# Residual physiological abnormalities after pulmonary endarterectomy and balloon pulmonary angioplasty in CTEPH

**Authors:** Rita Calé, Filipa Ferreira, Mariana Martinho, Sofia Alegria, Débora Repolho, Ana Rita Pereira, João Luz, Tiago Lobão, Patrícia Araújo, Sílvia Vitorino, Hélder Pereira, Daniel Caldeira, R. Widmer, R. Widmer, R. Widmer, R. Widmer

PMC · DOI: 10.1371/journal.pone.0344192 · 2026-03-06

## TL;DR

This study finds that while surgeries for pulmonary hypertension improve resting heart function, exercise performance and quality of life remain limited long-term.

## Contribution

The study provides new insights into long-term physiological recovery after pulmonary endarterectomy and balloon pulmonary angioplasty in CTEPH patients.

## Key findings

- Both BPA and PEA significantly reduce mean pulmonary arterial pressure and vascular resistance at long-term follow-up.
- Persistent exercise pulmonary vascular abnormalities remain despite improvements in resting hemodynamics.
- Physical quality of life remains impaired long-term after both procedures.

## Abstract

Pulmonary endarterectomy (PEA) is the first-line treatment for chronic thromboembolic pulmonary hypertension (CTEPH), while balloon pulmonary angioplasty (BPA) is an established alternative for inoperable patients. Although both interventions improve resting pulmonary hemodynamics, the extent of long-term physiological recovery during exercise and the persistence of functional limitations remain incompletely characterized.

Prospective single-center registry (2017–2023) including 14 patients completing BPA (71 sessions) and 15 undergoing PEA, with median follow-up of 50 months (IQR 36–61). Clinical assessment included resting hemodynamics, invasive exercise right heart catheterization to derive the exercise slope of the mean pulmonary arterial pressure to cardiac output relashionship (mPAP/CO slope), and health-related quality of life (HRQOL) evaluated using the SF-36 questionnaire. Analyses were descriptive and focused on within-pathway changes over time.

Both BPA and PEA significantly reduced mPAP (44.8 ± 12.4 → 26.1 ± 9.3 mmHg; 42.1 ± 12.9 → 22.6 ± 5.4 mmHg, both p < 0.001) and pulmonary vascular resistance (9.8 ± 4.6 → 3.0 ± 1.3 WU; 9.0 ± 5.4 → 2.9 ± 1.9 WU, both p < 0.001) at long term follow-up. Despite sustained improvements in resting hemodynamics, abnormal exercise pulmonary vascular responses persisted, with mean mPAP/CO slopes of 7.0 ± 5.6 mmHg/L/min after BPA and 4.0 ± 2.3 mmHg/L/min after PEA. Physical HRQOL remained impaired at long-term follow-up, with Physical Component Summary (PCS) scores below population norms in both pathways (44.4 ± 12.7 after BPA and 44.5 ± 7.3 after PEA).

BPA and PEA provide durable improvements in resting pulmonary hemodynamics; however, incomplete physiological recovery is common, with persistent exercise abnormalities and reduced physical quality of life at long-term follow-up.

## Linked entities

- **Diseases:** chronic thromboembolic pulmonary hypertension (MONDO:0013024), pulmonary hypertension (MONDO:0005149)

## Full-text entities

- **Diseases:** dermatitis (MESH:D003872), COPD (MESH:D029424), hemoptysis (MESH:D006469), contrast nephropathy (MESH:D005119), small-vessel disease (MESH:D059345), stenoses (MESH:D003251), CTEPH (MESH:D011655), BP (MESH:D010146), quality (MESH:D012893), pulmonar injury (MESH:D014947), ventricular overload (MESH:D019190), cancer (MESH:D009369), PEA (MESH:D008171), pulmonary vascular disease (MESH:D014652), physiological abnormalities (MESH:D012735), chronic thromboembolic disease (MESH:D013923), RHC (MESH:D006333), Pulmonary Hypertension (MESH:D006976), exercise abnormalities (MESH:D000092202), left heart involvement (MESH:D018636), venous thromboembolism (MESH:D054556), webs (MESH:C563636), death (MESH:D003643), occlusions (MESH:D001157), BPA (MESH:D054549), hypothermia (MESH:D007035), thrombotic (MESH:D013927), pulmonary vascular and microvascular dysfunction (MESH:D002561), vascular injury (MESH:D057772), mPAP (MESH:D000071079), vascular remodelling (MESH:D066253), intimal thickening (MESH:D013585), cardiac output (MESH:D002303)
- **Chemicals:** oxygen (MESH:D010100), BPA (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12965537/full.md

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Source: https://tomesphere.com/paper/PMC12965537