Eisenmenger syndrome (ES) represents an advanced stage of pulmonary arterial hypertension (PAH) associated with congenital heart disease. It is characterized by elevated pulmonary vascular resistance, with a right-to-left shunt and resting hypoxemia. ES is associated with high morbidity and mortality.
Portopulmonary hypertension (PoPH) is a subtype of pulmonary arterial hypertension (PAH) associated with portal hypertension, occurring in 2%–6% of cirrhotic patients. Although guidelines recommend routine echocardiography before transplantation, the prevalence, and outcomes of PAH-specific therapy in cirrhotic patients remain unclear.
Integrating routine mental health support in pulmonary hypertension care is not just a matter of efficiency but also of recognition, equity, and epistemic justice.
Schistosomiasis-associated pulmonary arterial hypertension (Sch-PAH) is one of the most frequent etiologies of pulmonary arterial hypertension in Brazil and globally. The disease is a complication of hepatosplenic schistosomiasis characterized by portal hypertension, egg deposition, and granuloma formation in the pulmonary arteries leading to inflammation, vascular remodeling, increased pulmonary vascular resistance, and progressive right heart failure.
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.
