Baseline galectin 3 predicted mitral valve intervention (HR 1.9, 95% CI 1.7-2.8) and correlated strongly with myocardial fibrosis in primary mitral regurgitation.
Do NT-proBNP and galectin 3 correlate with subclinical left ventricular dysfunction, myocardial fibrosis, and predict the need for mitral valve intervention in patients with primary mitral regurgitation?
237 patients, comprising 117 with moderate and severe chronic primary mitral regurgitation (MR) and a control group of 120 subjects with mild MR.
Assessment of biomarkers NT-proBNP and galectin 3, along with cardiac magnetic resonance imaging (T1 mapping, LGE) and echocardiography (LV GLS).
Control group of patients with mild mitral regurgitation.
Composite endpoint consisting of criteria for mitral valve intervention.composite
Galectin 3 correlates with myocardial fibrosis and is an independent predictor for mitral valve intervention in primary mitral regurgitation, whereas NT-proBNP is not.
Abstract The aim of this study was to correlate the biomarker of heart failure, NT proBNP and the marker of myocardial fibrosis - galectin 3, with imaging changes reflecting subclinical left ventricular dysfunction -left ventricular global longitudinal strain (LV GLS) and myocardial fibrosis by cardiac magnetic resonance techniques - and with a composite endpoint consisting of criteria for intervention, in primary mitral regurgitation (MR). Material and methods: we conducted a prospective, case-control study on a group of 117 patients with moderate and severe chronic primary MR, respectively a control group of 120 subjects with mild MR, enrolled within a four-year interval (2019-2023). Results: the mean values at baseline for both biomarkers were significantly higher in the study group compared to the control group, and increased during follow up, compared with controls. The values of galectin 3 at inclusion did not correlate with the severity parameters of the MR (RVol and RF), but correlated with the ECV measured at T1 mapping (r=0.73) and with the presence of replacement fibrosis by LGE (r=0.81). In the study group, 71 patients experienced interstitial fibrosis (60.6%), significantly more than in the control group (7 patients, 5.8%) (p0.01), and replacement fibrosis was recorded in 27 patients (23%) in the study group, compared to 3 patients (2.5%) in the control group (p0.01). Patients with interstitial fibrosis on T1 mapping and those with replacement fibrosis had significantly higher mean galectin 3 values, with a significant increase from baseline starting at month 6 of follow-up. Patients with normal LV GLS values had lower mean values of both NT proBNP and galectin 3 compared to those with LVGLS 21%. In patients with LVGLS 21%, there was an accelerated and earlier increase in both NT-ProBNP and galectin 3, with a similar trend for both biomarkers . During the follow-up, 27 patients in the study group reached the composite endpoint, requiring mitral valve (MV) intervention . Following the multivariate analysis, only the value of Galectin 3 at baseline was a predictive factor for the composite endpoint (HR 1.9, 95% CI 1.7-2.8), the value of NTProBNP not being associated with an increased risk of MV intervention. In conclusion, both NT proBNP and galectin 3 are useful markers in the monitoring of asymptomatic patients with primary MR. The prognostic role of NT proBNP in MR is still controversial. The data from the present study did not reveal NT ProBNP as an independent predictor of prognosis, but this may be due to the relatively small number of patients. Galectin 3 correlated with the presence of interstitial and replacement myocardial fibrosis, probably playing an active role in its onset and progression, with negative prognostic implications on the reverse of remodeling VS post-MR correction.
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Catalina Ileana Badau Riebel
L Agoston Coldea
European Heart Journal
Iuliu Hațieganu University of Medicine and Pharmacy
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Riebel et al. (Sat,) reported a other. Baseline galectin 3 predicted mitral valve intervention (HR 1.9, 95% CI 1.7-2.8) and correlated strongly with myocardial fibrosis in primary mitral regurgitation.
www.synapsesocial.com/papers/698829520fc35cd7a88497e9 — DOI: https://doi.org/10.1093/eurheartj/ehaf784.2473
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