ABC | Volume 114, Nº4, April 2020

Original Article Carrion et al. Right ventricular dysfunction and heart transplant Arq Bras Cardiol. 2020; 114(4):638-644 Table 2 – Cardiovascular structure and function Variables 0R/1R N = 155 2R N = 15 p-value Aortic diameter (mm) 33.0 ± 4.1 32.4 ± 5.7 0.575 Left atrial diameter (mm) 40.8 ± 5.6 42.5 ± 7.7 0.372 IS thickness (mm) 11.2 ± 1.4 11.5 ± 1.6 0.439 PW thickness (mm) 10.4 ± 1.4 11.3 ± 1.5 0.013 Relative wall thickness 0.49 ± 0.08 0.53 ± 0.08 0.115 LV end-diastolic diameter (mm) 42.4 ± 4.1 43.0 ± 2.7 0.550 LV end-systolic diameter (mm) 28.2 ± 4.4 28.3 ± 3.7 0.936 LV end-diastolic volume (mL) 88.2 ± 24.3 84.6 ± 18.0 0.593 LV end-systolic volume (mL) 35.7 ± 12.9 37.2 ± 12.9 0.618 RV basal diameter (mm) 40.2 ± 4.4 40.9 ± 2.9 0.550 RV end-diastolic area (cm 2 ) 20.2 ± 4.3 21.4 ± 3.8 0.302 RV end-systolic area (cm 2 ) 10.9 ± 3.1 12.8 ± 3.8 0.024 LV mass (g) 157.2 ± 33.9 173.9 ± 33.7 0.057 LV ejection fraction, Teichholz (%) 62.3 ± 7.9 63.2 ± 8.4 0.714 LV ejection fraction, Simpson (%) 59.6 ± 7.9 56.5 ± 8.6 0.122 TAPSE (mm) 13.8 ± 3.4 10.9 ± 2.2 0.009 RV fractional area change (cm/s) 46.2 ± 8.6 40.8 ± 10.2 0.016 E/A 1.56 ± 0.55 2.07 ± 0.82 0.017 Deceleration time (ms) 183.0 ± 41.8 158.2 ± 20.8 0.157 Medial e′ (cm/s) 7 ± 2 7 ± 2 0.653 Lateral e′ (cm/s) 12 ± 3 9 ± 2 0.100 Medial E/e′ 11.9 ± 4.4 20.6 ± 4.4 0.001 Lateral E/e′ 7.6 ± 3.5 13.3 ± 5.2 0.006 S wave (cm/s) 10.0 ± 2.1 8.3 ± 1.8 0.035 LV global longitudinal strain (%) −20.2 ± 3.3 −19.5 ± 3.3 0.351 Data are shown as mean ± SD. P-value calculated byANOVAadjusted for heart transplantation patients. E/A: early to late mitral inflow velocity ratio; e’: mitral relaxation velocity; E/e´: mitral inflow to mitral relaxation velocity ratio; IS: interventricular septal; LV: left ventricular; PW: posterior wall; RV: right ventricular; S wave: tricuspid lateral systolic velocity; TAPSE: tricuspid annular plane systolic excursion. by tissue Doppler imaging (TDI). Marciniak et al., 10 studying a group of 31 patients with 106 biopsy/echocardiogram pairs, demonstrated a decrease in strain and strain rate on TDI in basal and apical segments of the RV free wall and in basal and middle segments of the LV lateral wall in the group with ≥ 1B rejection, suggesting that these findings could be an additional tool for detecting acute rejection. The same authors also observed that, when histopathological involvement was mild (< 2B), these alterations took on a pattern of segmental involvement, with little or no impact on GLS, revealing a low sensitivity of the latter for low-grade rejection. 10 More recently, the advent of evaluation of regional or global myocardial function by speckle tracking has provided a more robust technique for the detection of subclinical myocardial dysfunction, overcoming the limitations of TDI-measured strain, especially the dependence on prospective acquisition and the angle of acquisition. 10,11 At least three studies, published almost concomitantly, showed a rejection-related decrease in LV GLS, 14-16 while another group, as in our study, found no such differences in LV GLS when comparing exams from patients with no rejection or mild rejection to patients with moderate rejection. 17 It bears stressing that, even in the 0R group of our study, LV GLS values exceeded the range reported as normal after HTx in the literature. 18,19 Evaluation of RV parameters as potential markers of subclinical rejection was relatively less explored in previous studies. Clemmensen et al. studied a group of 36 HTx recipients and found that TAPSE was reduced in the group with cellular rejection. 16 Another group, which studied a similar number of patients (n = 34), found a reduction in RV free wall strain associated with ≥ 2R rejection. 15 These findings were observed as a similar trend in our study, where the decrease in RV function was shown by TAPSE, S wave, FAC, and RV peak GLS in moderate rejection. Eleid et al. demonstrated a decline in LV GLS in the early post-HTx period, and the association of non-improvement in GLS throughout follow‑up was an independent predictor of worse prognosis for these patients, regardless of the histopathological results of endomyocardial biopsies. 20 642