Key result
Persistent pulmonary hypertension after valve replacement is linked to increased pulmonary arterial stiffness and wall thickness.
Why the study?
Pulmonary hypertension regression is often incomplete after successful left-sided valve replacement, and proximal pulmonary arterial wall disease may be involved in persistent pulmonary hypertension, affecting right ventricular to pulmonary arterial coupling.
Does proximal pulmonary arterial wall disease contribute to persistent pulmonary hypertension and RV-PA coupling impairment after successful left-sided valve replacement?
Cross-Sectional (n=25)
No
Does proximal pulmonary arterial wall disease contribute to persistent pulmonary hypertension and RV-PA coupling impairment after successful left-sided valve replacement?
Proximal pulmonary arterial remodeling is present in patients with persistent PH after left-sided valve replacement, contributing to RV-PA uncoupling even in isolated post-capillary PH.
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Proximal PA remodeling may contribute to persistent PH and RV uncoupling post-valve replacement; leaves open therapeutic targeting of wall stiffness.
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.
Domingo et al. (2018) conducted a cross-sectional in Persistent pulmonary hypertension after successful left-sided valve replacement (n=25). Persistent pulmonary hypertension after left-sided valve replacement vs. Control individuals without apparent cardiopulmonary disease was evaluated on Proximal pulmonary arterial stiffness (elastic modulus) and relative area wall thickness (p=<0.05). Patients with persistent pulmonary hypertension after successful left-sided valve replacement had significantly increased proximal pulmonary arterial stiffness and wall thickness compared to controls.