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TOPLINE
In patients with mild pulmonary hypertension (PH), neither mean pulmonary artery pressure (mPAP) nor pulmonary vascular resistance (PVR) predicted mortality risks, whereas measures reflecting pulmonary artery stiffness and right-ventricular adaptation had independent prognostic value.
METHODOLOGY
- Researchers analyzed data from an international meta-registry to evaluate the prognostic relevance of measures of right ventricular afterload and adaptation in patients with mild PH and across the full spectrum of PH.
- They included 16,910 incident treatment‑naive adults with PH (median age, 65 years; 59% women) using data entered up to January 2026.
- Mild PH was defined as mPAP greater than 20 mm Hg and less than 25 mm Hg, with pulmonary vascular resistance of three Wood units or less. Overall, 1095 patients met this definition.
- Researchers used baseline right‑heart catheterization data to derive pulmonary artery compliance, arterial elastance, and stroke volume index, and evaluated these against all‑cause mortality with adjustment for clinical confounders.
- Outcomes were compared with conventional measures (mPAP and PVR). The median follow‑up duration was 24 months.
TAKEAWAY
- mPAP and PVR did not predict mortality in patients with mild PH.
- In patients with mild PH, the risk for mortality was higher in those with arterial elastance > 0.36 mmHg/mL (adjusted hazard ratio [aHR], 1.49), in those with stroke volume index ≤ 31 mL/m2 (aHR, 1.28), and in those with higher heart rate (aHR, 1.24; P < .05 for all) even after adjusting for total pulmonary resistance.
- In the full PH cohort, arterial elastance and stroke volume index remained significant independent of PVR and total pulmonary resistance; pulmonary artery compliance remained significant independent of PVR alone.
- The findings remained consistent across etiological subgroups.
IN PRACTICE
"Complementing resistance-based metrics with variables that more comprehensively capture the interdependence of pulsatile load and RV [right-ventricular] performance may be especially relevant for hemodynamic phenotyping of so-called mild PH patients, whereas reliance on PVR alone may lead to systematic underestimation of the hemodynamic burden and risk profile in this patient population," the authors wrote.
SOURCE
The study was led by Athiththan Yogeswaran, MD, Universities of Giessen and Marburg Lung Center, Member of the German Center for Lung Research, in Giessen, Germany. It was published online on August 26 in Chest.
LIMITATIONS
The study was retrospective and may have introduced bias. Some data were missing and required imputation. The study lacked an external prospective validation cohort, which may have limited the generalizability of the results.
DISCLOSURES
The study received funding from the Pulmonary Vascular Research Institute and the Cardiovascular Medical Research and Education Fund, the National Institutes of Health. Several authors reported receiving research grants, trial funding, non‑financial support, travel support, and honoraria from various companies. Several authors reported receiving personal fees for consulting or advisory roles, and some disclosed having patent interests or planned patents. One author reported serving as a director, officer, and shareholder of two companies and another held equity in a company. Detailed disclosures are available in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
