There is a need for objective, continuous and remote assessment of exercise capacity in patients with pulmonary arterial hypertension (PAH). Using data from the TRACE study, in which 108 adult patients with PAH were continuously monitored with a wrist-worn accelerometer, we evaluated whether actigraphy can facilitate continuous monitoring of exercise capacity. 

Patients with congenital heart disease-related pulmonary arterial hypertension (CHD-PAH) often require regular follow-up through invasive right heart catheterization (RHC) to assess disease progression and potential interventions. 

Artificial intelligence-based cardiac motion mapping offers predictive insights into pulmonary hypertension (PH) disease progression and its impact on the heart. We proposed an automated deep learning pipeline for bi-ventricular segmentation and 3D wall motion analysis in PH rodent models for bridging the clinical developments. 

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare complication of pulmonary embolism, characterized by the presence of organized fibro-thrombotic material that partially or fully obstructs the lumen of large pulmonary arteries, microvasculopathy, and enlargement of the bronchial systemic vessels. The precise mechanisms underlying CTEPH remain unclear. However, defective angiogenesis and altered pulmonary arterial endothelial cell (PAEC) function may contribute to disease progression. 

Combined post- and precapillary pulmonary hypertension (CpcPH) comprises the most severe form of postcapillary PH. A severe precapillary component (pulmonary vascular resistance [PVR] > 5 WU) is critical for therapeutic decisions. Current treatment guidelines focus on optimizing underlying cardiac disease, while there are conflicting data regarding the efficacy and safety of pulmonary arterial hypertension (PAH) drugs in selected patients. 

Substantial evidence from animal models supports the concept of inhibiting peripheral serotonin synthesis for the treatment of pulmonary arterial hypertension (PAH), as demonstrated by pharmacological blockade or genetic deletion of tryptophan hydroxylase 1 (TPH1) [1-5]. Most recently, we have shown that daily inhalation of TPT-004, a novel class TPH1 inhibitor, can alleviate PAH in the Sugen-hypoxia (SuHx) rat model [1]. 

Phenotypic transition of pulmonary artery smooth muscle cells (PASMCs) under hypoxic conditions, which in turn causes increased proliferation and migration capacity, is an important pathological process in Hypoxic pulmonary hypertension (HPH). Although research on the phenotypic transition of PASMCs has been ongoing, little is known about the specific molecular mechanisms underlying this process.

Activin-A is elevated in pulmonary arterial hypertension (PAH) patients, and reportedly suppresses BMPR-II. This suggests one mechanism of action for PAH drug, sotatercept, an activin-ligand trap. However, we were unable to confirm that activin-A reduces BMPR-II in pulmonary endothelial cells. Thus, it seems unlikely that sotatercept influences BMPR-II or PAH via this mechanism.

The 2025 PVRI International Conference was held in Rio de Janeiro, Brazil under the theme “Embracing Heterogeneity” over 4 days of insightful discussions on pulmonary hypertension (PH). The conference covered a diverse array of topics spanning basic science, translational research, and clinical observations from around the world. Attendees included experts from backgrounds ranging from early-career investigators to senior scientists and clinicians and industry partners, representing 25 countries across 5 continents.

Fibrosing mediastinitis (FM) can block pulmonary vessels and airways, hindering treatment efficacy. Pulmonary artery (PA) stenting might provide a solution in such cases. This study involved 30 patients who had 49 PA stenting procedures for FM. Data on baseline characteristics, CT pulmonary angiography images, stent patency, and hemodynamics were collected.