We read with great interest the comments by Teruhiko Imamura on our study.1
A pulmonary capillary wedge pressure ≤ 15mmHg was found to be a reliable indicator of normal left ventricular (LV) filling pressure and is a reference value in clinical guidelines to diagnose postcapillary pulmonary hypertension and to guide prognosis and management in selected patients with heart failure. Other authors have considered higher cutoff values of pulmonary capillary wedge pressure to define a normal LV filling pressure in patients with chronic heart failure treated with a left ventricular assist device (LVAD). However, there is currently no evidence that a different cutoff value could better predict prognosis in these patients.
Regarding the involvement of right ventricular (RV) failure in patients with incomplete LV unloading, our results add to accumulating evidence underlining the impact of RV failure after LVAD on LV hemodynamics and supports the evidence of the strong interaction between the left and right filling pressures that occur during long-term LVAD support. Regarding our methods to evaluate RV function, we used the echocardiographic variables that are commonly employed in clinical practice, including RV dimensions, tricuspid annular plane systolic excursion, and tricuspid regurgitation. We agree that the new evidence addressed by our study, regarding the association between LV unloading and RV hemodynamics, merits further investigation with specific echocardiographic methods to evaluate RV function.
Due to our limited cohort, we evaluated a small number of variables in the multivariable analysis, including age. Brain natriuretic peptide emerged as an independent factor for LV unloading. Although we cannot rule out the influence of renal failure and obesity in the predictive value of brain natriuretic peptide, the mean creatinine (1.3mg/dL) and body mass index (26kg/m2) were only mildly elevated.
Ours was a noninterventional clinical study and we did not perform right-heart catheterization with the intention to optimize LVAD rotor speed setting or medication if patients were otherwise clinically stable. Therefore, the events would not be affected by the timing of the day 0 that we chose. We considered that global surveillance from the time of LVAD implantation was of greater clinical interest for survival analysis. In this line, our study cannot address the question of whether changes in medications or rotor speed setting based on right-heart catheterization might impact hemodynamics. Although worse hemodynamics after LVAD seem to be associated with more adverse events, there is still a clear knowledge gap regarding the clinical implications of a strategy guided by hemodynamics on quality of life and event-free survival in clinically stable patients.
FUNDINGNone.
CONFLICTS OF INTERESTThe author has no conflicts of interests to declare regarding this manuscript.