Systemic Inflammation and Myocardial Repolarization Heterogeneity in Heart Failure and Obstructive Sleep Apnea: Impact on Arrhythmic Risk.

Background and Objectives: Obstructive sleep apnea syndrome (OSAS) and heart failure (HF) frequently coexist, amplifying cardiovascular risk through mechanisms involving chronic inflammation and autonomic dysfunction. This study investigates the impact of systemic inflammation, measured by the systemic immune-inflammation index (SII), and OSAS severity, assessed by the apnea-hypopnea index (AHI), on myocardial repolarization heterogeneity in patients with both conditions. Materials and Methods: In this retrospective study, 160 patients with HF and polysomnography-confirmed OSAS (AHI ≥ 5 events/h) were evaluated between January 2018 and November 2024. Patients were stratified by QT dispersion (QTd < 40 ms vs. ≥40 ms) to assess electrical heterogeneity. SII was calculated from neutrophil, platelet, and lymphocyte counts, and electrocardiographic markers (QTd, frontal QRS-T angle, T wave peak-to-end interval [TPEI]) were measured. Logistic regression and receiver operating characteristic (ROC) analyses were used to identify predictors of repolarization heterogeneity and ventricular arrhythmias. Results: Patients with QTd ≥ 40 ms (n = 78) exhibited higher SII (p < 0.001) and AHI (p < 0.001) compared to those with QTd < 40 ms (n = 82). SII and AHI independently predicted increased QTd in multivariate analysis (p = 0.01 and p < 0.001, respectively). ROC analysis identified SII ≥ 625.4 (sensitivity 73.1%, specificity 72%) and AHI ≥ 22.4 (sensitivity 79.5%, specificity 79.3%) as optimal cut-offs for predicting repolarization heterogeneity. SII, QTd, and TPEI were significantly associated with ventricular arrhythmias (p < 0.05). Patients with moderate-to-severe OSAS (AHI ≥ 15) had higher rates of ventricular tachyarrhythmias (17.8% vs. 5.7%, p = 0.03) and sudden cardiac death (9.3% vs. 1.9%, p = 0.05). Conclusions: Elevated SII and AHI are independent predictors of myocardial repolarization heterogeneity in patients with HF and OSAS, contributing to increased arrhythmic risk. These findings highlight the potential use of SII and AHI as accessible biomarkers for risk stratification, particularly in patients with a preserved ejection fraction, and underscore the need for targeted interventions to mitigate inflammation and OSAS severity.