Frontiers in cardiovascular medicine · 2026
Delayed late ventricular depolarization is associated with inflammation in epicardial Fat Among females: a New avenue in cardiac electrophysiology.
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Ahmed Nadeem A, Sánchez-López David, Basdas Rumeysa, Núñéz-Caamaño José Ramón, Martínez-Cereijo José Manuel, Reija-López Laura, Fernández Ángel L, García-Seara Javier, Rodriguez-Mañero Moisés, González-Juanatey José R, Eiras Sonia
Аннотация
BACKGROUND: Epicardial adipose tissue (EAT) has been linked to cardiac conduction through direct myocardium interaction and endocrine activity. We investigated sex-specific associations between ventricular electrical activity and the molecular composition of EAT.
METHODS: EAT biopsies from 146 cardiac surgery patients were analysed for inflammatory cell markers (CD16, DEFA3, CXCR2, CD68, CD14), fatty acid transporters (FABP4, CD36), fibroblast-related markers (COL1A2 and PREF1), and neuroreceptor-related markers (CHRM3, CHRM2, ADRB3) using real-time PCR. High-quality electrocardiograms (ECGs) from 100 patients were analysed for 36 ventricular depolarization and repolarization parameters. Principal component analysis was used to explore the internal ECG structure. Spearman correlation with Benjamini-Hochberg correction and sex-stratified linear regression assessed ECG-EAT associations, adjusting for clinical covariates.
RESULTS: In females, EAT fibrotic and inflammatory profile were correlated with delayed late anteroseptal depolarization (prolonged S-wave upstroke time) in V2 (COL1A2, p= 0.642, adj.p = 0.025; DEFA3, p = 0.572, adj.p = 0.038), and V3 (COL1A2, p = 0.592; DEFA3, p = 0.629; CD16, p = 0.642; CD14, p = 0.596; CHRM3, p = 0.600; all adj.p ≤ 0.027). Linear regression models confirmed strong positive associations between the interaction ECGxSex and CD14, CD16, DEFA3, and COL1A2 (β = 1 to 5, all p ≤ 0.02). Clinical factors reduced but did not eliminate sex dependent effects. Akaike information criteria (AIC)-refined models identified coronary artery disease, hypertension, and valvular heart disease as key covariates, yet inflammatory markers (CD14 and CD16) retained sex-specific explanatory power (adjusted R 2 = 0.13-0.20).
CONCLUSION: Despite similar absolute ECG values, females exhibited a stronger electrical response to the EAT inflammatory profile. These findings highlight inflammation-driven sex-specific depolarization alterations and support ECG as a simple tool to indicate adverse EAT phenotypes.
METHODS: EAT biopsies from 146 cardiac surgery patients were analysed for inflammatory cell markers (CD16, DEFA3, CXCR2, CD68, CD14), fatty acid transporters (FABP4, CD36), fibroblast-related markers (COL1A2 and PREF1), and neuroreceptor-related markers (CHRM3, CHRM2, ADRB3) using real-time PCR. High-quality electrocardiograms (ECGs) from 100 patients were analysed for 36 ventricular depolarization and repolarization parameters. Principal component analysis was used to explore the internal ECG structure. Spearman correlation with Benjamini-Hochberg correction and sex-stratified linear regression assessed ECG-EAT associations, adjusting for clinical covariates.
RESULTS: In females, EAT fibrotic and inflammatory profile were correlated with delayed late anteroseptal depolarization (prolonged S-wave upstroke time) in V2 (COL1A2, p= 0.642, adj.p = 0.025; DEFA3, p = 0.572, adj.p = 0.038), and V3 (COL1A2, p = 0.592; DEFA3, p = 0.629; CD16, p = 0.642; CD14, p = 0.596; CHRM3, p = 0.600; all adj.p ≤ 0.027). Linear regression models confirmed strong positive associations between the interaction ECGxSex and CD14, CD16, DEFA3, and COL1A2 (β = 1 to 5, all p ≤ 0.02). Clinical factors reduced but did not eliminate sex dependent effects. Akaike information criteria (AIC)-refined models identified coronary artery disease, hypertension, and valvular heart disease as key covariates, yet inflammatory markers (CD14 and CD16) retained sex-specific explanatory power (adjusted R 2 = 0.13-0.20).
CONCLUSION: Despite similar absolute ECG values, females exhibited a stronger electrical response to the EAT inflammatory profile. These findings highlight inflammation-driven sex-specific depolarization alterations and support ECG as a simple tool to indicate adverse EAT phenotypes.