Altered Global Longitudinal Strain is a common finding in Liver Transplant Recipients with Mild Cardiometabolic Burden
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Background and aim of the study : Liver transplant (LT) recipients are a population at elevated cardiovascular (CV) risk, yet conventional assessment tools often fail to capture early myocardial dysfunction. Global longitudinal strain (GLS) has emerged as a sensitive marker of subclinical myocardial dysfunction, although its role in the long-term post-transplant setting remains insufficiently defined. The study aimed to evaluate left ventricular (LV)-GLS in a population of stable LT recipients with mild cardiometabolic burden and explored the possible associations with metabolic, lifestyle, inflammatory, and transplant-related variables. Secondary aims included longitudinal GLS variation over 12 months. Subjects and methods: We conducted a cross-sectional observational study in 40 LT recipients. Data on cardiometabolic parameters, body composition (including bioimpedance analysis), diet, physical activity were collected. Carotid ultrasound and echocardiography were performed. Levels of circulating inflammatory cytokines were measured. CV risk scores were calculated. Results : GLS impairment was detected in 47.5% of patients, despite preserved ejection fraction. Antihypertensive therapy correlated with more favorable GLS, whereas higher IL-17A and IL-1β levels were paradoxically linked to preserved strain. No association emerged with immunosuppressive regimen or lifestyle indices. GLS remained unchanged at 12 months, irrespective of weight loss or dietary improvement. Conclusions : GLS appears more sensitive than EF in detecting subclinical myocardial dysfunction in LT recipients, highlighting its potential role in post-transplant CV surveillance. Antihypertensive treatment may exert protective effects, whereas cytokine patterns suggest non-traditional mechanisms of cardiac modulation. Larger longitudinal studies are needed to confirm prognostic implications and integrate GLS into CV risk stratification pathways post-LT.