In 567 PH-COPD patients from the PVRI GoDeep Meta-Registry, ACE inhibitor use was associated with improved survival only in severe PH (PVR > 5 WU), supporting prospective trials targeting this high-risk subgroup.
The authors of “The Pulmonary Hypertension Global Patient Survey: Physical and Psychosocial Impacts on Health-Related Quality of Life,” along with the participants who bravely shared their experiences, are to be commended for this important contribution to the field.
Chronic thromboembolic pulmonary hypertension (CTEPH) is a distinct and potentially curable form of pulmonary hypertension; however, a substantial proportion of patients remain inoperable or experience persistent or recurrent disease. Pharmacological therapies targeting the nitric oxide–soluble guanylate cyclase–cyclic guanosine monophosphate (NO–sGC–cGMP) pathway have emerged as promising treatment options.
Previous studies have shown that red blood cell distribution width (RDW) is an independent risk factor for the prognosis of pulmonary arterial hypertension (PAH) and is also associated with cardiovascular events in patients with congenital heart disease (CHD). However, its role in patients with CHD-associated pulmonary hypertension (PAH-CHD) has not been reported.
Pulmonary hypertension (PH) is a condition characterized by elevated mean pulmonary arterial pressure confirmed by right heart catheterization. PH involves both structural and functional changes in the pulmonary vascular bed.
Diagnosing pulmonary hypertension (PH) requires invasive right heart catheterization (RHC). However, mean pulmonary artery pressure (mPAP) can be non-invasively estimated using 4D analysis of cardiovascular magnetic resonance (CMR) flow imaging to assess the duration of pathological vortex flow (Tvortex) in the main pulmonary artery (MPA).
Right heart failure is due to both right atrial and right ventricular dysfunction. While the two chambers are distinct, the proteomic response to pressure overload is undefined.
Methamphetamine-associated pulmonary arterial hypertension (Meth-APAH) is an increasingly recognized cause of pulmonary arterial hypertension (PAH) and is associated with worse outcomes than idiopathic PAH (IPAH).
To elucidate the complex pathophysiology of chronic thromboembolic pulmonary hypertension (CTEPH), a disease associated with bilateral fibrotic obstructions of the pulmonary arteries (PA) and microvascular changes, research relies on animal models, which often depend on invasive techniques, including open surgery.
Pulmonary hypertension (PH) and right ventricular (RV) dysfunction increase mortality in multivessel pediatric pulmonary vein stenosis (PVS). Pulmonary vasodilator use is limited in PVS due to the perceived risk of pulmonary edema. We aimed to describe our experience with pulmonary vasodilators in PVS and to assess changes in RV function and hemodynamics over time.
