Hemodynamic Implications of Sildenafil in Candidates for Heart Transplantation with Group 2 Pulmonary Hypertension: A Single Latin-American Center Registry

Purpose

Heart failure is the most common cause of Group 2 pulmonary hypertension (PH). When it becomes fixed, it increases morbidity and mortality in heart transplantation (HTx). Reversing this situation is difficult, but the use of selective pulmonary vasodilators such as sildenafil could be a simple pharmacological tool in this setting.

Objectives

To analyze the prevalence of PH and the effect of Sildenafil in HTx candidates and its impact on mortality.

Methods

Patients who had undergone HTx over a ten-year period were analyzed retrospectively. PH was defined as mean pulmonary artery pressure (PAP) ≥25mmHg and/or pulmonary vascular resistance (PVR) > 3UW. Among the P with PH those who received sildenafil (Group A) and those who did not (Group B) were compared. Quantitative variables were compared with t-test or Mann-Whitney, and nominals with Fisher's test. Survival was analyzed using the log-rank test. A p<0.05 was considered significant

Results

From 01/2008 to 12/2018, 294 P undergone HTx, 30 P (10%) with combined transplantation, pediatric, re-transplantation, and without data, were excluded. Of the 217 P analyzed, 153 P (70%) presented PH, of whom 77P (51%) received sildenafil. Baseline characteristics are described in Table 1a. The causes for which 76 P (49%) with PH did not receive treatment with sildenafil were: intolerance to vasodilators, treatment with vasopressors, pulmonary congestion, and a tendency to reserve selective pulmonary vasodilators for those patients under previous treatment with ACEIs, ARAII or ARNI. Table 1b describes the hemodynamic variables for both groups. Table 1a shows a decrease in MPAP, transpulmonary gradient, and PVR without changes in cardiac index in Group A. There was no difference in mortality between both groups (graphic 1)

Conclusion

The use of Sildenafil in P with Group 2 PH could be an effective strategy to improve the hemodynamic profile during the candidacy for HTx, without impact on survival.