Pulmonary arterial hypertension (PAH) is estimated to affect between 10 and 50 people per million worldwide. The lack of cure and devastating nature of the disease means that treatment is crucial to arrest rapid clinical worsening. Current therapies are limited by their focus on inhibiting residual vasoconstriction rather than targeting key regulators of the cellular pathology. Potential disease-modifying therapies may come from research directed towards causal pathways involved in the cellular and molecular mechanisms of disease. It is widely acknowledged that targeting reduced expression of the critical bone morphogenetic protein type-2 receptor and its associated signalling pathways is a compelling therapeutic avenue to explore. In this review, we highlight the advances that have been made in understanding this pathway and the therapeutics that are being tested in clinical trials and the clinic to treat PAH.
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http://dx.doi.org/10.1093/cvr/cvaa350 | DOI Listing |
J Invasive Cardiol
January 2025
Department of Echocardiography, Wuhan Asia Heart Hospital Affiliated to Wuhan University of Science and Technology. No.753 Jinghan Road, Hankou District, Wuhan, China. Email:
Heart Fail Rev
January 2025
Division of Cardiovascular Medicine, University of Utah Health & School of Medicine, 30 N Mario Capecchi Drive, HELIX Building 3rd Floor, Salt Lake City, UT, 84112, USA.
Right heart catheterization (RHC) provides critical hemodynamic insights by measuring atrial, ventricular, and pulmonary artery pressures, as well as cardiac output (CO). Although the use of RHC has decreased, its application has been linked to improved outcomes. Advanced hemodynamic markers such as cardiac power output (CPO), aortic pulsatility index (API), pulmonary artery pulsatility index (PAPi), right atrial pressure to pulmonary capillary wedge pressure ratio (RAP/PCWP) and right ventricular stroke work index (RVSWI) have been introduced to enhance risk stratification in cardiogenic shock (CS) and end-stage heart failure (HF) patients.
View Article and Find Full Text PDFAnn Intensive Care
January 2025
Department of Intensive Care, CHIREC Hospitals, Université Libre de Bruxelles, Brussels, Belgium.
J Thorac Cardiovasc Surg
January 2025
Coronary Center, Department of Thoracic and Cardiovascular Surgery, Miller Family Heart, Vascular, & Thoracic Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address:
JMIR Form Res
January 2025
Department of Anesthesiology and Perioperative Medicine, The First Affiliated Hospital of Nanjing Medical University, No. 300 Guangzhou Road, Nanjing, 210029, China, 86 2568303569.
Background: Ventricular fibrillation (VF) is a vicious arrhythmia usually generated after removal of the aortic cross-clamp (ACC) in patients undergoing open-heart surgery, which could damage cardiomyocytes, especially in patients with left ventricular hypertrophy (LVH). Amiodarone has the prominent properties of converting VF and restoring sinus rhythm. However, few studies concentrated on the effect of amiodarone before ACC release on reducing VF in patients with LVH.
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