The role of early right ventricular maladaptation to its load in adult heart transplant recipients

J. M. Mentzel (Hannover)1, A. Görler (Hannover)2, S. Soltani (Hannover)3, B. Schmack (Essen)4, J. D. Schmitto (Hannover)2, A. Ruhparwar (Hannover)2, J. Bauersachs (Hannover)3, D. Berliner (Hannover)3, A. M. Jakstaite (Hannover)3
1Hannover Medical School Department of Cardiology and Angiology Hannover, Deutschland; 2Medizinische Hochschule Hannover Klinik für Herz-, Thorax-, Transplantations- und Gefäßchirurgie, OE 6217 Hannover, Deutschland; 3Medizinische Hochschule Hannover Kardiologie und Angiologie Hannover, Deutschland; 4Universitätsmedizin Essen Klinik für Thorax- und Kardiovaskuläre Chirurgie Essen, Deutschland

Background: Right ventricular (RV)–pulmonary artery (PA) coupling has emerged as a load-adjusted marker of intrinsic RV contractility, yet its role and prognostic significance in heart transplant recipients remain poorly understood. This study aims to analyze RV–PA coupling and its association with post-transplant outcomes. We hypothesize that maladaptive RV, demonstrated as RV–PA uncoupling, is associated with reduced survival in heart transplant recipients.

Methods: We retrospectively analyzed RV–PA coupling in heart transplant recipients from our center who underwent transplantation between 2012 and 2023. Early RV–PA coupling after transplantation was assessed using fractional area change adjusted for systolic pulmonary artery pressure (FAC/PASP), estimated from baseline transthoracic echocardiographic examinations performed within the first four weeks after transplantation. The composite endpoint was all-cause mortality.

Results: 80 heart transplant recipients were included in the study (median age 51 years, 75% male). Over a median follow-up period of 74 months (IQR 42–102), 15 patients (18.8%) died. There were no significant differences in comorbidity burden between survivors and non-survivors. Non-survivors exhibited higher pulmonary pressures pre-transplant (mean pulmonary arterial pressure (mPAP) 34 mmHg (IQR 25-37) vs. 21 mmHg (IQR 15-29), p=0.015, pulmonary arterial wedge pressure (PAWP) 25 mmHg (IQR 17-27) vs. 13 mmHg (IQR 8-20), p=0.012). The median FAC/PASP value of 1.20 (IQR 0.92–1.72) was used to define RV–PA uncoupling and stratify the study population. Patients exhibiting RV–PA uncoupling had worse RV function (tricuspid annular plane systolic excursion (TAPSE) 14±3 mm vs.18±3 mm, p=0.001, RV free wall strain (RVFWS) 14.7±5.1 % vs. 19.9±3.0 %, p<0.001) and higher post-transplant RV afterload, as reflected by echocardiography-estimated PASP (33 mmHg (IQR 30-40) vs. 25 mmHg (IQR 22-30), p<0.001). There were no differences in pre-transplant precapillary pressures (pulmonary vascular resistance (PVR) 1.78±0.75 WU vs. 1.75±0.84 WU, transpulmonary pressure gradient 8.9±3.1 mmHg vs. 8.4±4.1 mmHg, both p>0.05) between the patient cohorts with and without RV–PA uncoupling after transplantation. When analyzing the prognostic value of RV-PA uncoupling, FAC/PASP-defined RV–PA uncoupling was not predictive of outcomes in the Kaplan–Meier analysis (log-rank: p=0.596).

Conclusion: FAC/PASP-defined early RV–PA uncoupling was not prognostic in patients after heart transplantation. Our findings suggest that early RV–PA uncoupling possibly reflects temporary RV impairment rather than a prognostic marker in heart transplant recipients.