# Pulmonary arterial flow alterations in systemic lupus erythematosus on 4D flow CMR: a case-control study

**Authors:** Xin Chen, An Sun, Junxian Liao, Zhenhuan Wang, Xinyi Wan, Yi Xiao

PMC · DOI: 10.1186/s41747-026-00692-4 · 2026-03-04

## TL;DR

This study shows that 4D flow CMR can detect early blood flow changes in the lungs of SLE patients before pulmonary hypertension develops.

## Contribution

The study introduces 4D flow CMR as a noninvasive method to detect subclinical pulmonary hemodynamic changes in SLE patients.

## Key findings

- SLE patients showed lower wall shear stress in the main pulmonary artery compared to controls.
- Asymmetric flow redistribution was observed in SLE patients, with higher pressure in the left pulmonary artery.
- Pulmonary flow changes were linked to left atrial remodeling and diastolic dysfunction in SLE patients.

## Abstract

Pulmonary arterial hypertension is a severe complication of systemic lupus erythematosus (SLE). Current screening methods often miss early vascular changes. This study aimed to characterize subclinical pulmonary hemodynamic alterations in SLE patients without known pulmonary arterial hypertension using four-dimensional (4D) flow cardiovascular magnetic resonance (CMR) and to investigate their association with left ventricular diastolic function.

Twenty-five SLE patients without known pulmonary arterial hypertension and 25 age-matched healthy controls were enrolled. All participants underwent 3-T 4D flow CMR to quantify hemodynamic parameters, including wall shear stress (WSS), flow volume, and relative pressure in the pulmonary arteries. SLE patients were further stratified based on echocardiographic assessment of diastolic function to analyze hemodynamic coupling.

Compared to controls, SLE patients exhibited significantly lower maximum WSS in the main pulmonary artery (0.29 versus 0.33 Pa, p = 0.040) and asymmetric flow redistribution, characterized by higher relative pressure in the left pulmonary artery (0.54 versus 0.30 mmHg, p = 0.008) and increased flow rate in the right pulmonary artery (3.51 versus 2.90 L/min, p = 0.015). Qualitative analysis revealed vortical flow patterns in SLE patients. Subgroup analysis demonstrated that the reduction in WSS was primarily driven by patients with diastolic dysfunction (p = 0.006 versus controls).

SLE patients without pulmonary arterial hypertension exhibit distinct subclinical pulmonary hemodynamic alterations, including lower WSS and flow asymmetry. These alterations are intimately coupled with left ventricular diastolic dysfunction, suggesting that 4D flow CMR serves as a sensitive noninvasive tool for early risk stratification in this population.

4D flow CMR identifies subclinical pulmonary hemodynamic alterations coupled with diastolic dysfunction in SLE patients, serving as a sensitive noninvasive tool for early risk stratification before irreversible vascular remodeling occurs.

SLE patients without known pulmonary arterial hypertension show early pulmonary blood flow changes.4D flow CMR detected asymmetric pulmonary flow redistribution in SLE patients.SLE patients exhibited altered left atrial function despite normal ventricles.Pulmonary flow changes correlated with left atrial remodeling in SLE.4D flow CMR detects subclinical pulmonary hemodynamic differences in SLE.

SLE patients without known pulmonary arterial hypertension show early pulmonary blood flow changes.

4D flow CMR detected asymmetric pulmonary flow redistribution in SLE patients.

SLE patients exhibited altered left atrial function despite normal ventricles.

Pulmonary flow changes correlated with left atrial remodeling in SLE.

4D flow CMR detects subclinical pulmonary hemodynamic differences in SLE.

## Linked entities

- **Diseases:** systemic lupus erythematosus (MONDO:0007915), pulmonary arterial hypertension (MONDO:0015924)

## Full-text entities

- **Genes:** LPA (lipoprotein(a)) [NCBI Gene 4018] {aka AK38, APOA, LP}, RPA1 (replication protein A1) [NCBI Gene 6117] {aka HSSB, MST075, PFBMFT6, REPA1, RF-A, RP-A}
- **Diseases:** endothelial (MESH:D005642), LA (MESH:D059446), chronic (MESH:D002908), pulmonary hypertension (MESH:D006976), tricuspid regurgitation (MESH:D014262), heart failure (MESH:D006333), cardiac functional impairment (MESH:D006331), MPA (MESH:D003324), CMR (MESH:D002318), infections (MESH:D007239), chamber dilation (MESH:D002311), pulmonary vascular alterations (MESH:D057772), pulmonary artery (MESH:D000071079), connective tissue disease (MESH:D003240), hypertension (MESH:D006973), PAH (MESH:D000081029), smoker (MESH:C000719328), SLE (MESH:D008180), systemic sclerosis (MESH:D012595), LV diastolic dysfunction (MESH:D018487), arrhythmia (MESH:D001145), Function (MESH:D003291), ventricular stroke (MESH:D020521), vasculopathy (MESH:D000090122), valvular heart disease (MESH:D006349), pulmonary (MESH:D008171), inflammation (MESH:D007249), vasculitis (MESH:D014657), hyperlipidemia (MESH:D006949), myocardial fibrosis (MESH:D005355)
- **Chemicals:** gadolinium (MESH:D005682), LA (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12961025/full.md

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Source: https://tomesphere.com/paper/PMC12961025