Pulmonary arterial hypertension (PAH) is a rare and progressive disease characterized by remodeling of the pulmonary vasculature, which leads to increased pulmonary artery pressure and ultimately right ventricular failure. Although Japanese guidelines recommend combination therapy, real-world data show inconsistencies in its implementation.
Level 3 cardiopulmonary exercise testing (CPET) can unmask the dynamic burden of pulmonary vascular disease (PVD), while submaximal exercise testing offers a simpler, noninvasive alternative.
Abnormal pulmonary hemodynamics during exercise may persist even after balloon pulmonary angioplasty (BPA) for inoperable chronic thromboembolic pulmonary hypertension (CTEPH).
Idiopathic pulmonary arterial hypertension (IPAH) exhibits significant clinical heterogeneity, necessitating a precision medicine approach. This study aimed to identify distinct IPAH phenotypes using machine learning-based clustering and to evaluate their longitudinal therapeutic responses and long-term survival.
Despite major advances in antiretroviral treatment, pulmonary arterial hypertension (PAH) remains a common, severe complication in patients diagnosed with HIV.
Rheumatic heart disease (RHD) is frequently complicated by pulmonary hypertension (PH) and right ventricular (RV) dysfunction. However, the prognostic significance of invasive hemodynamic parameters obtained at index right heart catheterization (RHC) in adults with RHD and echocardiographic RV–pulmonary artery (PA) uncoupling remains incompletely defined.
Hereditary hemorrhagic telangiectasia (HHT) is an autosomal‑dominant vascular disease characterized by telangiectasias and visceral arteriovenous malformations (AVMs), commonly in the lungs, liver, and brain.
This study aimed to investigate the therapeutic effects of Poncirin on hypoxic pulmonary hypertension (HPH) and to elucidate the underlying mechanism, with a specific focus on transactive response DNA-binding protein 43 (TDP43)-mediated macrophage pyroptosis.
Mechanosensitive cation channels expressed in pulmonary arterial smooth muscle (SMC) and endothelial (EC) cells contribute to the regulation of vasoconstriction and vasodilation of the pulmonary vasculature.
Poverty and social deprivation have been associated with impaired clinical outcomes and survival in several chronic diseases. The association between poverty and clinical outcomes in patients with pulmonary arterial hypertension (PAH) remains unclear.
