Myocardial mechanisms causing heart failure early after cardiac transplantation

Early after heart transplantation, some patients have heart failure (HF) with preserved left ventricular ejection fraction (LVEF), in the absence of rejection. The purpose of this study was to define the mechanisms causing HF early after transplantation and to determine whether these mechanisms involve changes that occur in active or passive myocardial properties. Eleven consecutive patients 1 week after heart transplantation underwent right heart catheterization and echocardiography with an endomyocardial biopsy. Hemodynamic measurements were obtained at spontaneous heart rate, and then were repeated at three atrially paced rates increased in 20-bpm increments above spontaneous heart rate. At baseline, 5 patients (group 1) had clinical HF and a pulmonary capillary wedge pressure (PCWP) > or = 16 mmHg, and 6 patients (group 2) had no clinical evidence of HF and a PCWP < 16 mmHg. LVEF was normal in all 11 patients. The relationships between cardiac index versus heart rate (HR) and PCWP versus HR were normal in all 11 patients. These normal function-versus-frequency relationships suggested that there were no significant abnormalities in the active myocardial processes of contraction or relaxation. In group 1 patients, the PCWP was significantly increased but the left ventricular end diastolic dimension was normal, suggestive of diastolic stiffness. Early after transplantation, there was a significant increase in LV wall thickness in group 1 patients as compared with preexplantation values despite myocardial biopsies in all 11 patients, showing no evidence of rejection, cardiomyocyte hypertrophy, or interstitial fibrosis thus suggestive of myocardial edema.