RESUMO
BACKGROUND: Right ventricular (RV) dysfunction remains one of the most prominent complications during the period immediately after heart transplantation (HT); however, late adaptation of the RV has not been well described. The aim of our study was to evaluate RV function and remodeling using magnetic resonance imaging (MRI) and to correlate it with exercise capacity and also with hemodynamic data obtained before HT. METHODS: We prospectively evaluated RV function of 25 heart-transplanted patients, without cardiac allograft vasculopathy, who were documented by negative dobutamine stress echocardiography during late follow-up (Group 1, 6 +/- 4.3 years) using MRI. We then compared Group 1 with a control group consisting of 10 patients, who were < or =1 year post-HT (Group 2), hemodynamically stable, and with the same pre-operative hemodynamic features as Group 1. Their pulmonary arterial systolic blood pressure (PSBP) varied from 17 to 67 mm Hg (43.2 +/- 15.3) and pulmonary vascular resistance (PVR) from 1.0 to 5.4 Wood units (2.5 +/- 1.12). The following parameters were studied: RV end-diastolic volume (EDV) and systolic volume (ESV); stroke volume (SV); ejection fraction (EF); and mass (M). We also evaluated the VO2 peak and slope VE/VCO2 values during a treadmill test. Data were analyzed and correlated with the hemodynamic values of PVR and PSBP obtained pre-HT. RESULTS: In Group 1, treadmill evaluation data showed exercise VO2 peak (19.9 +/- 3.19 ml/kg/min) and slope VE/VCO2 (36.9 +/- 4.5) values comparable to those of sedentary individuals; RV variables according to MRI were within normal ranges, with the following mean values for Groups 1 and 2, respectively: RVEDV, 99.6 +/- 4.0 ml vs 127 +/- 16 ml (p = 0.03); RVESV, 42 +/- 2 ml vs 58.5 +/- 9 ml (p = 0.01); RVSV, 57 +/- 3 ml vs 71 +/- 10 ml (p = 0.1); RVEF, 58 +/- 1.4% vs 54 +/- 3.8% (p = 0.29); and RVM, 43.4 +/- 1.9 g vs 74 +/- 8.8 g (p = 0.001). There was no correlation between hemodynamic pulmonary values before HT or any other index of late RV performance, including RV remodeling and hypertrophy, in our study population (p = not significant). CONCLUSIONS: In contrast to what we would expect for heart transplant patients at late follow-up, the RV may adapt to pulmonary pressure and resistance, with reverse remodeling characterized by volume and mass reduction, leading to normalization of RV function despite abnormal hemodynamic pulmonary values being measured before HT. There was no influence on the low exercise capacity observed in these patients, in the absence of cardiac allograft vasculopathy.
