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 2 – Baseline and ambulatory Holter electrocardiography parameters of the study population Variables Group 1 (n = 32) Group 2 (n = 36) Group 3 (n = 32) p values (groups)* 1 vs 2 1 vs 3 2 vs 3 Maximum Heart Rate (beats/min) 123.60 ± 17.10 120.40 ± 20.10 116.80 ± 13.20 0.720 0.259 0.671 Minimum Heart Rate (beats/min) 58.90 ± 7.40 54.90 ± 8.60 57.10 ± 7.30 0.097 0.638 0.481 Average Heart Rate (beats/min) 73.40 ± 13.40 72.40 ± 14.60 73.90 ± 12.00 0.940 0.980 0.855 Number of VPCs (median/24 h) 543.00 ± 288.00 2779 ± 1041 8358 ± 2911 < 0.001 < 0.001 < 0.001 Number of VPCs (median/h) 22.80 ± 12.40 117.50 ± 46.30 358.00 ± 125.20 < 0.001 < 0.001 < 0.001 Percent of VPC number (24 h) 0.50 ± 0.23 2.76 ± 1.03 7.90 ± 2.72 < 0.001 < 0.001 < 0.001 Lead V2 QT (ms) 358.00 ± 22.80 378.10 ± 35.50 387.00 ± 25.30 0.013 < 0.001 0.419 QTc (ms) 414.30 ± 32.20 410.50 ± 27.00 427.30 ± 33.80 0.867 0.222 0.071 Tp-e (ms) 94.30 ± 9.40 100.50 ± 9.70 106.50 ± 7.90 0.016 < 0.001 0.023 cTp-e (ms) 108.60 ± 14.80 110.00 ± 16.30 117.70 ± 11.50 0.923 0.038 0.079 Tp-e/QT 0.26 ± 0.02 0.27 ± 0.03 0.28 ± 0.02 0.854 0.239 0.493 Tp-e/QTc 0.23 ± 0.02 0.24 ± 0.03 0.25 ± 0.03 0.007 0.001 0.689 Lead V5 QT (ms) 363.70 ± 26.20 380.50 ± 41.50 389.30 ± 20.50 0.075 0.004 0.485 QTc (ms) 421.00 ± 37.00 413.00 ± 29.30 429.70 ± 29.10 0.554 0.524 0.084 Tp-e (ms) 91.30 ± 9.20 94.00 ± 12.20 101.10 ± 8.80 0.519 0.001 0.015 cTp-e (ms) 106.50 ± 15.10 102.3 ± 13.9 112.0 ± 14.0 0.453 0.280 0.018 Tp-e/QT 0.25 ± 0.02 0.25 ± 0.03 0.26 ± 0.03 0.895 0.372 0.163 Tp-e/QTc 0.22 ± 0.02 0.23 ± 0.03 0.24 ± 0.03 0.244 0.021 0.465 QTd (ms) 23.30 ± 6.40 26.3 ± 13.1 34.3 ± 13.4 0.537 0.001 0.015 QTc: corrected QT; QTd: QT dispersion; Tp-e: T wave peak-to-end interval; cTp-e: corrected Tp-e; ms: millisecond; VPC: ventricular premature contraction; Data are presented as mean ± SD. Statistically significant p values shown in bold; *ANOVA test was performed to study differences among the three groups. The post hoc Tukey’s test was performed after ANOVA to study between groups differences for group 1 vs. group 2, group 1 vs. group 3 and group 2 vc. group 3. who experienced cardiac arrest during ambulatory ECG recording, heart rate and VPC frequency increased before the onset of VF. 21 Savelieva et al. 22 found significant QT turbulence after VPC in individuals with a structurally healthy heart. Although these data provide information on the cause of malignant arrhythmias for VPC, they do not provide enough information about the importance of VPC frequency. Several mechanisms have been proposed to explain the relationship between VPC and life-threatening arrhythmias. VPC may play a key role in the initiation of malignant cardiac arrhythmias. Various factors such as increased sympathetic tonus, altered hemodynamic status, or electrolyte imbalances (e.g., the hypokalemia and hypercalcemia), which all disrupt the stability of the myocardium, may cause a transition from VPC to malignant arrhythmia. 17 Increased sympathetic tonus due to anxiety or physiological stress may cause the release of catecholamines such as adrenaline. This condition causes the flow of calcium from an extracellular space into the myocyte cells by increasing the production of cyclic AMP (cAMP). The contraction force of the myocytes increases, and the myocyte is depolarized rapidly. For this reason, myocytes become more sensitive than normal and may depolarize spontaneously without sino-atrial node depolarization. Therefore, VPC formation and frequency may increase. 23,24 Armaganijan et al. 25 reported the relationship of sympathetic activation with patients with ventricular arrhythmias and suggested the effectiveness of renal sympathetic denervation by catheter to reduce arrhythmic burden. Another factor that increases the frequency of VPC is excessive caffeine consumption. Caffeine, a phosphodiesterase inhibitor, is also a central stimulant that can enhance sympathetic activity. It can increase intracellular calcium concentration by inhibiting the enzyme that catalyzes the breakdown of cAMP. Animal studies showed that caffeine administration at high doses could induce and increase the frequency of VPCs. 26,27 Prolongation in the dispersion of myocardial repolarization predisposes the malignant ventricular arrhythmia and has prognostic importance in terms of sudden cardiac death (SCD). Prolongation of QT and QTd durations may be associated with polymorphic ventricular tachycardia, Torsades de pointes, and SCD. 28,29 Recently, some myocardial repolarization markers, such as Tp-e interval, Tp-e/QT, and Tp-e/QTc ratios, have been reported to be useful in predicting lethal ventricular arrhythmias in various clinical disorders without structural 537