Endothelial Function Correlates With Pulmonary Pressures in Subjects With Clinically Suspected Pulmonary Hypertension.

Impaired pulmonary circulation hemodynamics are characteristic of pulmonary hypertension (PH). We therefore sought to evaluate possible correlations between endothelial function noninvasively assessed by brachial artery flow-mediated dilation (FMD) and hemodynamic parameters at right-sided cardiac catheterization in patients with clinically suspected PH. Consecutive outpatients with suspected PH were enrolled in the study. In all patients, endothelial function was assessed by FMD and hemodynamic parameters (pulmonary artery pressure [PAP]); pulmonary vascular resistances [PVR]) were derived by right-sided cardiac catheterization. For this study, 95 consecutive patients with suspected PH were enrolled (mean age 63 ± 13 years, 58% male) and included in the analysis. FMD values were significantly correlated with systolic (s)PAP levels (r = -0.29, p = 0.016); correlation with PVR was of borderline significance (r = -0.21, p = 0.78). After multivariable regression analysis including age, gender, tricuspid annular plane systolic excursion and peak tricuspid regurgitation velocity (peak TRV), and FMD, the latter remained significantly correlated with systolic pulmonary artery pressure (sPAP) values (B = -47, p = 0.02). After classifying patients according to median levels of peak TRV and FMD into 3 groups (neither, either, or both impaired), progressively increased levels of sPAP, mean PAP, and PVR were found (p for trend <0.001 in all cases). FMD values were inversely related to sPAP levels in a small population of patients with clinically suspected PH. In combination with peak TRV levels, FMD values noninvasively assessed were predictive of increased sPAP, mean PAP, and PVR.

Circulating Biomarkers in Pulmonary Arterial Hypertension: An Update.

Pulmonary arterial hypertension (PAH) is a rare subtype of group 1 pulmonary hypertension (PH) diseases, characterized by high pulmonary artery pressure leading to right ventricular dysfunction and potential life-threatening consequences. PAH involves complex mechanisms: vasoconstriction, vascular remodeling, endothelial dysfunction, inflammation, oxidative stress, fibrosis, RV remodeling, cellular hypoxia, metabolic imbalance, and thrombosis. These mechanisms are mediated by several pathways, involving molecules like nitric oxide and prostacyclin. PAH diagnosis requires clinical evaluation and right heart catheterization, confirming a value of mPAP ≥ 20 mmHg at rest and often elevated pulmonary vascular resistance (PVR). Even if an early and accurate diagnosis is crucial, PAH still lacks effective biomarkers to assist in its diagnosis and prognosis. Biomarkers could contribute to arousing clinical suspicion and serve for prognosis prediction, risk stratification, and dynamic monitoring in patients with PAH. The aim of the present review is to report the main novelties on new possible biomarkers for the diagnosis, prognosis, and treatment monitoring of PAH.

Endothelial Function in Pulmonary Arterial Hypertension: From Bench to Bedside.

Pulmonary arterial hypertension is a complex pathology whose etiology is still not completely well clarified. The pathogenesis of pulmonary arterial hypertension involves different molecular mechanisms, with endothelial dysfunction playing a central role in disease progression. Both individual genetic predispositions and environmental factors seem to contribute to its onset. To further understand the complex relationship between endothelial and pulmonary hypertension and try to contribute to the development of future therapies, we report a comprehensive and updated review on endothelial function in pulmonary arterial hypertension.