“Why is there more variation in the females? Could it be due to their estrous cycle?” This was the question my co-mentor, Dr. Irina Petrache, posed when I shared the first data I generated as a first-year research fellow. It was 2007, and was in the lab of cardiothoracic surgeon Dr. Dan Meldrum at Indiana University. 

This study quantified prior authorization (PA)—insurance-required approval—burden for pediatric pulmonary hypertension (PH) at an accredited center. Among 53 patients, 72% of 283 prescriptions between 2021 and 2023 required PA, with non-FDA-approved medications showing highest volume.

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.

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.