Right ventricle (RV) dysfunction is central to pulmonary arterial hypertension (PAH) yet its molecular mechanisms remain unclear. This study aimed to identify biomarkers and therapeutic targets for RV remodeling in PAH.
Patients with chronic thromboembolic pulmonary disease (CTEPD) without resting pulmonary hypertension (PH) frequently experience dyspnea which is not explained by stationary assessment and therefore requires cardiopulmonary exercise testing for further diagnostic insight.
Twelve patients with severe pulmonary hypertension (PH) who had a pulmonary artery-to-descending aorta (Potts) shunt were treated with the novel PH drug sotatercept for an average of 12 months.
Pulmonary arterial hypertension (PAH) is characterized by excessive pulmonary vasoconstriction and vascular remodelling, with mutations in bone morphogenetic protein receptor type 2 (BMPR2) being the most common genetic alteration associated with the disease.
Accurate measurement of cardiopulmonary hemodynamics and exercise capacity is vital for PAH diagnosis and management. Terminal digit bias in clinical measures introduces non-differential error.
Pediatric idiopathic pulmonary arterial hypertension (IPAH) refractory to maximal medical therapy is associated with high morbidity and mortality, and therapeutic options remain limited.
Pulmonary hypertension (PH) is widely recognized as a disease driven by both vasoconstriction and vascular remodeling. Vasoconstriction is thought to play a predominant role in the early stages of PH, whereas the contribution of vascular remodeling increases as the disease progresses. However, clinical or histological evidence of this pathological progression has not been reported.
