Single-center pilot study suggests a threefold increase in self-reported history of adverse pregnancy outcomes (APO) among women with subsequent diagnosis of pulmonary arterial hypertension (PAH). Females with PAH and a history of APO were younger and had higher mean pulmonary artery pressures at diagnosis compared to those without a history of APO.

Pulmonary arterial hypertension (PAH) requires lifelong medication, with patients taking an average of 12 tablets/day. Several chronic diseases can be treated with a fixed-dose combination (FDC) tablet, decreasing patient pill burden and increasing adherence.

Part of the Hypoxia in pulmonary vascular research – altitude and beyond webinar series

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.