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The ECG diagnosis of LVH is predominantly based on the QRS voltage criteria. The classical paradigm postulates that the increased left ventricular mass generates a stronger electrical field, increasing the leftward and posterior QRS forces, reflected in the augmented QRS amplitude. However, the low sensitivity of voltage criteria has been repeatedly documented. We discuss possible reasons for this shortcoming and proposal of a new paradigm. The theoretical background for voltage measured at the body surface is defined by the solid angle theorem, which relates the measured voltage to spatial and non-spatial determinants. The spatial determinants are represented by the extent of the activation front and the distance of the recording electrodes. The non-spatial determinants comprise electrical characteristics of the myocardium, which are comparatively neglected in the interpretation of the QRS patterns. Various clinical conditions are associated with LVH. These conditions produce considerable diversity of electrical properties alterations thereby modifying the resultant QRS patterns. The spectrum of QRS patterns observed in LVH patients is quite broad, including also left axis deviation, left anterior fascicular block, incomplete and complete left bundle branch blocks, Q waves, and fragmented QRS. Importantly, the QRS complex can be within normal limits. The new paradigm stresses the electrophysiological background in interpreting QRS changes, i.e., the effect of the non-spatial determinants. This postulates that the role of ECG is not to estimate LV size in LVH, but to understand and decode the underlying electrical processes, which are crucial in relation to cardiovascular risk assessment., (© 2023 The Authors. Annals of Noninvasive Electrocardiology published by Wiley Periodicals LLC.)

Background Race is an established risk factor for sudden cardiac death (SCD). We sought to determine whether the association of electrophysiological substrate with SCD varies between black and white individuals. Methods and Results Participants from the ARIC (Atherosclerosis Risk in Communities) study with analyzable ECGs (n=14 408; age, 54±6 years; 74% white) were included. Electrophysiological substrate was characterized by ECG metrics. Two competing outcomes were adjudicated: SCD and non-SCD. Interaction of ECG metrics with race was studied in Cox proportional hazards and Fine-Gray competing risk models, adjusted for prevalent cardiovascular disease, risk factors, and incident nonfatal cardiovascular disease. At the baseline visit, adjusted for age, sex, and study center, blacks had larger spatial ventricular gradient magnitude (0.30 mV; 95% CI, 0.25-0.34 mV), sum absolute QRST integral (18.4 mV*ms; 95% CI, 13.7-23.0 mV*ms), and Cornell voltage (0.30 mV; 95% CI, 0.25-0.35 mV) than whites. Over a median follow-up of 24.4 years, SCD incidence was higher in blacks (2.86 per 1000 person-years; 95% CI, 2.50-3.28 per 1000 person-years) than whites (1.37 per 1000 person-years; 95% CI, 1.22-1.53 per 1000 person-years). Blacks with hypertension had the highest rate of SCD: 4.26 (95% CI, 3.66-4.96) per 1000 person-years. Race did not modify an association of ECG variables with SCD, except QRS-T angle. Spatial QRS-T angle was associated with SCD in whites (hazard ratio, 1.38; 95% CI, 1.25-1.53) and hypertension-free blacks (hazard ratio, 1.52; 95% CI, 1.09-2.12), but not in blacks with hypertension (hazard ratio, 1.15; 95% CI, 0.99-1.32) ( P -interaction=0.004). Conclusions Race did not modify associations of electrophysiological substrate with SCD and non-SCD. Electrophysiological substrate does not explain racial disparities in SCD rate.

Background: The risk of sudden cardiac death (SCD) is known to be dynamic. However, the accuracy of a dynamic SCD prediction is unknown. We aimed to measure the dynamic predictive accuracy of ECG biomarkers of SCD and competing non-sudden cardiac death (non-SCD)., Methods: Atherosclerosis Risk In Community study participants with analyzable ECGs in sinus rhythm were included (n = 15,716; 55% female, 73% white, age 54.2 ± 5.8 y). ECGs of 5 follow-up visits were analyzed. Global electrical heterogeneity and traditional ECG metrics (heart rate, QRS, QTc) were measured. Adjudicated SCD was the primary outcome; non-SCD was the competing outcome. Time-dependent area under the receiver operating characteristic curve (ROC(t) AUC) analysis was performed to assess the prediction accuracy of a continuous biomarker in a period of 3,6,9 months, and 1,2,3,5,10, and 15 years using a survival analysis framework. Reclassification improvement as compared to clinical risk factors (age, sex, race, diabetes, hypertension, coronary heart disease, stroke) was measured., Results: Over a median 24.4 y follow-up, there were 577 SCDs (incidence 1.76 (95%CI 1.63-1.91)/1000 person-years), and 829 non-SCDs [2.55 (95%CI 2.37-2.71)]. No ECG biomarkers predicted SCD within 3 months after ECG recording. Within 6 months, spatial ventricular gradient (SVG) elevation predicted SCD (AUC 0.706; 95%CI 0.526-0.886), but not a non-SCD (AUC 0.527; 95%CI 0.303-0.75). SVG elevation more accurately predicted SCD if the ECG was recorded 6 months before SCD (AUC 0.706; 95%CI 0.526-0.886) than 2 years before SCD (AUC 0.608; 95%CI 0.515-0.701). Within the first 3 months after ECG recording, only SVG azimuth improved reclassification of the risk beyond clinical risk factors: 18% of SCD events were reclassified from low or intermediate risk to a high-risk category. QRS-T angle was the strongest long-term predictor of SCD (AUC 0.710; 95%CI 0.668-0.753 for ECG recorded within 10 years before SCD)., Conclusion: Short-term and long-term predictive accuracy of ECG biomarkers of SCD differed, reflecting differences in transient vs. persistent SCD substrates. The dynamic predictive accuracy of ECG biomarkers should be considered for competing SCD risk scores. The distinction between markers predicting short-term and long-term events may represent the difference between markers heralding SCD (triggers or transient substrates) versus markers identifying persistent substrate.

Background: Phthalates are used as plasticizers in the manufacturing of flexible, plastic medical products. Patients can be subjected to high phthalate exposure through contact with plastic medical devices. We aimed to investigate the cardiac safety and biocompatibility of mono-2-ethylhexyl phthalate (MEHP), a phthalate with documented exposure in intensive care patients., Methods: Optical mapping of transmembrane voltage and pacing studies were performed on isolated, Langendorff-perfused rat hearts to assess cardiac electrophysiology after MEHP exposure compared with controls. MEHP dose was chosen based on reported blood concentrations after an exchange transfusion procedure., Results: Thirty-minute exposure to MEHP increased the atrioventricular node (147 versus 107 ms) and ventricular (117 versus 77.5 ms) effective refractory periods, compared with controls. Optical mapping revealed prolonged action potential duration at slower pacing cycle lengths, akin to reverse use dependence. The plateau phase of the action potential duration restitution curve steepened and became monophasic in MEHP-exposed hearts (0.18 versus 0.06 slope). Action potential duration lengthening occurred during late-phase repolarization resulting in triangulation (70.3 versus 56.6 ms). MEHP exposure also slowed epicardial conduction velocity (35 versus 60 cm/s), which may be partly explained by inhibition of Na v 1.5 (874 and 231 µmol/L half-maximal inhibitory concentration, fast and late sodium current)., Conclusions: This study highlights the impact of acute MEHP exposure, using a clinically relevant dose, on cardiac electrophysiology in the intact heart. Heightened clinical exposure to plasticized medical products may have cardiac safety implications-given that action potential triangulation and electrical restitution modifications are a risk factor for early after depolarizations and cardiac arrhythmias.

Background: A few studies have recently reported clockwise and counterclockwise rotations of QRS transition zone as predictors of mortality. However, their prospective correlates and associations with individual cardiovascular disease (CVD) outcomes are yet to be investigated., Methods and Results: Among 13 567 ARIC (Atherosclerosis Risk in Communities) study participants aged 45 to 64 years, we studied key correlates of changes in the status of clockwise and counterclockwise rotation over time as well as the association of rotation status with incidence of coronary heart disease (2408 events), heart failure (2196 events), stroke (991 events), composite CVD (4124 events), 898 CVD deaths, and 3469 non-CVD deaths over 23 years of follow-up. At baseline, counterclockwise rotation was most prevalent (52.9%), followed by no (40.5%) and clockwise (6.6%) rotation. Of patients with no rotation, 57.9% experienced counterclockwise or clockwise rotation during follow-up, with diabetes mellitus and black race significantly predicting clockwise and counterclockwise conversion, respectively. Clockwise rotation was significantly associated with higher risk of heart failure (hazard ratio, 1.20; 95% confidence interval [CI], 1.02-1.41) and non-CVD death (hazard ratio, 1.28; 95% CI, 1.12-1.46) after adjusting for potential confounders including other ECG parameters. On the contrary, counterclockwise rotation was significantly related to lower risk of composite CVD (hazard ratio, 0.93; 95% CI, 0.87-0.99]), CVD mortality (hazard ratio, 0.76; 95% CI, 0.65-0.88), and non-CVD deaths (hazard ratio, 0.92; 95% CI, 0.85-0.99 [borderline significance with heart failure])., Conclusions: Counterclockwise rotation, the most prevalent QRS transition zone pattern, demonstrated the lowest risk of CVD and mortality, whereas clockwise rotation was associated with the highest risk of heart failure and non-CVD mortality. These results have implications on how to interpret QRS transition zone rotation when ECG was recorded., (© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)

Background: Several reports have demonstrated that prolongation of the QT interval is associated with sudden cardiac death (SCD). However, it is unknown whether any of the components within the QT interval are responsible for its association with SCD., Methods and Results: We examined the association of the individual QT-interval components (R-wave onset to R-peak, R-peak to R-wave end, ST-segment, T-wave onset to T-peak, and T-peak to T-wave end) with SCD in 12 241 participants (54±5.7 years; 26% black; 55% women) from the ARIC study (Atherosclerosis Risk in Communities). The QT interval and its components were measured at baseline (1987-1989) from 12-lead ECGs. SCD cases were adjudicated by a group of physicians through December 31, 2012. During a median follow-up of 23.6 years, a total of 346 cases of SCD were identified. Although prolongation of the QT interval was associated with a 49% increased risk of SCD (hazard ratio, 1.49; 95% confidence interval, 1.01-2.18), only the T-wave onset to T-peak component (per 1-SD increase: hazard ratio, 1.19; 95% confidence interval, 1.06-1.34) was associated with SCD and not any of the other components in separate models. When all of the QT-interval components were included in the same model, T-wave onset to T-peak remained the strongest predictor of SCD (per 1-SD increase: hazard ratio, 1.21; 95% confidence interval, 1.06-1.37)., Conclusions: The risk of SCD with the QT interval is driven by prolongation of the T-wave onset to T-peak component. This suggests that shifting the focus from the overall QT interval to its individual components will refine SCD prediction in the community., (© 2017 American Heart Association, Inc.)

Denervated post-infarct scar is arrhythmogenic. Our aim was to compare QRS frequency content in denervated and innervated left ventricular (LV) scar. In-vivo single lead ECG telemetry device was implanted in 17 heterozygous PTPσ (HET) and 7 lacking PTPσ (KO) transgenic mice. Myocardial infarction (MI) with reperfusion and sham surgery was performed. HET mice developed a denervated scar, whereas KO mice developed innervated scar. The power spectral density was used to assess the QRS frequency content. Denervated as compared to innervated post-MI scar was characterized by the higher relative contribution of 300-500 Hz (14 ± 1 vs. 9 ± 1%; P = 0.001) but reduced relative contribution of 200-300 Hz (86 ± 1 vs. 91 ± 1%; P = 0.001). Norepinephrine concentration in peri-infarct zone correlated with both 1-200 Hz (r = 0.75; P = 0.03) and 200-500 Hz QRS power (r = 0.73; P = 0.04). Sympathetic fiber density within the infarct correlated with 200-300/200-500 Hz QRS power ratio (r = 0.56; P = 0.005). Intracellular sigma peptide injections in post-MI HET mice restored the QRS power., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The ventricular gradient, an electrocardiographic concept calculated by integrating the area under the QRS complex and T-wave, represents the degree and direction of myocardial electrical heterogeneity. Although the concept of the ventricular gradient was first introduced in the 1930s, it has not yet found a place in routine electrocardiography. In the modern era, it is relatively simple to calculate the ventricular gradient in three dimensions (the spatial ventricular gradient (SVG)), and there is now renewed interest in using the SVG as a tool for risk stratification of ventricular arrhythmias and sudden cardiac death. This manuscript will review the history of the ventricular gradient, describe its electrophysiological meaning and significance, and discuss its clinical utility., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Asymptomatic individuals account for the majority of sudden cardiac deaths (SCDs). Development of effective, low-cost, and noninvasive SCD risk stratification tools is necessary., Methods and Results: Participants from the Atherosclerosis Risk in Communities study and Cardiovascular Health Study (n=20 177; age, 59.3±10.1 years; age range, 44-100 years; 56% female; 77% white) were followed up for 14.0 years (median). Five ECG markers of global electric heterogeneity (GEH; sum absolute QRST integral, spatial QRST angle, spatial ventricular gradient [SVG] magnitude, SVG elevation, and SVG azimuth) were measured on standard 12-lead ECGs. Cox proportional hazards and competing risks models evaluated associations between GEH electrocardiographic parameters and SCD. An SCD competing risks score was derived from demographics, comorbidities, and GEH parameters. SCD incidence was 1.86 per 1000 person-years. After multivariable adjustment, baseline GEH parameters and large increases in GEH parameters over time were independently associated with SCD. Final SCD risk scores included age, sex, race, diabetes mellitus, hypertension, coronary heart disease, stroke, and GEH parameters as continuous variables. When GEH parameters were added to clinical/demographic factors, the C statistic increased from 0.777 to 0.790 (P=0.008), the risk score classified 10-year SCD risk as high (>5%) in 7.2% of participants, 10% of SCD victims were appropriately reclassified into a high-risk category, and only 1.4% of SCD victims were inappropriately reclassified from high to intermediate risk. The net reclassification index was 18.3%., Conclusions: Abnormal electrophysiological substrate quantified by GEH parameters is independently associated with SCD in the general population. The addition of GEH parameters to clinical characteristics improves SCD risk prediction., (© 2016 American Heart Association, Inc.)

Background: The goal of this study was to compare the time series predictors of beat-to-beat variability in repolarization in healthy individuals., Methods: Spatial QRS- and T-vector amplitudes, spatial QRS-T, RR' and TT' angles, RR' and QT intervals, and QRS- and T-loop roundness were measured on 453 consecutive sinus beats in 168 healthy subjects (mean age 39.8±15.6years; 50% men; 93% white). Panel time-series regression models were adjusted by age, sex, and race. Appropriate time series of ECG metrics served as predictors and outcomes., Results: Increase in T-loop roundness index by 0.1 was associated with 1.1° (95%CI 0.9-2.2; P=0.048) increase in corresponding TT' angle. One unit increase in a respiration index was associated with 4ms (95%CI 0.6-7.0; P=0.021) increase in QT interval., Conclusions: Spatial TT' angle and beat-to-beat variability in T-loop roundness represent intrinsic measures of repolarization variability. QT interval variability characterizes the effect of respiration and heart rate variability., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The spectrum of frequencies producing the QRS complex has not been fully explored. In this manuscript we review previous studies of QRS frequency content, and discuss our novel method of the conjoint analysis of the ECG signal in six dimensions: in the domain of three space dimensions, in time domain, and in frequency domain. Orbital frequency of QRS loop is introduced as a six-dimensional characteristic of ventricular conduction, which helped to reveal inapparent ventricular conduction, and to characterize electrophysiological substrate. In this paper, we review our novel method in the historical context., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Identifying individuals at risk for sudden cardiac death (SCD) is of critical importance. Electrocardiographic (ECG) deep terminal negativity of P wave in V1 (DTNPV1), a marker of left atrial abnormality, has been associated with increased risk of all-cause and cardiovascular mortality. We hypothesized that DTNPV1 is associated with increased risk of sudden cardiac death (SCD)., Methods and Results: This analysis included 15 375 participants (54.1±5.8 years, 45% men, 73% whites) from the Atherosclerosis Risk in Communities (ARIC) study. DTNPV1 was defined from the resting 12-lead ECG as presence of biphasic P wave (positive/negative) in V1 with the amplitude of the terminal negative phase >100 μV, or one small box on ECG scale. After a median of 14 years of follow-up, 311 cases of SCD occurred. In unadjusted Cox regression, DTNPV1 was associated with an 8-fold increased risk of SCD (HR 8.21; [95%CI 5.27 to 12.79]). Stratified by race and study center, and adjusted for age, sex, coronary heart disease (CHD), and ECG risk factors, as well as atrial fibrillation (AF), stroke, CHD, and heart failure (HF) as time-updated variables, the risk of SCD associated with DTNPV1 remained significant (2.49, [1.51-4.10]). DTNPV1 improved reclassification: additional 3.4% of individuals were appropriately reclassified into a higher SCD risk group, as compared with traditional CHD risk factors alone. In fully adjusted models DTNPV1 was associated with increased risk of non-fatal events: AF (5.02[3.23-7.80]), CHD (2.24[1.43-3.53]), HF (1.90[1.19-3.04]), and trended towards increased risk of stroke (1.88[0.99-3.57])., Conclusion: DTNPV1 is predictive of SCD suggesting its potential utility in risk stratification in the general population., (© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Background: Reproducibility of spatial TT' angle on the 10-second ECG and its agreement with QT variability has not been previously studied., Methods: We analyzed 2 randomly selected 10-second segments within 3-minute resting orthogonal ECG in 172 healthy IDEAL study participants (age 38.1±15.2years, 50% male, 94% white). Repolarization lability was measured by the QT variance (QTV), short-term QT variability (STV(QT)), and spatial TT' angle. Bland-Altman analysis was used to assess the agreement between different log-transformed metrics of repolarization lability, and to assess the reproducibility., Results: The heart rate showed a very high reproducibility (bias 0.14%, Lin's rho_c=0.99). As expected, noise suppression by averaging improves reproducibility. Agreement between two 10-second LogQTV was poor (bias -0.04; 95% limits of agreement [-1.89; 1.81]), while LogSTV(QT) (0.04 [-1.01; 1.10]), and especially LogTT' angle (-0.009 [-0.84; 0.82]) was better., Conclusion: TT' angle is a satisfactory reproducible metric of repolarization lability on the 10-second ECG., (Copyright © 2014 Elsevier Inc. All rights reserved.)

We examined whether there is a relationship between repolarization abnormalities on electrocardiography (EKG) and deformation abnormalities by echocardiography. Analysis of baseline EKGs and mechanical (echo-based deformation) changes was performed in 128 patients with a clinical diagnosis of hypertrophic cardiomyopathy (HCM). Patients with left ventricular hypertrophy (LVH) or repolarization abnormalities had higher septal thickness when compared to patients with normal EKG. Patients with EKG evidence of LVH or QTc prolongation had lower systolic velocity, systolic strain, systolic strain rate, late diastolic velocity, and late diastolic strain rate than patients with a normal EKG. Patients with strain pattern or ST depression/T-wave inversion had lower systolic velocity, systolic strain, systolic strain rate, early diastolic velocity, and late diastolic velocity when compared to patients with normal EKGs. LVH and repolarization abnormalities on surface EKG are markers of impaired systolic and diastolic mechanics in HCM.

Background: Experimental studies have demonstrated that unstable repolarization dynamics is a risk factor of arrhythmia. We have recently developed an algorithm to detect QT interval (QTI) instability from the clinical electrocardiogram (ECG)., Objective: To develop a clinical arrhythmia risk stratification index based on the detection of QTI instability., Methods: Intracardiac ECGs were recorded at rest in 114 patients with implanted implantable cardioverter-defibrillators (ICDs). Patients were followed up until appropriate implantable cardioverter-defibrillator therapy or death occurred, whichever came first. Each ECG recording was divided into 1-minute episodes (minECGs); the instability in QTI dynamics, if any, of each minECG was detected with our algorithm. An arrhythmia risk index termed QTI instability index (QTII) was defined as the number of minECGs with unstable QTI dynamics normalized by the number of minECGs with premature activations. The performance of QTII in arrhythmia risk stratification was examined with survival analysis and was compared with other risk indices, such as the mean RR interval (RRI), the standard deviation of the RRI and the QTI, and the frequency of premature activation. We hypothesized that the index QTII, which accounts for multiple risk factors and their interdependence, performs better than indices quantifying individual arrhythmia risk factors in the stratification of arrhythmia risk., Results: The results of survival analysis show that QTII outperformed all other studied indices in arrhythmia risk stratification and was the only independent indicator of arrhythmia propensity in a multivariate survival model., Conclusion: QTII is a promising arrhythmia risk stratification index., (Copyright © 2013 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: The goal of the present study was to determine the predictive value of beat-to-beat QT variability in heart failure patients across the continuum of left ventricular dysfunction., Methods and Results: Beat-to-beat QT variability index (QTVI), log-transformed heart rate variance, normalized QT variance, and coherence between heart rate variability and QT variability have been measured at rest during sinus rhythm in 533 participants of the Muerte Subita en Insuficiencia Cardiaca heart failure study (mean age, 63.1±11.7; men, 70.6%; left ventricular ejection fraction >35% in 254 [48%]) and in 181 healthy participants from the Intercity Digital Electrocardiogram Alliance database. During a median of 3.7 years of follow-up, 116 patients died, 52 from sudden cardiac death (SCD). In multivariate competing risk analyses, the highest QTVI quartile was associated with cardiovascular death (subhazard ratio, 1.67 [95% CI, 1.14-2.47]; P=0.009) and, in particular, with non-SCD (subhazard ratio, 2.91 [1.69-5.01]; P<0.001). Elevated QTVI separated 97.5% of healthy individuals from subjects at risk for cardiovascular (subhazard ratio, 1.57 [1.04-2.35]; P=0.031) and non-SCD in multivariate competing risk model (subhazard ratio, 2.58 [1.13-3.78]; P=0.001). No interaction between QTVI and left ventricular ejection fraction was found. QTVI predicted neither noncardiac death (P=0.546) nor SCD (P=0.945). Decreased heart rate variability rather than increased QT variability was the reason for increased QTVI in the present study., Conclusions: Increased QTVI because of depressed heart rate variability predicts cardiovascular mortality and non-SCD but neither SCD nor extracardiac mortality in heart failure across the continuum of left ventricular dysfunction. Abnormally augmented QTVI separates 97.5% of healthy individuals from heart failure patients at risk.

Background: Prediction of sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) could help to guide preventive interventions in at-risk patients. The QRST integral (∫QT) reflects intrinsic repolarization properties., Objective: The objective of this study was to determine whether intracardiac ∫QT predicts VT/VF in the next few months in patients with implantable cardioverter defibrillators (ICDs)., Methods: Far-field (FF) and near-field (NF) right ventricular intracardiac electrograms (EGMs) were recorded via telemetry in 46 patients with structural heart disease and ICDs implanted for secondary prevention of sudden cardiac death. Epochs of 4.9 ± 0.4 minutes during sinus rhythm (mean heart rate 70.9 ± 15.2 beats/min) and ventricular pacing at 105 beats/min were analyzed. Mean ∫QT was calculated on FF and NF EGMs as the algebraic sum of areas under the QRST curve and adjusted by mean heart rate. Patients were followed up for at least 3 months. True VT/VF events treated by the ICD served as the end point., Results: During a mean follow-up of 4.6 months, 22 patients (48%) were treated for VT/VF. Unadjusted and adjusted by heart rate, FF EGM ∫QT in sinus rhythm was a significant predictor of VT/VF (unadjusted ∫QT hazard ratio 1.007; 95% confidence interval 1.002 to 1.0013; P = .007; adjusted ∫QT hazard ratio 1.68; 95% confidence interval 1.19 to 2.36; P = .002). The highest quartile of intracardiac ∫QT predicted VT/VF (log-rank test P = .042) and identified patients at risk with a specificity of 86% and positive predictive value of 73%., Conclusion: Increased intracardiac FF EGM ∫QT predicts VT/VF in patients with structural heart disease and secondary prevention ICDs., (Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Reverse electrical remodeling (RER) of the native conduction with cardiac resynchronization therapy (CRT) is associated with decreased mortality and antiarrhythmic effect of CRT. Still, mechanisms of RER are largely unknown. In this study, we explored repolarization lability during biventricular pacing., Methods and Results: The width of native QRS was measured in lead II electrocardiogram before and at least 6 months after implantation of Cardiac Resynchronization Therapy Defibrillator (CRT-D) devices (Medtronic, Inc [Minneapolis, MN, USA] and Boston Scientific Corporate [Natick, MA, USA]) in 69 patients (mean age, 66.3 ± 13.9 years; 39 men [83%]) with either bundle-branch block (44 patients [64%]) or nonspecific intraventricular conduction delay (25 patients [36%]) and New York Heart Association class III and IV heart failure. Narrowing of the native QRS duration for at least 10 milliseconds was considered a marker of RER. Beat-to-beat QT variability and coherence was measured on surface electrocardiogram and intracardiac near-field electrogram during biventricular pacing. Reverse electrical remodeling was observed in 22 patients (32%) in whom coherence between heart rate variability and intracardiac repolarization lability was stronger (0.483 ± 0.243 vs 0.237 ± 0.146, P = .018) and normalized intracardiac QT variance was smaller (0.28 ± 0.0031 vs 0.46 ± 0.0048, P = .049), as compared with that in patients without RER. During a further 24 ± 13 months of follow-up, 21 patients (33%) died or experienced sustained ventricular tachycardia (VT)/ventricular fibrillation. Low intracardiac coherence (≤0.116) was associated with increased risk of death or sustained VT/VT (hazard ratio, 4.33; 95% confidence interval, 1.51-12.40; P = .006)., Conclusion: Strong coherence between heart rate variability and intracardiac repolarization lability during biventricular pacing is associated with RER of the native conduction with CRT. Low coherence is associated with increased risk of VT/ventricular fibrillation or death., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background: Monitoring arrhythmic risk may improve management of patients with implantable cardioverter-defibrillators (ICD) and prevent ICD shocks. Changes in repolarization duration between subsequent beats quantified as short-term variability (STV) is associated with ventricular arrhythmias in several animal models., Objective: We evaluated STV of QT from right ventricular intracardiac ICD electrograms in patients with structural heart disease and compared its predictive value with the QT variability index (QTVI)., Methods: In 233 patients, STV over 60 beats for QT and RR intervals and their ratio was calculated (STV(QT), STV(RR), STV(Ratio), respectively). QTVI was derived from mean and SD of QT and heart rate. Follow-up duration was 26 ± 15 months. Predictive value was determined for sudden arrhythmic death (SAD) defined as sudden cardiac death or fast ventricular tachycardia/fibrillation [CL < 240 ms]., Results: In univariate analysis, STV(Ratio), but not STV(QT) or STV(RR), was predictive of SAD. Hazard ratios for highest quartile STV(Ratio) and QTVI were comparable (STV(Ratio): 1.9, 95% confidence interval [CI] 1.1 to 3.3, P = .038, QTVI: 2.2, 95% CI 1.2 to 3.8, P = .010). In a multivariate model, highest quartile STV(Ratio) was predictive of SAD after adjustment for New York Heart Association class, history of ischemia, ICD indication, and use of class I antiarrhythmics (hazard ratio 1.8, 95% CI 1.0 to 3.4, P < .050). A combined criterion of highest quartile for both STV(Ratio) and QTVI identified patients at highest risk (hazard ratio 2.4, 95% CI 1.3 to 4.3, P = .005, positive predictive value 38%, negative predictive value 82%)., Conclusion: STV(Ratio) from ICD electrograms is predictive of SAD. Predictive value is similar for order-based STV(Ratio) and distribution-based QTVI, but the combination of both parameters can further improve results., (Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Antiarrhythmic and proarrhythmic effects of cardiac resynchronization therapy (CRT) remain controversial. We hypothesized that reverse electrical remodeling (RER) with CRT is associated with reduced frequency of ventricular tachyarrhythmias (VTs)., Methods: The width of native and paced QRS was measured in lead II electrocardiogram before and 13 ± 7 months after implantation of a CRT defibrillator device in 69 patients (mean age 66.3 ± 13.9; 39 males [83%]) with bundle branch block (BBB) (41 patients with left BBB and three patients with bifascicular block) or nonspecific intraventricular conduction delay (25 patients, 36%), and New York Heart Association class III-IV heart failure. Biventricular pacing was inhibited for 10 seconds to record native QRS. RER was defined as a decrease in the native QRS duration ≥10 ms compared to preimplant. Patients were followed prospectively 24 ± 13 months after assessment for electrical remodeling., Results: RER was observed in 22 patients (32%), among whom QRS duration decreased by 30.9 ± 14.1 ms (P < 0.00001) with similar heart rate and QRS morphology. Native QRS duration increased by 10.3 ± 16.6 ms in the other 47 patients (68%) (P = 0.0001). Baseline mean ejection fraction did not differ between patients with and those without RER (24.9 ± 10.0 vs 24.2 ± 8.6%, NS). During 2 ± 1 years of further follow-up, 19 patients had VTs and 12 patients died. RER was associated with a fourfold decrease in the risk of death or sustained VTs requiring appropriate implantable cardioverter-defibrillator therapies, whichever came first (hazard ratio 0.25; 95% confidence interval 0.08-0.85; P = 0.026)., Conclusion: RER of the native conduction with CRT is associated with decreased mortality and antiarrhythmic effect of CRT., (©2010, The Authors. Journal compilation ©2010 Wiley Periodicals, Inc.)

Background: Arrhythmic sudden cardiac death (SCD) is generally mediated by ventricular fibrillation (VF) or fast ventricular tachycardia (FVT). We studied the predictive value of temporal QT variability detected from various sources of cardiac electric signal: surface ECG, far-field (FF), and near-field (NF) intracardiac electrograms (EGMs) in patients with implantable cardioverter-defibrillators (ICDs)., Methods and Results: Surface ECG and FF and NF intracardiac EGMs were simultaneously recorded at rest (mean heart rate, 74+/-15 bpm) for 4.5+/-1.3 minutes in 298 patients (mean age, 59+/-14; 216 male [73%]) with structural heart disease and an implanted Medtronic ICD for primary (231 patients, 78%) or secondary (67 patients, 22%) prevention of SCD. During mean follow-up of 16+/-8 months, 52 (13.1% per person-year of follow-up) patients sustained VT/VF and received appropriate ICD therapies, but only 19 (4.8% per person-year of follow-up) patients sustained FVT/VF with cycle length

Terminal PV1 Negativity in NHANES III Introduction Deep terminal negativity of P wave in V1 (DTNPV1), defined as negative P prime larger than one small box (1 mm, or 0.1 mV), could be easily detected by simple visual inspection of the resting 12-lead ECG. The objective of this study was to determine the relationship between DTNPV1 and all-cause-, cardiovascular disease (CVD), and ischemic heart disease (IHD) mortality in the National Health and Nutrition Examination Survey III (NHANES III). Methods and Results After exclusion of participants with atrial fibrillation and missing data, DTNPV1 was automatically measured from standard 12-lead ECG in 8,146 participants. Minnesota and Novacode algorithms were used for the determination of major and minor ECG abnormalities. National Death Index was used to identify the date and cause of death. During a median follow-up of 13.8 years, a total of 2,975 deaths (1,303 CVD and 742 IHD deaths) occurred. After adjustment for age, gender, race/ethnicity, IHD, heart failure, chronic obstructive pulmonary disease, cancer, diabetes, body mass index, smoking, dyslipidemia, hypertension, use of antihypertensive and lipid-lowering medications, and ECG abnormalities, DTNPV1 was associated with significantly increased risk of all-cause death (HR [95% CI]: 1.30 [1.10, 1.53]; P = 0.002), CVD death (HR [95% CI]: 1.36 [1.08, 1.72]; P = 0.010), and IHD death (HR [95% CI]: 1.36 [1.00, 1.85]; P = 0.047). Conclusion In a large sample of the adult United States population, DTNPV1 is independently associated with increased risk of death due to all-cause, CVD, and IHD, findings suggesting its potential usefulness as a simple marker to identify individuals at risk of poor outcomes. [ABSTRACT FROM AUTHOR]