ArticleJournal of the American Heart Association2025
Right Ventricular Dysfunction in Lung Disease/Hypoxia-Associated Pulmonary Hypertension.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Hypoxia-injured pulmonary vascular targeting and microenvironment-responsive nanoparticle to treat hypoxic pulmonary hypertension.Journal of nanobiotechnology · 2026Article
- Burden of chronic obstructive pulmonary disease, related heart failure and risk factors among middle-aged and elderly patients, 1990-2050.Journal of thoracic disease · 2026Article
- Broiler Ascites Syndrome as a Potential Spontaneous Animal Model for Human Pulmonary Arterial Hypertension: A Narrative Review.Life (Basel, Switzerland) · 2026Review
- Right Ventricular Free Wall Strain in Healthy Lowlanders and Highlanders-A Case-Control Study.Journal of clinical medicine · 2026Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLimited data exist on right ventricular (RV) function in lung disease/hypoxia-associated pulmonary hypertension (PH). We aimed to clarify the presence, characteristics, and clinical significance of RV dysfunction in patients with lung disease/hypoxia-associated PH.
methodsWe analyzed data from 3 groups of patients: those with lung disease/hypoxia-associated PH, those without PH, and those with pulmonary arterial hypertension (PAH). RV volume was assessed using cardiac magnetic resonance imaging, and RV pressure data were obtained by right heart catheterization and analyzed using dedicated software and a single-beat method. We then evaluated RV contractility by end-systolic elastance (Ees), diastolic function by β and end-diastolic elastance, and RV-pulmonary artery coupling by Ees/arterial elastance.
resultsWe studied 68 patients with lung disease/hypoxia-associated PH, 40 without PH, and 93 with PAH. In the lung disease/hypoxia-associated PH group, Ees was sustained (0.46 [95% CI, 0.26-0.75] mm Hg/mL), whereas β (0.035 [95% CI, 0.022-0.049]) and end-diastolic elastance (0.19 [95% CI, 0.11-0.38] mm Hg/mL) were higher, and Ees/arterial elastance was lower (0.59 [95% CI, 0.27-0.79]) compared with the no-PH group. There were no differences in these values between the groups with lung disease/hypoxia-associated PH and PAH. Ees/arterial elastance was significantly correlated with the 6-minute walk distance and associated with mortality (hazard ratio, 0.18 [95% CI, 0.04-0.79]) in the group with PAH, but it was not in the group with lung disease/hypoxia-associated PH. Similarly, whereas the group with PAH showed improvement in β and Ees/arterial elastance with pulmonary vasodilator therapy, such improvement was not observed in the group with lung disease/hypoxia-associated PH.
conclusionsIn lung disease/hypoxia-associated PH, RV contractility is preserved, whereas diastolic function and RV-pulmonary artery coupling are impaired. Further investigation is needed to elucidate the distinct clinical relevance of RV dysfunction in lung disease/hypoxia-associated PH.
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