Increased Corrected Index of Cardiac Electrophysiological Balance in Behçet’s Disease: Association with Disease Duration

Background/Objectives: Behçet’s disease (BD) is a chronic multisystem inflammatory vasculitis associated with an increased risk of ventricular arrhythmias and sudden cardiac death. The index of cardiac electrophysiological balance (iCEB) and its corrected form (iCEBc) are novel electrocardiographic markers reflecting the balance between ventricular depolarization and repolarization and have been proposed as indicators of arrhythmic risk. This study aimed to evaluate iCEB and iCEBc in patients with BD and to investigate their associations with disease duration and inflammatory activity. Methods: This observational, cross-sectional study included 81 patients with clinically inactive BD (Behçet’s Disease Current Activity Form score 0–1) and 84 age- and sex-matched healthy controls. All participants underwent laboratory testing, transthoracic echocardiography and standard 12-lead electrocardiography. QT, QTc, QRS, iCEB (QT/QRS), and iCEBc (QTc/QRS) values were calculated. Correlation analyses were performed to evaluate the relationships between disease duration and QTc, iCEB, iCEBc, and CRP levels in the Behçet group. Disease duration, age, and CRP levels were subsequently entered into a multivariable linear regression model to identify independent predictors of iCEBc. Results: Patients with BD exhibited significantly higher QTc (431.41 ± 24.18 vs. 410.60 ± 18.65 ms, p < 0.001), iCEB (4.49 ± 0.33 vs. 4.36 ± 0.35, p = 0.016), and iCEBc (5.20 ± 0.47 vs. 4.93 ± 0.33, p < 0.001) values compared with healthy controls. CRP levels were also significantly elevated in the Behçet group (23.34 ± 34.05 vs. 6.07 ± 4.57 mg/L, p < 0.001). Disease duration demonstrated significant positive correlations with QTc (r = 0.539, p < 0.001), iCEB (r = 0.447, p < 0.001), iCEBc (r = 0.747, p < 0.001), and CRP levels (r = 0.419, p < 0.001). In multivariable linear regression analysis, disease duration emerged as the sole independent predictor of iCEBc (β = 0.077, 95% CI: 0.057–0.097, p < 0.001), whereas CRP was not independently associated with iCEBc (p = 0.286). Conclusions: Patients with BD have significantly increased iCEB and iCEBc values, indicating impaired cardiac electrophysiological balance. The strong association between disease duration and iCEBc suggests a relationship between disease duration and electrophysiological alterations associated with ventricular arrhythmia risk. iCEBc may serve as a simple and noninvasive electrocardiographic marker of electrophysiological alterations associated with ventricular arrhythmia risk in patients with BD.