraction, systemic blood pressure, and number of rejection episodes did not differ significantly between groups. The excess LV mass index in group 2 regressed significantly during the first year after transplantation from 133 ± 37 to 93 ± 17 g/BSA1.5 (p < 0.005). Similarly, LV mass/volume ratio decreased from 2.4 ± 0.9 to 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 = 0.86, p < 0.0001). This correlation persisted at 6 months after transplantation (r = 0.72, p = 0.0015), but was not present at 12 months. The initial LV mass in group 2 was significantly smaller when indexed to the donorʹs BSA (Z score = 2.0 ± 1.8 SD) than when indexed to the recipientʹs BSA (Z score = 6.9 ± 3.3 SD, p = 0.0008). There was no significant difference between LV mass measured in the donor before transplantation and the mass measured in the recipient 2 weeks after transplantation. These results indicate that increased LV mass found immediately after transplantation can largely be accounted for by donor-recipient size mismatch. In patients with LV hypertrophy, the left ventricle remodels during the first year after transplantation, with regression of excess mass and a decrease in mass/volume ratio toward the normal range.