4D flow CMR identified that systemic lupus erythematosus patients without pulmonary arterial hypertension had significantly lower main pulmonary artery maximum wall shear stress (0.29 vs 0.33 Pa, p=0.040), higher left pulmonary artery relative pressure (0.54 vs 0.30 mmHg, p=0.008), and increased right pulmonary artery flow rate (3.51 vs 2.90 L/min, p=0.015) compared to healthy controls.
Cross-Sectional (n=50)
No
Does 4D flow CMR detect subclinical pulmonary hemodynamic alterations in SLE patients without known PAH compared to healthy controls?
4D flow CMR identifies subclinical pulmonary hemodynamic alterations, such as reduced wall shear stress and asymmetric flow, in SLE patients without PAH, which are coupled with left ventricular diastolic dysfunction.
Effect estimate: p = 0.040 (WSS in MPA)
Absolute Event Rate: 0.29% vs 0.33%
p-value: p=0.040
Abstract Objective 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. Materials and methods 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. Results 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). Conclusion 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. Relevance statement 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. Key Points 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. Graphical Abstract
Chen et al. (2026) conducted a cross-sectional in Adults with systemic lupus erythematosus without known pulmonary arterial hypertension (n=50). 4D flow cardiovascular magnetic resonance (CMR) imaging vs. Age-matched healthy controls without cardiovascular or autoimmune disease was evaluated on Pulmonary artery hemodynamic parameters measured by 4D flow CMR including main pulmonary artery (MPA) max wall shear stress (WSS), left pulmonary artery (LPA) relative pressure, right pulmonary artery (RPA) velocity flow rate (p = 0.040 (WSS in MPA), p=0.040). 4D flow CMR identified that systemic lupus erythematosus patients without pulmonary arterial hypertension had significantly lower main pulmonary artery maximum wall shear stress (0.29 vs 0.33 Pa, p=0.040), higher left pulmonary artery relative pressure (0.54 vs 0.30 mmHg, p=0.008), and increased right pulmonary artery flow rate (3.51 vs 2.90 L/min, p=0.015) compared to healthy controls.