Key result
Mitral valve prolapse is linked to ~3-point higher liver ECV regardless of MR severity.
Why the study?
Persistent volume overload in mitral valve prolapse (MVP) and mitral regurgitation (MR) may cause systemic venous congestion affecting the liver, but whether and to what extent liver extracellular volume (ECV) is elevated in these patients was unknown.
Observational (n=142)
Patients with mitral valve prolapse exhibit significantly elevated liver extracellular volume on CMR compared to healthy controls regardless of mitral regurgitation severity, suggesting early extracardiac hepatic involvement beyond hemodynamic volume overload alone.
Higher liver ECV in MVP should not yet change practice; leaves open its value for systemic fibrosis assessment or monitoring.
Background Mitral valve prolapse (MVP) is a common cause of mitral regurgitation (MR), leading to chronic volume overload and maladaptive left ventricular (LV) remodelling. Persistent volume overload may also result in systemic venous congestion, potentially affecting extracardiac organs such as the liver. Cardiovascular magnetic resonance (CMR) allows non-invasive quantification of extracellular volume (ECV), reflecting diffuse interstitial expansion and fibrosis. Whether and to which extent liver ECV is elevated in patients with MVP and MR is unknown. Objectives To compare liver ECV between MVP patients and healthy controls, to assess differences across MR severity, and to identify clinical and CMR-related characteristics associated with elevated liver ECV. Methods A total of 142 subjects were prospectively included among whom 20 were healthy controls, and 122 were patients with MVP categorized as mild (n=27), moderate (n=54), or severe MR (n=41). All subjects underwent 1.5T CMR including ECV imaging. A free region of interest was manually drawn in the liver parenchyma in ECV maps, carefully avoiding the inferior vena cava, hepatic veins, and visible coregistration artifacts. Liver ECV was compared between MR severity groups and controls. Univariable and age- and sex-adjusted linear regression analyses were performed. Results Liver ECV was significantly higher in all MVP groups than in controls (29.2±4.14%, 29.4±3.06%, and 28.9±3.59% in mild, moderate, and severe MR vs. 26.2±2.16% in controls; p<0.01 for all, Figure 1), with no significant difference across MR severity groups (p=0.63). In adjusted analyses, higher liver ECV in patients with MVP was independently associated with diabetes (β=5.27, p=0.01), atrial fibrillation (β=2.58, p=0.01), larger indexed LV end-diastolic volume (β=0.03, p=0.03), larger indexed LV end-systolic volume (β=0.06, p=0.01), higher myocardial native T2 (β=0.53, p<0.001), higher myocardial ECV (β=0.55, p<0.001), and higher liver native T1 (β=0.02, p<0.001). Anterior leaflet prolapse (β=3.26, p=0.02) was positively associated with liver ECV in patients with MVP. Conclusions Liver ECV was significantly increased in patients with MVP with mild, moderate or severe MR, compared with healthy controls. Hepatic extracellular expansion appears to occur early and does not scale with the degree of MR-related volume overload, suggesting extracardiac involvement beyond hemodynamic burden alone.
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Lodin et al. (2026) conducted an observational in Mitral valve prolapse and mitral regurgitation (n=142). Mitral valve prolapse with mitral regurgitation vs. Healthy controls was evaluated on Liver extracellular volume (ECV) (p=<0.01). Mitral valve prolapse with mild, moderate, or severe MR was associated with higher liver ECV vs controls (29.2%, 29.4%, and 28.9% vs 26.2%; p<0.01), without differences across MR severity (p=0.63).
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