We read with great interest the recent article on patient-specific hemodynamic modeling to estimate microvascular disease burden and predict response to pulmonary endarterectomy (PEA) in chronic thromboembolic pulmonary hypertension (CTEPH) [1]. The integration of multiscale structure-based modeling with routine clinical data addresses the key challenges of quantifying distal microvascular remodeling and anticipating heterogeneous hemodynamic responses after technically successful PEA.
In this Living Legends in PH session, Rubin Tuder reflects on a career that has shaped modern pulmonary hypertension research. He discusses key scientific advances, including the Sugen–hypoxia rat model, and shares personal insights on discovery, mentorship, and the evolution of the PH field, joined by Paul Hassoun and Jason Hong.
Assessing operability in late-presenting ventricular septal defects (VSD) with pulmonary arterial hypertension (PAH) is complex. Although a comprehensive assessment is often recommended, pulmonary vascular resistance index (PVRI) is the cornerstone of most decisions
In 1980, while working as a pediatric resident in the newborn intensive care unit of a University-affiliated hospital, I was called urgently to the delivery room. The attending obstetrician had delivered a full-term infant without complications just minutes before my arrival.
Transition from parenteral prostanoids to oral selexipag may be considered in select patients with pulmonary arterial hypertension (PAH) to reduce the therapeutic burden imposed on patients and caregivers, but its safety and efficacy remain uncertain.
Pulmonary hypertension (PH) significantly impacts outcomes in heart failure with preserved ejection fraction (HFpEF), especially with right ventricular dysfunction (RVD), yet effective treatments are limited. This study retrospectively evaluated sacubitril-valsartan's effects on pulmonary pressures, RV function, and clinical outcomes in 20 severe HFpEF-PH patients.
Pulmonary arterial hypertension (PAH) is a pulmonary disease associated with alterations in gut microbiota. We aimed to identify potential diagnostic genes causally associated with gut microbiota and PAH.
In the recent paper, Pulmonary Vascular Compromise is Associated with Survival in Pediatric Pulmonary Hypertension: a New Computational Model by Niccum et al. [1] presents an innovative computational model reframing pulmonary vascular disease through the concept of pulmonary vascular compromise (PVC), a quantifiable estimate of the proportion of pulmonary vascular surface area lost relative to an idealized normal pulmonary vascular capacity.
Pulmonary arterial hypertension (PAH) is a life-threatening condition with no cure, making research into its underlying mechanisms critical. The platelet-derived growth factor (PDGF) signaling pathway plays a crucial role in vascular remodeling, a key factor in PAH progression.
Pulmonary Arterial Hypertension (PAH) is a rare, chronic and progressive disease affecting the heart and lungs. Endothelin receptor antagonist (ERA) + phosphodiesterase type 5 inhibitor (PDE5i) treatment is recommended for all PAH patients.
