Abstract 4147111: Correlation between Plasma Adiponectin, Leptin Levels, and Adverse Outcomes in Hypertrophic Cardiomyopathy Patients

Introduction: Hypertrophic cardiomyopathy (HCM) stands as a significant cause of sudden cardiac death in the younger population. Adipokines, originating from adipose tissue, regulate processes such as heart inflammation, fibrosis, and hypertrophy. Among these adipokines, adiponectin and leptin are particularly linked to cardiac remodeling in HCM. This study aimed to examine the association between plasma levels of adiponectin and leptin and the occurrence of all-cause mortality as well as ventricular tachycardia/fibrillation (VT/VF) in individuals with HCM. Methods and Materials: In a multicenter prospective cohort study involving individuals diagnosed with HCM, we assessed plasma adiponectin and leptin concentrations upon enrollment. We examined the combined occurrence of all-cause mortality and new-onset VT/VF. Subsequently, the cohort was stratified into four categories based on adiponectin and leptin levels. Using the Cox proportional hazards model, we compared the likelihood of experiencing the outcome event across these groups, adjusting for age, body mass index, left atrial diameter, and maximum left ventricular wall thickness, with the largest group serving as the reference. Results: The endpoint event occurred in 48 of 384 individuals throughout a 2.8-year median follow-up period. The four groups based on adiponectin and leptin levels exhibited varying risks of the outcome event (log-rank P < 0.001). The Cox proportional hazards model showed that the High-Adiponectin, Low-Leptin group had a considerably higher risk (adjusted HR 7.34, 95% CI 1.12-14.25, P < 0.005) than the reference (Low-Adiponectin, High-Leptin) group. Conclusion: High plasma adiponectin and low leptin levels are independently linked with mortality and new-onset VT/VF in HCM patients. These adipokines can potentially be novel biomarkers for risk stratification in HCM, improving current prediction models.