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.
Pulmonary hypertension (PH) is a frequent complication of interstitial lung diseases (ILD) that worsens morbidity and mortality. Cigarette smoking has a detrimental effect on transplant-free survival of patients with ILD, including patients with idiopathic pulmonary fibrosis (IPF).
Iron deficiency aggravates hypoxic pulmonary vasoconstriction, exacerbating the increase of pulmonary arterial pressure at high altitude (HA). This may be especially relevant for patients with pulmonary hypertension (PH) travelling to HA, who moreover have a high prevalence of iron deficiency.
Pulmonary arterial hypertension (PAH) is a disease of abnormal pulmonary vascular remodeling and vascular obliteration that results in right heart failure and death. PAH pathogenesis is strongly associated with mutations of the Transforming Growth Factor Beta (TGF-β) superfamily signaling pathway, which has previously been challenging to target therapeutically.
Pulmonary hypertension (PH) is a chronic and devastating disease that currently lacks effective therapies, often ultimately requiring lung transplantation. Pulmonary vascular cells are subjected to various mechanical forces, which contribute to cardiovascular remodeling in PH.
