Total anomalous pulmonary venous connection (TAPVC) is a rare but life-threatening congenital heart defect that requires surgical correction. The sutureless technique has been developed as an alternative to conventional repair to minimize postoperative complications.

The typical pathology of pulmonary hypertension (PH) is characterized by pulmonary vasoconstriction and irreversible pulmonary vascular remodeling. Vascular remodeling is the process of structural changes and cellular rearrangement of blood vessels due to injury and is a significant factor in conditions such as PH.

There is a limited understanding of how pulmonary hypertension (PH) patients are managed worldwide. The Pulmonary Vascular Research Institute (PVRI) Innovative Drug Discovery Initiative (IDDI) global survey attempted to obtain insights into access to PH care in diverse international regions to pave future action plans. Responses from 151 centers (19.9% from Europe, 3.9% Middle East, 6% South Asia, 17.9% East Asia, 2% Sub-Saharan Africa, 31.8% Latin America, and 18.5% North America) were received. 

Chronic thromboembolic pulmonary hypertension (CTEPH) is due to unresolved pulmonary embolism (PE), however the pathophysiology of how PE evolves into CTEPH is unclear. Study of populations of acute PE patients at increased risk for CTEPH, such as those with prior splenectomy, may clarify the mechanisms driving transition from acute PE to CTEPH. 

I graduated from the University of Hamburg Faculty of Medicine in 1972. In 1973, as a second-year resident in Internal Medicine at the University Hospital in Hamburg-Eppendorf, I experienced a night on call that remains vivid in my memory.

This study evaluates the utility of CT-derived PA/A and RV/LV ratios in distinguishing surgically accessible CTEPH from acute PE and negative controls. Unlike the RV/LV ratio, PA/A ratio was significantly higher in CTEPH patients compared to low and intermediate/high-risk acute PE cohorts, indicating its utility as a marker of clot chronicity.

Schistosomiasis and sickle cell disease (SCD) both cause pulmonary hypertension (PH). We identified a subject with sickle cell trait and hepatosplenic schistosomiasis, who on right heart catheterization had PH, but due to high cardiac output. In a pre-clinical model, we found SCD mice were protected from developing schistosomiasis-induced PH.

In patients with pulmonary arterial hypertension (PAH), limited real-world data are available on persistence to oral treprostinil therapy, particularly while transitioning from parenteral prostacyclins. 

An on-demand recording of PVRI’s December PH Community Call, featuring informal discussion on emerging science and patient-focused research in pulmonary hypertension. The session covers new insights into hypoxic PH mechanisms and exercise interventions in PAH, with expert-led moderation and open exchange.

The establishment of the pulmonary hypertension center in Giessen, initiated in the late 1980s and further developed over the following decades by the founding team of Friedrich Grimminger, Ardeschir Ghofrani, Ralph Schermuly, and myself, has its roots in research projects on acute lung injury, ARDS. Employing the multiple gas elimination technique (MIGET), we observed severe ventilation/perfusion (V/Q) mismatch with high shunt in the ARDS lungs, accompanied by elevated pulmonary artery pressure levels.