ABC | Volume 114, Nº2, February 2020

Original Article Inanır et al. Arrhythmia predictors in type 1 diabetes mellitus Arq Bras Cardiol. 2020; 114(2):275-280 Electrocardiography Twelve-lead ECGs were obtained following a 10-minute rest period, with 10 mm/mV amplitude and 25 mm/s rate with standard lead positions in a supine position, using a commercially available machine (Nihon Kohen Cardiofax ECG-1950 VET). Depending on heart rate, there were four to six beats per lead. ECGs were manually measured, using a magnifying glass (TorQ 150 mm Digital Caliper LCD) by two blinded cardiologists who had no information about the patients. QT intervals were taken from the onset of the QRS complex to the end of the T wave, whichwas defined as its return to the TP baseline. If Uwaves were present, the QT interval was measured at the nadir of the curve between the T and U waves. The R-R interval was measured and used to compute the heart rate and to correct QT interval (QTc) with Bazett’s Formula. 8 QT dispersion (QTd) was determined as the difference between the maximum and minimumQT interval in different leads. The Tp-e interval was defined from the peak of T wave to the end of T wave. Measurements of Tp-e interval were performed from precordial leads. Rate QTc and corrected QT dispersion (QTdc) were calculated using Bazett’s formula (QTc =QT/√RR). JT intervals were measured from the end of the QRS complex (J point) to the end of the Twave (JTend interval). JTc was calculated using Bazett’s formula (JTc= JT/√RR). Tp-e/QT and Tp-e/QTc ratios were also calculated. No patient had fewer than nine measurable leads. Intraobserver and interobserver variations for measurements were less than 5%, and themeans of the values defined by the cardiologists were used for analysis. Statistical analysis Analyses were carried out using SPSS 20.0 Statistical Package Program for Windows (SPSS Inc, Chicago, Illinois, USA). Quantitative variables are expressed as mean ± standard deviation (SD), and qualitative variables are expressed as numbers and percentages. The Kolmogorov- Smirnov Test was used to determine if the data were normally distributed. ECG parameters were normally distributed, and disease duration and hemoglobin A1c (HbA1c) levels were not normally distributed. Differences between independent groups were assessed by Student t-test for quantitative variables that were normally distributed and chi-square test for qualitative variables. Spearman correlation analysis was used to examine possible associations between T1DM duration, HbA1c, and ventricular repolarization parameters. P values lower than 0.05 were considered statistically significant. Results Mean diabetes duration was 16.6 ± 7.1 years, and mean HbA1c was 10.81% ± 3.27% in the T1DM group. Mean age, systolic blood pressure (BP), diastolic BP, body mass index (BMI), and frequencies of sex, smoking, and hyperlipidemia were not significantly different between study patients and control group (Table 1). In comparison with the control group, heart rate, QTc, QTd, QTdc, Tp-e and JTc intervals, and Tp-e/QT and Tp-e/QTc ratios were significantly higher in T1DM patients (Table 2). T1DM duration and HbA1c levels were significantly correlated with QTc, QTd, QTdc, Tp-e and JTc intervals, and Tp-e/QT and Tp-e/QTc ratios (Table 3). There were no significant correlations between gender, age, BMI, blood pressure, and the measured ECG parameters. Discussion In this study we have found that, in correlation with disease duration and HbA1c levels, QTc, QTd, QTdc, Tp-e, and JTc intervals and Tp-e/QT and Tp-e/QTc ratios on surface ECG, whichmay be associatedwith ventricular arrhythmias and sudden death, were significantly increased in T1DMpatients. As far as we know, there is no study in the literature that investigates Tp-e and JT intervals or Tp-e/QT and Tp-e/QTc ratios in T1DM patients. T1DM patients are at major risk for ventricular arrhythmias and sudden cardiac death. 9 Presence of reentry circuits, triggered activity, and increased autonomy are among possible mechanism for ventricular arrhythmias. The pathophysiological mechanisms behind arrhythmias have not been fully established in diabetic patients. Structural abnormalities caused by prolonged hyperglycemia and increased fibrosis in the myocardium have been speculated. 10,11 Myocardial fibrosis, cell loss in the living myocardial tissue and myocardial conduction pathways can create a favorable environment for the formation of micro-reentry circuits. Ventricular arrhythmias may also be triggered by the contribution of impaired electrical balance of the heart and increased sympathetic activity. 12,13 QT, QTc, and QTd have been shown to predict ventricular arrhythmic events and sudden death in various clinical situations. 14,15 QT interval is an independent predictor of all-cause and cardiovascular mortality in individuals with type 2 diabetes. 16 QT interval represents the time from beginning of ventricular Table 1 – General characteristics of the study groups Baseline characteristics T1DM (n = 46) Control group (n = 46) p value Age (years) 33.8 ± 8.8 33.8 ± 6.2 1.000 Male/female 28/18 28/18 1.000 Systolic BP (mmHg) 124.4 ± 8.7 121.4 ± 6.7 0.069 Diastolic BP (mmHg) 81.0 ± 4.1 78.4 ± 3.3 0.581 Smoking 7 (15.2%) 9 (19.6%) 0.587 Hyperlipidemia 3 (6.5%) 3 (6.5%) 1.000 BMI 24.2 ± 4.7 24.1 ± 4.8 0.955 BMI: body mass index; BP: blood pressure; T1DM: type 1 diabetes mellitus. 276