Background: Although the pathophysiology of coronary slow flow (CSF) has not been fully elucidated, emerging data increasingly support potential role for subclinical diffuse atherosclerosis in the etiology of CSF. We aimed to investigate relationship between atherogenic indices and CSF. Methods: 130 patients with CSF diagnosed according to Thrombolysis in Myocardial Infarction (TIMI)-frame count (TFC) method and 130 controls who had normal coronary flow (NCF) were included in this retrospective study. Atherogenic indices (atherogenic index of plasma [AIP], Castelli risk indices I and II [CRI-I and II]) were calculated using conventional lipid parameters. Results: The logistic regression analyses demonstrated that AIP (OR, 5.463; 95% confidence interval [CI], 1.357–21.991; p = 0.017) and CRI-II (OR, 1.624; 95% CI, 1.138–2.319; p = 0.008) were independent predictors of CSF. Receiver operating characteristic analysis showed that the optimal cutoff value to predict the occurrence of CSF was 0.66 for AIP (sensitivity, 59%; specificity, 73%; area under curve [AUC], 0.695; p < 0.001) and 3.27 for CRI-II (sensitivity, 60%; specificity, 79%; AUC, 0.726; p < 0.001). Conclusions: AIP and CRI-II levels were independent predictors of CSF. Prospective studies in larger cohorts of patients may elucidate the role of atherogenic dyslipidemia in the pathophysiology of CSF.

Background and Objectives: Epilepsy patients have a higher risk of sudden unexplained death compared to the rest of the population. Cardiac repolarization abnormalities might be seen in epilepsy during interictal periods. We aimed to evaluate the changes in electrocardiography (ECG) parameters in generalized tonic-clonic seizure patients treated with carbamazepine or valproic acid (VPA) drug. Materials and Methods: A totally of 129 subjects (66 epilepsy patients, 63 healthy subjects) were enrolled in the study. Of the patients, 36 were on carbamazepine and 30 were on VPA. There were 12-lead ECGs obtained from all participants. RR interval (time between consecutive R peaks), QT interval (defines the period of ventricular repolarization), corrected QT (QT interval corrected for heart rate; QTc), QTc-maximum (QTc-max), QTc-minimum (QTc-min), QTc dispersion (QTcd), P (atrial depolarization )-maximum (P-max), P-minimum (P-min) and P dispersion (Pd) were measured. Results: QTd (QT dispersion), QTcd, and Pd values were significantly higher in the patients compared to the controls (p < 0.01). QTcd, Pd, and P-max values were statistically higher in male patients compared to healthy male controls. QTcd values were significantly higher in female patients using carbamazepine compared to the female patients on VPA and healthy controls (p = 0.01). Male patients using VPA had significantly higher QTcd values against the male population in carbamazepine and control groups. Conclusions: This study demonstrated that QTd, QTcd, and Pd values were significantly higher in epilepsy patients than in healthy controls. In addition, female patients using carbamazepine and male patients using VPA were prone to ventricular arrhythmia compared to the control group.

Background and Objectives: The autonomic nervous system (ANS) is involved in panic disorders. ANS dysfunction has been shown to be associated with ventricular arrhythmia and increased heterogeneity of ventricular repolarization. However, there remains limited evidence of the relationship between panic disorders and ventricular depolarization markers, including the Tp-e interval and Tp-e/QT ratio. This study aimed to evaluate ventricular repolarization parameters in patients with panic disorder. Materials and Methods: In total, 40 patients with panic disorder, diagnosed using the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) criteria, were included in the study group. The control group comprised of 50 age- and sex-matched healthy individuals. A standard 12 lead electrocardiogram was recorded on all participants, and heart rate, QT interval, QRS duration, Tp-e interval, and Tp-e/QT ratio were measured. Results: QRS durations and QT intervals were similar in the study and control groups. Compared to the control group, QTd, Tp-e, and cTp-e intervals as well as Tp-e/QT and Tp-e/QTc ratios were significantly increased in patients with panic disorder (p < 0.05 for all). In the study group, the Severity Measure for Panic Disorder—Adult score had a significant positive correlation with the Tp-e interval (r = 0.369, p < 0001), cTp-e interval (r = 0.531, p < 0.001), Tp-e/QT ratio (r = 0.358, p = 0.001), and Tp-e/QTc ratio (r = 0.351, p = 0.001). Conclusion: These findings indicate that panic disorders are associated with increased ventricular repolarization heterogeneity, which may be attributed to ANS dysregulation.

AIM: The aim of the current study was to evaluate the index of Cardiac Electrophysiological Balance (iCEB) in hospitalized COVID-19 patients receiving Hydroxychloroquine / azithromycin (HCQ / AZ) combination therapy to determine the susceptibility to ventricular arrhythmia among these patients. METHOD: Sixty-seven COVID-19 patients admitted to the ward were included in the study. Electrocardiograms (ECGs) were obtained from all patients before the initiation of treatment and on treatment day 5. QT/QRS (iCEB) and QTc/QRS (iCEBc) ratios were calculated. RESULTS: QRS, QT and QTc intervals were signifi cantly prolonged on day 5 measurements compared to pre-treatment period (p <0.05). Overall, mean iCEB was 3.6 +/- 0.4 before treatment and 3.8 +/- 0.4 on day 5 in the study population (p <0.001). Considering the iCEBc values, a signifi cant increase was observed in patients receiving HCQ/AZ treatment compared to pre-treatment period (4.1 +/- 0.5 vs 4.4 +/- 0.6; p <0.001). CONCLUSIONS: To the best of our knowledge, this was the fi rst study to investigate iCEB and iCEBc parameters in patients with COVID-19 on HCQ/AZ therapy. In this study, we demonstrated signifi cantly increased iCEB and iCEBc values following HCQ/AZ treatment in COVID-19 patients. iCEB and iCEBc may serve as a noninvasive, simple, and novel biomarker for detecting increased pro-arrhythmia risk in COVID-19 patients (Tab. 3, Fig. 3, Ref. 36). Text in PDF www.elis.sk