Balloon pulmonary angioplasty improves right ventricular-pulmonary arterial coupling during exercise in patients with chronic thromboembolic pulmonary disease without pulmonary hypertension

Background Symptomatic chronic thromboembolic pulmonary disease (CTEPD) without pulmonary hypertension is a clinical indication for mechanical reperfusion therapy such as pulmonary endarterectomy or balloon pulmonary angioplasty (BPA) (1). Although clinical benefit may be achieved, the effect of BPA on dynamic right ventricular (RV) function and interaction with pulmonary artery (PA) during exercise remains unclear. Purpose To investigate the therapeutic impact of BPA on RV-PA coupling, which serves as a critical indicator of RV compensatory function against afterload, using exercise cardiac magnetic resonance imaging (exCMR) and exercise right heart catheterisation (exRHC). Methods Five symptomatic chronic thromboembolic pulmonary disease without pulmonary hypertension patients underwent exCMR and exRHC at rest and 40% of peak workload (determined by cardiopulmonary exercise testing) before and after BPA. MRI data were analysed using CVI42 software to obtain RV end-diastolic volume (RVEDV) and end-systolic volume (RVESV). RV stroke volume (RVSV) was defined as the difference between RVEDV and RVESV. RV pressure-volume loops were analyzed via the single-beat method (Figure A) (2). End-systolic elastance (Ees), representing load-independent RV contractility, was calculated as Ees = (Piso - Pes) / RVSV, where Piso was derived using sine curve fitting and Pes was estimated using a formula derived from the mean pulmonary arterial pressure (mPAP) (3). Effective arterial elastance (Ea) was defined to evaluate the interaction between the ventricle and the pulmonary arterial system. Data are presented as mean ± SD. Statistical analysis was performed using two-way repeated-measures ANOVA with Tukey’s post-hoc tests. Results Mean age was 71 ± 10 years (3 females, 2 males). Resting mPAP was unchanged after BPA (18.4 ± 3.8 to 18.4 ± 2.8 mmHg, p=0.307), while pulmonary vascular resistance tended to decrease (3.1 ± 1.6 to 2.2 ± 0.8 Wood units, p=0.066) with no change in cardiac index (2.7 ± 0.4 to 2.6 ± 0.3 L/min/m2, p=0.236) by exRHC. Peak oxygen uptake increased (16.1 ± 1.2 to 17.2 ± 1.8 mL/min/kg, p=0.013) and ventilatory efficiency (VE/VCO2 slope) tended to improve (42.3 ± 15.1 to 37.5 ± 5.5, p=0.057). ExCMR demonstrated the heart rate increased during exercise (Figure C). Exercise increased Ees in both before and after BPA (p=0.578, Figure D). Meanwhile, the exercise-induced increase in Ea was significantly attenuated after BPA (p=0.034, Figure E). Consequently, while RV-PA coupling (Ees/Ea) at rest remained unchanged, exercise-induced decline in Ees/Ea before BPA was not significant anymore after BPA (Figure F). Conclusion In symptomatic CTEPD without pulmonary hypertension, BPA preserves RV-PA coupling during exercise by suppressing the exercise-induced increase in Ea. These findings suggest that BPA improves exercise haemodynamics and RV functional reserve even when resting pulmonary pressure is normal.