ABC | Volume 110, Nº6, June 2018

Original Article Karaman et al Myocardial repolarization and VPC burden Arq Bras Cardiol. 2018; 110(6):534-541 Table 1 – Baseline characteristics, laboratory and echocardiographic parameters of the study population Variables Group 1 (n = 32) Group 2 (n = 36) Group 3 (n = 32) p* Age, years 49.60 ± 16.50 51.40 ± 17.00 52.10 ± 12.90 0.805 Female sex, n (%) 16.00 (50.00) 19.00 (52.80) 14.00 (43.8) 0.752 Body mass index, kg/m 2 24.10 ± 2.50 23.60 ± 3.60 23.40 ± 4.40 0.657 Hypertension, n (%) 8.00 (25.00) 12.00 (33.30) 10.00 (31.3) 0.743 Diabetes Mellitus, n (%) 1.00 (3.10) 4.00 (11.10) 5.00 (15.6) 0.240 Coronary Artery Disease, n (%) 7.00 (21.90) 10.00 (27.80) 11.00 (34.4) 0.538 Smoking, n (%) 6.00 (18.80) 5.00 (13.90) 7.00 (21.9) 0.687 Systolic Blood Pressure (mmHg) 125.40 ± 15.40 125.10 ±14.30 122.80 ±14.00 0.737 Diastolic Blood Pressure (mmHg) 78.70 ± 7.50 77.50 ± 8.10 76.70 ± 8.90 0.638 Left Ventricle Ejection Fraction, (%) 62.80 ± 3.70 61.30 ± 4.20 60.90 ± 4.70 0.167 Interventricular Septum, (mm) 9.80 ± 0.70 10.20 ± 0.80 10.00 ± 0.80 0.460 Creatinine, mg/dl 0.82 ± 0.22 0.85 ± 0.22 0.83 ± 0.21 0.816 Neutrophil to Lymphocyte Ratio 1.90 ± 0.57 2.36 ± 1.05 2.26 ± 1.67 0.267 Hemoglobin, gr/dl 14.60 ± 1.60 14.00 ± 1.40 14.20 ± 1.80 0.345 β-blockers, n (%) 15.00 (46.90) 16.00 (44.40) 11.00 (34.4) 0.559 Angiotensin-converting Enzyme Inhibitors, n (%) 8.00 (25.00) 9.00 (25.00) 6.00 (18.8) 0.787 Angiotensin Receptor Blockers, n (%) 4.00 (12.50) 5.00 (13.90) 4.00 (12.5) 0.981 Number of patients with Vc, n (%) 9.00 (28.10) 21.00 (58.30) 21.00 (65.6) 0.006 Number of patients with VT, n (%) 3.00 (9.40) 11.00 (30.60) 12.00 (37.5) 0.028 Vc: ventricular couplet; VT: ventricular tachycardia. Data are presented as mean ± SD, or n (%). Statistically significant p values shown in bold. *ANOVA and χ 2 tests were performed to study differences among the three groups. analysis, CADhad no effect on ECGparameters. Vcwas observed in 51 patients (9, 21, and 21 patients in groups 1, 2, and 3, respectively) and VT in 26 patients (3, 11, and 12 patients in groups 1, 2, and 3, respectively). The QTd duration of group 3 was significantly longer than those in groups 1 and 2 (p = 0.001, p = 0.015, respectively). According to Pearson’s correlation test, positive correlations were observed between VPC burden and Tp-e (in leads V2 and V5) and Tp-e/QTc (in leads V2 and V5) (r = 0.476, p < 0.001; r = 0.395, p =< 0.001and r = 0.296, p = 0.003; r = 0.256, p = 0.010, respectively) (Table 3, Figure 1). Table 3 shows the results of the multiple linear regression analyses performed to identify the ECG parameters affecting VPC burden. Thus, Tp-e interval ( β = 1.318, p = 0.043) and Tp-e/QTc ratio ( β = -405.136, p = 0.024) in lead V5 were independent predictors of VPC burden. Discussion In this study, we demonstrated that Tp-e interval and Tp-e/QTc ratios were significantly higher in patients with higher VPC burden than in those with lesser VPC burden and that a positive correlation was observed between these markers and VPC frequency. However, we did not find a relationship between Tp-e/QT ratio and VPC burden. Tp‑e interval and Tp-e/QTc ratio in lead V5 were identified as independent predictors of increased VPC burden. The prolongation of the duration of myocardial repolarization in patients with increased VPC burden is important because this condition may be related to the increased risk of life‑threatening arrhythmia. According to our results, myocardial repolarization parameters deteriorated with increasing VPC frequency. Therefore, we concluded that both VPC frequency and stage of myocardial repolarization were affected by similar causes. Idiopathic VPCs, generally regarded as a benign condition in healthy individuals without structural heart disease, are formed by the spread of an early stimulus originating from an ectopic focus. VPCs may cause serious complications, such as angina, syncope, or heart failure, when the ectopic beat number increases. 13-16 Although VPCs are known to be benign in individuals with a structurally normal heart, they have been shown to cause malignant arrhythmias in some cases. However, the clinical significance of VPC frequency in these individuals remains unclear once adequate human studies have not been performed. 17 Tilz et al. 18 found that ventricular fibrillation (VF) was triggered by VPCs after an implantable cardioverter-defibrillator was used on a 29-year-old patient, who was resuscitated following sudden cardiac death. All examinations, including echocardiography, angiography, ajmaline test, and myocardial biopsy, were normal. At the same time, some cases demonstrated that polymorphic VT and idiopathic VF were induced because specific VPCs with short coupling intervals could promote intracellular calcium overload. 19,20 In a study examining the records of 21 patients 536