Proximal pulmonary arterial wall disease in patients with persistent pulmonary hypertension after successful left-sided valve replacement according to the hemodynamic phenotype

Abstract

Regression of pulmonary hypertension (PH) is often incomplete after successful left-sided valve replacement (LSVR). Proximal pulmonary arterial (PPA) wall disease can be involved in patients with persistent-PH after LSVR, affecting the right ventricular to pulmonary arterial (RV-PA) coupling. Fifteen patients underwent successful LSVR at least one year ago presenting PH by echo (> 50 mmHg). Prosthesis-patient mismatch and left ventricular dysfunction were discarded. All patients underwent hemodynamic and intravascular ultrasound (IVUS) study. We estimated PPA stiffness (elastic modulus [EM]) and the relative area wall thickness (AWT). Acute vasoreactivity was assessed by inhaled nitric oxide (iNO) testing. RV-PA coupling was estimated by the tricuspid annular plane systolic excursion to systolic pulmonary arterial pressure ratio. Patients were classified as isolated post-capillary PH (Ipc-PH; pulmonary vascular resistance [PVR] ≤ 3 WU and/or diastolic pulmonary gradient [DPG] < 7 mmHg) and combined post- and pre-capillary PH (Cpc-PH; PVR > 3 WU and DPG ≥ 7 mmHg). Both Ipc-PH and Cpc-PH showed a significant increase of EM and AWT. Despite normal PVR and DPG, Ipc-PH had a significant decrease in pulmonary arterial capacitance and RV-PA coupling impairment. Cpc-PH had worse PA stiffness and RV-PA coupling to Ipc-PH ( P < 0.05). iNO decreased RV afterload, improving the cardiac index and stroke volume only in Cpc-PH ( P < 0.05). Patients with persistent PH after successful LSVR have PPA wall disease and RV-PA coupling impairment beyond the hemodynamic phenotype. Cpc-PH is responsive to iNO, having the worse PA stiffness and RV-PA coupling. The PPA remodeling could be an early event in the natural history of PH associated with left heart disease.

Keywords: inhaled nitric oxide; left-sided valve replacement; pulmonary arterial wall; pulmonary hypertension; right ventricular to pulmonary arterial coupling.

Fig. 1.

Scatter plot of transpulmonary pressure gradient, diastolic pulmonary gradient, pulmonary vascular resistance, and pulmonary arterial compliance with elastic modulus.

Fig. 2.

Changes in hemodynamic parameters and elastic modulus after inhaled nitric oxide (iNO) in combined post-capillary and pre-capillary pulmonary hypertension (Cpc-PH) and isolated post-capillary pulmonary hypertension (Ipc-PH) patients. mPAP, mean pulmonary arterial pressure; PA compliance, pulmonary arterial compliance; TPR, total pulmonary resistance. *P < 0.05 Ipc-PH vs. Cpc-PH within the same state; ^&P < 0.05 baseline vs. iNO within the same group.

Fig. 3.

Correlations between absolute changes in hemodynamic parameters and elastic modulus (EM) after iNO and baseline EM. Cpc-PH/Ipc-PH, combined pre and post-capillary/isolated post-capillary pulmonary hypertension; mPAP/pPAP, mean/pulsatile pulmonary arterial pressure; PAC, pulmonary arterial compliance; SV, stroke volume; TPR, total pulmonary resistance. Delta is computed as after NO minus before NO administration (baseline) values. *P < 0.05 Ipc-PH vs. Cpc-PH.

Fig. 4.

Correlation and concordance rate between the percentage of change after iNO of mean pulmonary arterial pressure (mPAP) and elastic modulus (EM). Gray area: area of data exclusion.