Ventricular Repolarization In Patients Research Articles

QT Interval Derived Measurements in Patients with Cardiac Syndrome X Compared to Coronary Artery Disease.

Previous studies assessing effect of ischemia on ventricular repolarization are mostly directed toward patients with coronary artery disease (CAD); however, similar reports on cardiac syndrome X (CSX) are scarce. Whether microvascular dysfunction of CSX and ischemia induced by CAD produce comparable effect on ventricular repolarization is unclear and deserve further studies. In the present study, ECG measures of ventricular repolarization were compared between CAD and CSX patients (40 subjects in each group). Following evaluation of sociodemographic characteristics, medical and past medical history, a resting ECG was used to assess measurements of ventricular repolarization in each patient, namely, QT interval (QT), corrected QT interval (QTc), QT dispersion (QTd), corrected QT dispersion (QTcd), adjacent QT dispersion (AdQTd), QT dispersion ratio (QTdR), JT dispersion (JTd), and Corrected JT dispersion (JTcd). Results showed comparable QT intervals and QTd in CAD and CSX patients even after adjustment for the possible variations in gender, age and body mass index of the studied groups. Although JTd was increased in CSX subjects (26.6 ± 7.2 ms) compared with CAD patients (22.7 ± 6.5 ms, p = 0.019), statistical significance disappeared after correcting JT for variations in heart rate. QT and QTc were significantly below 440 ms in CAD as well as CSX patients (p < 0.001). In contrast, maximum QTd, maximum QTcd and AdQTd of CAD and CSX patients were significantly above 440 ms (p < 0.001). The means of JTd and JTcd were significantly above 22 ms and 24 ms respectively (p < 0.001, p = 0.001) in CSX but not CAD patients (p = 0.529, p = 0.281). The present findings clearly demonstrate comparable measures of ventricular repolarization in CAD and CSX patients and consequently an equal risk of cardiac events in both groups.

Evaluation of Tp-e interval and Tp-e/ QTc ratio in patients with mild to moderate psoriasis

Objectives. Many systemic diseases including cardiovascular disturbances have been described in psoriatic patients. In the previous studies, left ventricle (LV) subclinical myocardial dysfunction was reported in the psoriasis patients. The T-wave peak to end (Tp-e) interval is a relatively new marker for ventricular arrhythmogenesis and repolarization heterogeneity. Prolongation of this interval represents a period of potential vulnerability to ventricular arrhythmias. However, there is no information available assessing the Tp-e interval and related calculations in patients with psoriasis disease. The aim of this study was to evaluate ventricular repolarization in patients with psoriasis disease by using QT, corrected QT (QTc) and Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. Methods. In this study, retrospective analysis of 30 patients who underwent the psoriasis treatment and of 30 healthy individuals was performed. The severity of the disease was evaluated by the “Psoriasis Area and Severity Index”. QT, corrected QT (QTc), Tp-e interval and Tp-e/QT ratio were measured by means of the 12-lead electrocardiogram. Left ventricular function was evaluated by echocardiography. Results. Baseline characteristics and QT and QTc intervals were similar in both groups. No difference was detected between the groups with regards to Tp-e interval (83.0±9 vs 82.3±10; p =0.81), Tp-e/QT (0.22±0.03 vs 0.23±0.04; p =0.3) and Tp-Te/QTc (0.20±0.04 vs 0.19±0.04; p =0.77). Conclusions. These findings suggest that ventricular repolarization in mild to moderate psoriasis patients might be unimpaired. Larger samples and severe degree psoriasis patients are needed to evaluate the arrhythmia risk in psoriasis patients.

Heart rate-guided, but not dose-guided titration of beta blockers stabilizes ventricular repolarization in patients with chronic heart failure

AimsWe compared the effects of heart rate-guided and dose-guided beta-blocker titration strategies on QT variability in patients with chronic heart failure (CHF). MethodsIn a prospective study we recorded 5-minute resting high-resolution ECGs (HRECG) in 100 patients with CHF and measured heart rate (HR) and ventricular repolarization by QT variability index (QTVI). In a subgroup of patients not reaching target HR (<70bpm) we uptitrated beta blockers and repeated HRECG measurements 3months thereafter. ResultsTarget HR was present in 46 patients (group A), and in 54 patients HR was above target (group B). The groups did not differ in age, gender, NYHA class, NT pro-BNP, creatinine, or beta blocker dose. Patients in group A displayed significantly lower QTVI than patients in group B (−1.25±0.55 vs. −1.52±0.42, P=0.013). When uptitrating beta-blockers we found a decrease in HR (from 91±15bpm to 71±15bpm, P<0.001), NTpro BNP levels (from 4474±3878pg/ml to 3042±2566pg/ml, P=0.024), and NYHA class (from 3.0±0.8 to 2.5±0.7, P=0.006). With beta-blocker uptitration QTVI decreased in 10 of 24 patients (42%). In these patients HR decreased more than in the remaining cohort (−25±20bpm vs. −15±17bpm, P=0.017). On multivariate analysis, the presence of target HR was a predictor of QTVI decrease (P=0.017), but beta-blocker dose was not. ConclusionsIn patients with CHF treated by beta-blockers, changes in QT variability appear to occur in parallel with changes of heart rate. This suggests that heart rate-guided titration of beta-blockers may be associated with decreased risk of sudden cardiac death.

Prolonged Tp-e Interval, Tp-e/QT Ratio and Tp-e/QTc Ratio in Patients with Type 2 Diabetes Mellitus.

BackgroundType 2 diabetes mellitus (T2DM) is associated with increased risk of malignant ventricular arrhythmias. Cardiac electrical inhomogeneity may be the leading cause of the increased arrhythmic risk in patients with T2DM. The peak and the end of the T wave (Tp-e) interval and associated Tp-e/QT ratio are promising measures of ventricular repolarization indicating transmural dispersion of repolarization. The aim of this study was to assess ventricular repolarization in patients with T2DM by using Tp-e interval, Tp-e/QT ratio and Tp-e/corrected QT interval (QTc) ratio.MethodsForty-three patients with T2DM and 43 healthy control subjects, matched by gender and age, were studied. All participants underwent electrocardiography (ECG) recording. PR, RR and QT intervals represents the ECG intervals. These are not abbreviations. In all literature these ECG intervals are written like in this text. Tp-e intervals were measured from 12-lead ECG. Rate QTc was calculated by using the Bazett's formula. Tp-e/QT ratio and Tp-e/QTc ratio were also calculated.ResultsMean Tp-e interval was significantly prolonged in patients with T2DM compared to controls (79.4±10.3, 66.4±8.1 ms, respectively; P<0.001). We also found significantly higher values of Tp-e/QT ratio and Tp-e/QTc ratio in patients with diabetes than controls (0.21±0.03, 0.17±0.02 and 0.19±0.02, 0.16±0.02, respectively; P<0.001). There was no difference in terms of the other ECG parameters between the groups.ConclusionTp-e interval, Tp-e/QT ratio and Tp-e/QTc ratio were prolonged in patients with T2DM. We concluded that T2DM leads to augmentation of transmural dispersion of repolarization suggesting increased risk for ventricular arrhythmogenesis.

Can QT/RR relationship differentiate between low- and high-risk patients with hypertrophic cardiomyopathy?

Abnormal dynamicity of repolarization is considered to be a marker of myocardial vulnerability contributing to increased risk of arrhythmic events and sudden death. However, little is known about QT dynamics in hypertrophic cardiomyopathy (HCM). In this study, we aimed to evaluate ventricular repolarization by QT dynamicity in patients with HCM, focusing on its value to define if it is able to differentiate among low- and high-risk HCM patients. The linear regression slopes of the QT interval, measured to the apex and to the end of the T wave plotted against RR intervals (QTapex/RR and QTend/RR slopes, respectively) were calculated from 24-hour Holter recordings using a standard algorithm in 36 HCM patients and 64 control subjects. QTapex/RR and QTend/RR slopes were significantly steeper in the HCM patients in contrary to healthy control subjects (QTapex/RR = 0.22 + 0.08 vs 0.20 + 0.05, P = 0.0367; QTend/RR = 0.25 + 0.10 vs 0.20 + 0.06, P = 0.023). Moreover, the slopes of QTend/RR and QTapex/RR of high-risk patients were significantly steeper than those of control subjects while no significant differences were found among low-risk HCM patients and control subjects and only QTe/RR of high-risk patients was significantly different between low- and high-risk HCM patients. Our study results suggest that QT dynamicity is impaired in patients with HCM and may help to differentiate among low- and high-risk patients. Further studies are needed to elucidate the prognostic significance and clinical implications of impaired ventricular repolarization in patients with HCM.

The Presence of Electromechanical Mismatch In Nonischemic Dilated Cardiomyopathy Is Associated With Ventricular Repolarization Instability

BackgroundWe analyzed electromechanical mismatch (EMM) and its relationship to ventricular repolarization in patients with nonischemic dilated cardiomyopathy (DCM). Methods and ResultsIn 39 DCM patients with left ventricular ejection fraction (LVEF) <40% and New York Heart Association functional class ≥III, electroanatomic mapping was used to quantify areas of EMM. High-resolution electrocardiograph was used to measure heart rate variability (HRV) and QT variability index (QTVI). EMM was present in 22 patients (56%, group 1), whereas 17 patients presented no mismatched segments (44%, group 2). The groups did not differ in age (56 ± 10 years in group 1 vs 57 ± 7 years in group 2; P = .82), sex (male: 82% vs 94%; P = .40), LVEF (27 ± 8% vs 25 ± 6%; P = .18), or N-terminal pro–B-type natriuretic peptide (2,350 pg/mL vs 2,831 pg/mL; P = .32). Although heart rate and HRV were similar in both groups (rate: 80 ± 20 beats/min in group 1 vs 74 ± 19 beats/min in group 2 [P = .47]; standard deviation of normal-to normal RR intervals: 106 ± 79 vs 88 ± 115 [P = .61]), we found significantly higher QTVI values in patients from group 1 (−1.15 ± 0.46 vs −1.62 ± 0.51 in group 2; P = .005). In patients with implantable cardioverter-defibrillators, ventricular arrhythmias recorded ≤1 year before enrollment were more frequent in group 1 than in group 2 (58% vs 13%; P = .02). ConclusionsEMM is present in a majority of patients with DCM and is associated with ventricular repolarization instability.

Intravenous amiodarone homogeneously prolongs ventricular repolarization in patients with life-threatening ventricular tachyarrhythmia

BackgroundThe most critical adverse effects of class III drugs are marked QT prolongation and torsade de pointes. Even though intravenous amiodarone (iv-Amio) is a representative class III drug, it peculiarly inhibits both clinical ventricular tachycardia/fibrillation (VT/VF) and proarrhythmic effects.To test the hypothesis that iv-Amio homogeneously prolongs repolarization, we evaluated electrocardiographic changes before and during short-term amiodarone therapy, focusing closely on the ventricular dispersion of repolarization. MethodsTwenty-seven consecutive patients treated with iv-Amio for VT/VF as a first-line antiarrhythmic therapy were enrolled in this study. Twelve-lead electrocardiography was recorded before and during amiodarone therapy to evaluate the following electrocardiographic intervals: R–R, QRS, QT, QRS to T-peak (QTp), and T-peak to T-end (Tp-e; as an index of dispersion of repolarization). Repolarization indices were corrected to the heart rate by Bazett's method (QTc, c-QTp, c-Tp-e). ResultsAmiodarone suppressed VT/VF in 19/27 (70%) patients without conferring any proarrhythmic effect. The QTc, c-QTp, and R–R interval were significantly prolonged during amiodarone (476±45ms vs 511±45ms, p<0.05; 338±40ms vs 364±35ms, p<0.05; 762±272ms vs 870±189ms, p<0.05; respectively), whereas the c-Tp-e and QRS durations did not change significantly (139±33ms vs 145±41ms, p=0.25; 96±20ms vs 97±21ms, p=0.33; respectively). ConclusionsIv-Amio homogeneously prolongs repolarization and properly inhibits original VT/VF recurrence without inducing torsade de pointes.

New markers for ventricular repolarization in coronary slow flow: Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio.

Coronary slow flow (CSF) is characterized by normal or near-normal coronary arteries with delayed opacification of the distal vasculature that it may cause angina pectoris, acute myocardial infarction, life-threatening arrhythmias, and sudden cardiac death. The Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio are also known as predictors of ventricular arrhythmogenesis. The aim of this study was to assess ventricular repolarization in patients with CSF by using Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. This study included 50 patients with CSF and 51 control subjects. Coronary flow rates of all subjects were documented by thrombolysis in myocardial infarction (TIMI) frame count (TFC). Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio were measured from the 12-lead electrocardiogram. These parameters were compared between groups. In electrocardiographic parameters analysis, QT, QTc, QTd, and QTcd were significantly increased in CSF patients compared with the control subjects (P < 0.001, P = 0.019, P < 0.001, P < 0.001, respectively). The Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio in the CSF patients were significantly higher than those in the control subjects (Tp-e: 117 ± 21 milliseconds [ms] vs 96 ± 16 ms, P < 0.001; Tp-e/QT: 0.30 ± 0.06 vs 0.27 ± 0.06, P = 0.005; Tp-e/QTc: 0.27 ± 0.06 vs 0.24 ± 0.05, P < 0.001). In the multivariate analysis, increased Tp-e and Tp-e/QT ratio were associated with CSF. Our study revealed that when compared to the control subjects, Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc were significantly increased in the CSF patients.

Does glycemic control reverse dispersion of ventricular repolarization in type 2 diabetes?

BackgroundAbnormal ventricular repolarization is a predictor of cardiovascular mortality. In this study, we tested the hypothesis that glycemic control reverses abnormal ventricular repolarization in patients with type 2 diabetes.MethodsWe analyzed longitudinal changes in repolarization indices of electrocardiograms in retrospectively enrolled 44 patients with type 2 diabetes and 44 age-matched healthy subjects.ResultsIn the diabetic group, BMI was greater, levels of HbA1c (10.0 ± 1.6 vs. 5.6 ± 0.3%) and triglyceride were higher and level of HDL cholesterol was lower than those in the control group. Although mean QTc intervals were similar (413.6 ± 18.5 vs. 408.3 ± 22.7 ms), QT dispersion (41.8 ± 15.4 vs. 28.7 ± 7.7 ms) and Tpeak-Tend in lead V5 (83.6 ± 13.6 vs. 71.3 ± 10.3 ms) were significantly longer in the diabetic group than in the control group, indicating increased heterogeneity of ventricular repolarization in type 2 diabetes. During follow-up of 36 patients in the diabetic group for 787 ± 301 days, HbA1c level decreased to 7.3 ± 1.6%, while BMI did not significantly change. In contrast to HbA1c, QT dispersion (45.8 ± 15.0 ms) and Tpeak-Tend in lead V5 (83.6 ± 10.6 ms) were not significantly reduced during the follow-up period. There was no correlation between the change in HbA1c and the change in QT dispersion or Tpeak-Tend.ConclusionsIncreased heterogeneity of ventricular repolarization in type 2 diabetic patients was not reduced during the relatively short follow-up period despite significantly improved glycemic control.

Evaluation of Tpe interval and Tpe/QT ratio in patients with slow coronary flow.

Objective:Slow coronary flow (SCF) phenomenon is described as the delayed opacification of the distal vasculature and angiographically normal coronary arteries. Considerable studies have suggested that the interval from the peak to the end of the electrocardiographic T wave (Tpe) may correspond to the transmural dispersion of repolarization and that increased Tpe interval and Tpe/QT ratio are associated with malignant ventricular arrhythmias. In this study, we intended to evaluate ventricular repolarization in patients with SCF by using the Tpe interval and Tpe/QT ratio.Methods:The study population included 33 patients with angiographically proven SCF and 33 control patients with angiographically proven normal coronary arteries without associated SCF. Coronary flow rates of patients and the control group were documented by TIMI (Thrombolysis in Myocardial Infarction) frame count. From the electrocardiograms, Tpe interval and Tpe/QT ratio were calculated and compared between groups.Results:No statistically significant difference was found between the two groups in terms of basic characteristics. Mean Tpe interval, Tpe/QT ratio, and Tpe/QTc ratio were prolonged in the study group compared to the control group (p<0.001).Conclusion:Tpe interval and Tpe/QT ratio were increased in SCF patients.

Effect of intravenous amiodarone on QT and T peak–T end dispersions in patients with nonischemic heart failure treated with cardiac resynchronization-defibrillator therapy and electrical storm

BackgroundThe effect of intravenous amiodarone on spatial and transmural dispersion of ventricular repolarization in patients receiving cardiac resynchronization therapy (CRT) remains unclear. MethodsWe studied 14 patients with nonischemic heart failure who received CRT with a defibrillator, experienced electrical storm and were treated with intravenous amiodarone. Each patient underwent 12-lead electrocardiography (ECG) and 187-channel repolarization interval-difference mapping electrocardiography (187-ch RIDM-ECG) before and during the intravenous administration of amiodarone infusion. ResultsA recurrence of ventricular tachyarrhythmia was observed in 2 patients during the early period of intravenous amiodarone therapy. Intravenous amiodarone increased the corrected QT interval (from 470±52ms to 508±55ms, P=0.003), but it significantly decreased the QT dispersion (from 107±35ms to 49±27ms, P=0.001), T peak–T end (Tp–e) dispersion (from 86±17ms to 28±28ms, P=0.001), and maximum inter-lead difference between corrected Tp–e intervals as measured by using the 187-ch RIDM-ECG (from 83±13ms to 50±19ms, P=0.001). ConclusionsIntravenous amiodarone suppressed the electrical storm and decreased the QT and Tp–e dispersions in patients treated by using CRT with a defibrillator.

Associations of Hemodynamic Load and Ventricular Repolarization in Patients With Newly Diagnosed Essential Hypertension: A Long‐Term Follow‐Up Study

The evolution of QT interval and its dispersion (QTd) were studied in 135 newly diagnosed nondiabetic patients, as well as the relationship between changes of these left ventricular (LV) repolarization parameters with blood pressure (BP) and LV mass changes, which were prospectively studied for a median period of 3.8 years. At baseline and at last follow-up visit, all patients underwent ambulatory BP monitoring, echocardiographic assessment, and 12-lead electrocardiography. At the end of follow-up, responders of antihypertensive treatment based on a reduced 24-hour systolic BP (n=122) exhibited a reduction in LV mass index (by 7.6 g/m2, P<.001) and corrected QT (by 4.3, P=.038), while corrected QTd was unchanged. In nonresponders (n=13), although no difference in LV mass index was observed, corrected QT increased by 12.4 ms (P=.048) and corrected QTd by 8.2 ms (P=.027). Changes in parameters of LV repolarization were related to BP changes but not to changes of myocardial size.

Effect of cardiac resynchronization therapy on ventricular repolarization: A meta-analysis

Objective:Cardiac resynchronization therapy (CRT) was thought to have a proarrhythmic effect on ventricular repolarization. But the results of previous studies were inconsistent. The aim of this study was to determine the effect of CRT on ventricular repolarization.Methods:A meta-analysis of studies focused on the effect of CRT on ventricular repolarization in patients undergoing CRT was conducted. Endpoints including QT interval (QT), JT interval (JT), QT dispersion(QTD) and interval between the peak to end of T wave (Tp-e).Results:A total of 14 studies were included in our meta-analysis. After pooling the data, no significant difference was observed in QT, JT and Tp-e between biventricular (BV) pacing and intrinsic ventricular rhythm. BV paced QTD was lower than intrinsic QTD, but the significance was ambiguous [mean difference (MD): -17.33, 95% CI -34.44 to -0.22, p=0.05]. Left ventricular (LV) paced Tp-e was significantly longer than intrinsic Tp-e (MD: 21.44, 95% CI 2.37 to 40.51, p=0.03). No significant difference was observed in QT, JT and QTD between LV pacing and intrinsic ventricular rhythm.Conclusion:In patients undergoing CRT, BV pacing has no deteriorating effect on ventricular repolarization, but LV pacing has a prolonging effect on Tp-e.

No association between high-density lipoprotein levels and ventricular repolarization indexes in subjects with primary hypercholesterolemia

Objective. Data regarding the effect of lipid parameters on repolarization are sparse. Recent data indicate that reconstituted HDL administration shortens repolarization in cardiomyocytes as well as the corrected QT (QTc) interval in human subjects. We investigated the potential association of high-density lipoprotein cholesterol (HDL-C) levels with conventional and novel electrocardiographic markers of ventricular repolarization in patients with hypercholesterolemia. Methods. Consecutive subjects with primary hypercholesterolemia were recruited. We recorded clinical and laboratory parameters as well as electrocardiographic indexes. With regard to ventricular repolarization, we calculated the QTc interval, the T peak-to-end (Tpe) interval, and the Tpe/QT ratio. Results. The study population consisted of 440 patients (199 men) with a median age of 56 [48–65] years. The correlation analysis (Spearman's) failed to show any association between HDL-C and any of the studied electrocardiographic parameter. Moreover, no correlation between other lipid parameters and the electrocardiograhic indexes was evident. Also, a comparison of the ventricular repolarization parameters between different HDL-C quartile groups (HDL-Q1: ≤ 1.11 mmol/L; HDL-Q2: 1.12–1.29 mmol/L; HDL-Q3: 1.30–1.53 mmol/L; HDL-Q4: ≥ 1.54 mmol/L) was performed. Specifically, the differences in QTc (p: 0.372), Tpe in leads II (p: 0.356), V2 (p: 0.372), V5 (p: 0.112), and Tpe/QT in leads II (p: 0.348), V2 (p: 0.162), V5 (p: 0.122) were not significant. Conclusion. HDL-C levels are not associated with the QTc interval or indexes of repolarization dispersion in patients with primary hypercholesterolemia. The potential antiarrhythmic efficacy of HDL should be further evaluated in the setting of myocardial ischemia where dynamic changes in the heterogeneity of ventricular repolarization ensue.

Effect of buspirone hydrochloride on dispersion of ventricular repolarization in patients with anxiety and depressive disorders and ischemic heart failure

Objectives: The purpose of the study was to investigate the effect of buspirone hydrochloride on QT interval dispersion (DQT) in patients with chronic heart failure (CHF) of ischemic etiology with anxiety and depressive disorders. Methods: 102 patients (65 males, 37 females; mean age 67.4±9.5) NYHA II-IV were randomized in the study. All the patients were prescribed buspirone hydrochloride 10 mg t.i.d. due to anxiety and depressive disorders. All the patients had II-III functional classes of angina, 67 of them (65.7%) had history of myocardial infarction. Randomized patients received standard CHF and coronary heart disease therapy. Informed consents were signed before the study initiation. Exclusion criteria were history of mental disorders, significant impairment of cognitive functions, alcohol/drug abuse, other psychoactive drug intake, severe concomitant pathology. Initially and in 3 months of buspirone hydrochloride intake rest ECG was recorded in 12 standard leads, 50 mm/s and QT (DQT) and QTc (DQTc) dispersions were calculated by the standard technique (DQT = QTmax-Qcmin, DQTc = QTcmax-QTcmin). Statistical data processing was carried out by using the program Statistica 8.0. Data was reported as mean ± standard deviation. The significance of differences was determined by Student's t-test. Results: Initially mean DQT and DQTc were 41.5 ± 13.0 ms and 36.0 ± 9.8 ms, respectively. At re-examination mean DQT was 43.9 ± 14.8 ms (p>0.05), and DQTc -37.5 ± 10.9 ms (p>0.05). Thus, indices of ventricular repolarization dispersion before and after 3 months of buspirone hydrochloride intake had no statistically significant differences. Conclusion: Buspirone hydrochloride treatment did not lead to an increase in dispersion of ventricular repolarization in the patients with ischemic CHF.

The association of premature ovarian failure with ventricular repolarization dynamics evaluated by QT dynamicity

The association between premature ovarian failure (POF) and cardiovascular diseases has been investigated in a few studies, but none have looked at ventricular repolarization abnormalities in these patients. In this study, we aimed to evaluate the ventricular repolarization by QT dynamicity in patients with POF. We enrolled 26 female patients (mean age 37.5 ± 10.1 years) with primary POF and 31 healthy female subjects (mean age 37.5 ± 9.0 years). The linear regression slopes of the QT interval measured to the apex and to the end of the T-wave plotted against RR intervals (QTapex/RR and QTend/RR slopes, respectively) were calculated from 24 h Holter recordings using a standard algorithm. QTapex/RR and QTend/RR slopes were more steeper in the POF patients in contrary to healthy control subjects (QTapex/RR = 0.184 ± 0.022 vs. 0.131 ± 0.019, P < 0.001; QTend/RR = 0.164 ± 0.021 vs. 0.128 ± 0.018, P < 0.001). Pearson's correlation analyses revealed a stronger negative correlation between oestradiol (E2) and QTapex/RR (r = -0.715, P < 0.001). There was also a moderate negative correlation between E2 and QTend/RR (r = -0.537, P < 0.001). Serum follicle-stimulating hormone level was positively correlated with QTapex/RR (r = 0.681, P < 0.001) and QTend/RR (r = 0.531, P < 0.001). Our study results suggest that QT dynamicity is impaired in patients with POF despite the absence of overt cardiovascular involvement. Further studies are needed to elucidate the prognostic significance and clinical implications of impaired ventricular repolarization in patients with POF.

Slower heart rate and altered rate dependence of ventricular repolarization in patients with lone atrial fibrillation

Electrophysiological alterations in atrial fibrillation (AF) may be genetically based and may lead to changes in ventricular repolarization. Short QT syndrome is a rare channelopathy with abbreviated ventricular repolarization and a propensity for AF. To determine if minor unrecognized forms of short QT syndrome can explain some cases of lone AF. We prospectively compared QT intervals in 66 patients with idiopathic lone AF and 132 age- and sex-matched controls. QT intervals were measured during sinus rhythm in each of the 12 surface electrocardiogram leads and corrected using Bazett's formula (QTc). QT intervals were also corrected using other formulae. Uncorrected QT and heart rate regression lines were compared between AF patients and controls. AF patients presented with a slower resting heart rate (64 ± 10 beats per minute [bpm] vs 69 ± 9 bpm; P=0.0006). QTc intervals were shorter in AF patients in 11/12 electrocardiogram leads (significant in 7/12, borderline in 2/12; mean QTc 381 ± 21 ms vs 388 ± 22 ms; P=0.02). QTc intervals were also shorter in AF patients, significantly or not, using other correction formulae. For similar heart rates, uncorrected QT intervals were shorter in patients when heart rates were greater than 70 bpm and longer when heart rates were less than 60 bpm. AF patients displayed steeper QT/heart rate regression line slopes than controls (P=0.009). Heart rate is significantly slower and the rate dependence of ventricular repolarization is significantly altered in patients with lone AF compared with controls. Further study is warranted to determine if AF induces subsequent ventricular repolarization changes or if these modifications are caused by an underlying primary electrical disease.

The relationship between left ventricular scar and ventricular repolarization in patients with coronary artery disease: insights from late gadolinium enhancement magnetic resonance imaging

The markers of ventricular repolarization corrected QT interval (QTc), QT dispersion (QTD) and Tpeak-to-Tend interval (Tpeak-end) have shown an association with sudden cardiac death (SCD) in the general population. However, their mechanistic relationship with SCD is unclear. The study aim was to evaluate the relationship between QTc, QTD, and Tpeak-end, and the extent and distribution of left ventricular (LV) scar in patients with coronary artery disease at high SCD risk. We included 64 consecutive implantable cardioverter defibrillator (ICD) recipients (66 ± 11 years, 80% male, median left ventricular ejection fraction 30%) who had undergone late gadolinium enhancement cardiac magnetic resonance (CMR) imaging prior to device implantation over 4 years. Scar was quantified using the CMR images and characterized in terms of percent LV scar and number of LV segments with subendocardial/transmural scar. Repolarization parameters were measured on an electrocardiogram performed prior to ICD implantation. After adjustment for potential confounders there was a strong association between the number of limited subendocardial (1-25% transmurality) scar segments and QTc (P = 0.003), QTD (P = 0.002), and Tpeak-end (P = 0.008). However, there was no association between the repolarization parameters and percent LV scar or the amount of transmural scar. During a mean follow-up of 19 ± 10 months 19 (30%) patients received appropriate ICD therapy, but none of the repolarization parameters were associated with its occurrence. In this pilot study there was a strong association between limited subendocardial LV scar and prolonged QTc, QTD, and Tpeak-end. However, there was no association between any of these repolarization markers and the delivery of appropriate ICD therapy.

Tp‐e Interval, Tp‐e/QT Ratio, and Tp‐e/QTc Ratio are Prolonged in Patients with Moderate and Severe Obstructive Sleep Apnea

Prolongation of the peak and the end of T wave (Tp-e) has been reported to be associated with ventricular arrhythmias. Tp-e/QT ratio and Tp-e/QTc ratio are used as an index of ventricular arrhythmogenesis. An increased incidence of ventricular arrhythmias has been reported in patients with obstructive sleep apnea (OSA). The aim of this study was to assess ventricular repolarization in patients with OSA by using Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. We have studied 72 patients who underwent overnight polysomnography (PSG) between the years 2010-2011 at our institution. Patients with moderate and severe OSA (23 patients; mean age: 45±10), according to the apnea-hypopnea index, constituted the study group. Patients with normal PSG (23 patients; mean age: 42±11) were used as the control group. In all patients, Tp-e interval, Tp-e/QT ratio, Tp-e/QTc ratio, as well as some other electrocardiogram intervals were measured. Independent samples t-tests were used for comparison of continuous and categorical variables and correlations were calculated by Spearman rank correlation. Although QT and QTc intervals were not different between the groups, mean Tp-e interval (81.6±11.1 msn; 63.9±7.3 msn; respectively; P < 0.001), Tp-e/QT ratio (0.21±0.03; 0.17±0.02; respectively; P < 0.001), and Tp-e/QTc ratio (0.20±0.03; 0.16±0.02; respectively; P < 0.001) were prolonged in the study group compared to the control group. Correlation analysis showed a significant positive correlation between the presence of moderate and severe OSA and Tp-e interval (r = 0.72; P < 0.001), Tpe/QT ratio (r = 0.70; P < 0.001), and Tp-e/QTc ratio (r = 0.70; P < 0.001). Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio are prolonged in patients with moderate and severe OSA patients. There is a positive correlation between the presence of OSA and Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio.

Sympathetic stimulation increases dispersion of repolarization in humans with myocardial infarction

The sympathetic nervous system is thought to play a key role in genesis and maintenance of ventricular arrhythmias. The myocardial effect of sympathetic stimulation on myocardial repolarization in humans is poorly understood. The purpose of this study was to evaluate the effects of direct and reflex sympathetic stimulation on ventricular repolarization in patients with postinfarct cardiomyopathy (ICM). The effects of direct sympathetic stimulation were assessed using isoproterenol, while those of reflex sympathetic stimulation were assessed with nitroprusside infusion in ICM patients (n = 5). Five patients without cardiomyopathy were also studied. Local repolarization was measured from intracardiac electrograms that were used to calculate the activation recovery interval (ARI), a surrogate of action potential duration. Isoproterenol significantly increased heterogeneity in repolarization in patients with ICM; the decrease in ARI from baseline was 72.9 ± 9.1 ms in more viable regions, 64.5 ± 8.9 ms in the scar, and 54.9 ± 9.1 ms in border zones (P = 0.0002 and 0.014 comparing normal and scar to border zones, respectively). In response to nitroprusside, the ARI at the border zones decreased significantly more than either scar or surrounding viable myocardium, which showed an increase in ARI (P = 0.014 and 0.08 comparing normal tissue and scar to border zones, respectively). Furthermore, isoproterenol increased ARI dispersion by 70%, while nitroprusside increased ARI dispersion by 230% when ICM patients were compared to those with structurally normal hearts (P = 0.0015 and P < 0.001, respectively). In humans, both direct and reflex sympathetic stimulations increase regional differences in repolarization. The normal tissue surrounding the scar appears denervated. Dispersion of ARI in response to sympathetic stimulation is significantly increased in patients with ICM.