Chronic obstructive pulmonary disease (COPD) is frequently accompanied by abnormalities of the pulmonary vasculature. This vasculopathy spans the spectrum from mild vascular dysfunction to pulmonary hypertension, which on rare occasions can be severe. Given the worldwide prevalence of COPD, it is conceivable that the morbidity and mortality associated with pulmonary vascular dysfunction have been vastly underappreciated, especially in countries and regions where the infrastructure and resources to define the magnitude of the problem are often limited.

Pulmonary hypertension in COPD patients and identifying accompanying factors in clinical decisions are very important. The current study aimed to determine the relationship between phenotypic and echocardiographic findings with the help of pulmonary artery pressure in patients with COPD. In this study, 100 COPD patients referred to a specialized clinic participated in the study.

This exploratory analysis assessed whether plasma biomarkers predict the response to switching from phosphodiesterase type 5 inhibitors (PDE5is) to the soluble guanylate cyclase stimulator riociguat in patients with pulmonary arterial hypertension. Selected biomarkers at baseline and their changes to Week 24 were evaluated in patients with and without a favorable response to riociguat in two trials: RESPITE, in which patients with an inadequate response to PDE5i were switched to riociguat; and REPLACE, in which patients at intermediate risk of 1-year mortality despite a PDE5i were randomized to remain on PDE5i or were switched to riociguat.

In 1976, my wife and I moved to Salt Lake City to start my fellowship in pulmonary and critical care medicine. The University of Utah program had applied principles of physiology to the care of critically ill patients; and that interested me. As a critical care fellow, I learned to perform pulmonary artery catheterization and to interpret hemodynamic measurements in patients with adult respiratory distress syndrome (ARDS).

The pathology of primary pulmonary hypertension was first described by Ernest Romberg in 1891 when he referred to histopathologic findings as pulmonary arterial sclerosis [1]. In the 1920s, Ayerza's Disease was described in a series of patients from Argentina with the proposed etiology being syphilis; this was subsequently disproven [2].

This serendipitous encounter, initially sparked by a single patient, began my profound and enduring interest in pulmonary vascular disease, particularly pulmonary hypertension. Learning from this, my career has been shaped, to a large extent, by clinical observation, translational research, and collaboration with peers, all driven by a curiosity to understand the complex mechanisms of pulmonary vascular disease. This journey underscores the value of curiosity-driven research, demonstrating how unexpected clinical encounters can profoundly influence a medical career, hopefully leading to advancements in understanding and treating pulmonary hypertension. You could easily say that pentazocine hooked me.

Acute lung injury (ALI) involves inflammatory cytokines and chemokines, resulting in lung and multiple organ injuries. This study explored the mechanism of mitophagy and cGAS/STING pathway in oleic acid (OA)-induced ALI. Mice and pulmonary microvascular endothelial cells were divided into four groups: control group (Con), ALI group, FUNDC1−/− control group (F-Con), and FUNDC1−/− ALI group (F-ALI). After 24 h of modeling, proceed with tissue collection. Lung tissues were stained using hematoxylin eosin.

My journey into studying nitric oxide (NO) bioavailability developed as I explored the role of nitrite ions. The traditional view that nitrite was merely an inactive byproduct of NO oxidation was a perspective I sought to challenge. As I continued my research at Papworth and Addenbrooke's Hospitals under Professor Higenbottam, I hypothesized that nitrite ions could be a source of NO bioactivity.

The article, “Survival Outcomes and Impact of Targeted PAH Therapy in Portopulmonary Hypertension in the PVRI GoDeep Meta-Registry” by Jose et al. addresses the controversial question on the survival benefit of PAH drugs in portopulmonary hypertension (PoPH) [1]. Treatment strategies in PoPH are often extrapolated from other PAH subtypes as PoPH have largely been excluded from large PAH drug randomized trials. In this context, the present study represents an important contribution to the management of PoPH.

Pfizer initiated their Phase III trial of sildenafil for the treatment of PAH (SUPER study), which later led to the publication of the results [4] and the approval of sildenafil (20 mg, three times a day) in 2006 for the management of PAH. This period marked a pivotal moment in the medical history of treating PAH. I witnessed firsthand how this development transformed the landscape of treatment options for patients suffering from this severe condition.