Real-Time Biventricular Pressure-Volume Loops During Percutaneous Pulmonary Valve Implantation in Patients With RVOT...

In patients with right ventricular (RV) outflow tract stenosis and pulmonary regurgitation (PR), percutaneous pulmonary valve implantation (PPVI) aims to preserve RV and left ventricular (LV) integrity and function. Our study aimed to assess acute changes in biventricular intrinsic myocardial function occurring with PPVI.

Twenty patients with RV outflow tract dysfunction (mean±1 SD; age, 23.0±10.9 years; mean peak echocardiographic RV outflow tract gradient, 64±25 mm Hg) underwent PPVI with biventricular assessment of pressure-volume loops using the conductance catheter technique during the same cardiac catheterization. Load-independent parameters of ventricular contractility (ventricular elastance) and ventricular compliance function, as well as pulmonary/systemic arterial elastance and ventriculoarterial coupling, were assessed before and directly after PPVI. Cardiac magnetic resonance for quantification of biventricular volumes, function, and PR was also performed.

After PPVI, both RV ventricular elastance (median [interquartile range], 0.26 [0.16-0.83] to 0.19 [0.13-0.42] mm Hg/mL per m²; P=0.029) and pulmonary systemic arterial elastance (0.32±0.20 to 0.25±0.19 mm Hg/mL per m²; P<0.001) decreased significantly, while right ventriculoarterial coupling (1.14±0.61 to 1.10±0.59; P=0.76) did not change statistically significant. LV ventricular elastance (1.31±0.93 to 1.23±0.72 mm Hg/mL per m²; P=0.68) and left ventriculoarterial coupling (0.75 [0.51-1.23] to 0.82 [0.53-1.10]; P=0.98) were not affected by PPVI although systemic arterial elastance increased significantly (0.83±0.26 to 0.90±0.34 mm Hg/mL per m²; P=0.032). Both RV (P=0.37) and LV (P=0.20) compliance showed no significant change after PPVI. Patients with relevant PR (≥25%; n=10) had lower RV ventricular elastance (P=0.043) before and higher LV compliance (P=0.010) after PPVI compared with patients with minor PR (<25%; n=10), whereas ventriculoarterial coupling was similar between the 2 groups.

Acute reduction of RV overload by PPVI is accompanied by an instantaneous decline in RV contractility with persistent and inefficient ventriculoarterial coupling. The LV adequately adapts to an increase in pre- and post-load with nonsignificant changes in LV intrinsic function and ventriculoarterial coupling. The relevance of these response patterns on long-term biventricular remodeling requires further investigation.