Repolarization heterogeneity in patients with cardiac resynchronization therapy and its relation to ventricular tachyarrhythmias

Cvijić, Marta; Antolič, Bor; Klemen, Luka; Zupan, Igor

doi:10.1016/j.hrthm.2018.06.023

Cited by 20 publications

(16 citation statements)

References 20 publications

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“…6d and 6e). Additionally, the ratio of TpTe to QT (an index of repolarization heterogeneity predictive of ventricular tachycardia and fibrillation [54]) remained increased during stress recovery ( Fig. 6f; all P < 0.05 vs. Air).…”

Section: Characterization Of Peps Exposurementioning

confidence: 90%

Inhalation of printer-emitted particles impairs cardiac conduction, hemodynamics, and autonomic regulation and induces arrhythmia and electrical remodeling in rats

et al. 2020

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Background: Using engineered nanomaterial-based toners, laser printers generate aerosols with alarming levels of nanoparticles that bear high bioactivity and potential health risks. Yet, the cardiac impacts of printer-emitted particles (PEPs) are unknown. Inhalation of particulate matter (PM) promotes cardiovascular morbidity and mortality, and ultra-fine particulates (< 0.1 μm aerodynamic diameter) may bear toxicity unique from larger particles. Toxicological studies suggest that PM impairs left ventricular (LV) performance; however, such investigations have heretofore required animal restraint, anesthesia, or ex vivo preparations that can confound physiologic endpoints and/or prohibit LV mechanical assessments during exposure. To assess the acute and chronic effects of PEPs on cardiac physiology, male Sprague Dawley rats were exposed to PEPs (21 days, 5 h/day) while monitoring LV pressure (LVP) and electrocardiogram (ECG) via conscious telemetry, analyzing LVP and heart rate variability (HRV) in four-day increments from exposure days 1 to 21, as well as ECG and baroreflex sensitivity. At 2, 35, and 70 days after PEPs exposure ceased, rats received stress tests. Results: On day 21 of exposure, PEPs significantly (P < 0.05 vs. Air) increased LV end systolic pressure (LVESP, + 18 mmHg) and rate-pressure-product (+ 19%), and decreased HRV indicating sympathetic dominance (root means squared of successive differences [RMSSD], − 21%). Overall, PEPs decreased LV ejection time (− 9%), relaxation time (− 3%), tau (− 5%), RMSSD (− 21%), and P-wave duration (− 9%). PEPs increased QTc interval (+ 5%) and low:high frequency HRV (+ 24%; all P < 0.05 vs. Air), while tending to decrease baroreflex sensitivity and contractility index (− 15% and − 3%, P < 0.10 vs. Air). Relative to Air, at both 2 and 35 days after PEPs, ventricular arrhythmias increased, and at 70 days post-exposure LVESP increased. PEPs impaired ventricular repolarization at 2 and 35 days postexposure, but only during stress tests. At 72 days post-exposure, PEPs increased urinary dopamine 5-fold and protein expression of ventricular repolarizing channels, K v 1.5, K v 4.2, and K v 7.1, by 50%. Conclusions: Our findings suggest exposure to PEPs increases cardiovascular risk by augmenting sympathetic influence, impairing ventricular performance and repolarization, and inducing hypertension and arrhythmia. PEPs may present significant health risks through adverse cardiovascular effects, especially in occupational settings, among susceptible individuals, and with long-term exposure.

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Section: Characterization Of Peps Exposurementioning

confidence: 90%

Inhalation of printer-emitted particles impairs cardiac conduction, hemodynamics, and autonomic regulation and induces arrhythmia and electrical remodeling in rats

et al. 2020

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“…10,11 However, the effect of BiV pacing on ECG markers of ventricular repolarization is inconsistently reported, 12 and prior studies on the association of BiV pacing-induced concomitant changes in ventricular repolarization with ventricular arrhythmia burden are conflicting. [13][14][15][16][17][18] This suggests that BiV pacing has differential effects on arrhythmogenic substrate. The proarrhythmic effect of BiV pacing may occur early due to the reversed direction of the activation of the LV wall, thus prolonging the QT interval and increasing intrinsic transmural dispersion of repolarization and creating a substrate for arrhythmias.…”

Section: Discussionmentioning

confidence: 99%

“…As described in animal models and simulation studies, BiV pacing induces a reversed sequence of ventricular depolarization and repolarization due to the epicardial pacing location, thus increasing transmural repolarization heterogeneity and prolonging ventricular repolarization 10,11 . However, the effect of BiV pacing on ECG markers of ventricular repolarization is inconsistently reported, 12 and prior studies on the association of BiV pacing‐induced concomitant changes in ventricular repolarization with ventricular arrhythmia burden are conflicting 13–18 . This suggests that BiV pacing has differential effects on arrhythmogenic substrate.…”

Section: Discussionmentioning

confidence: 99%

“…BiV pacing-induced increases in QT interval with excess ventricular arrhythmia burden, [13][14][15][16][17] others suggest no association. 18 Although QT prolongation is common with BiV pacing, and most patients benefit despite developing transmural repolarization heterogeneity, 19,20 little is known about the complex interaction between concomitant changes in ventricular depolarization and repolarization and their association with long-term outcomes of BiV pacing.…”

Section: Introductionmentioning

confidence: 98%

“…BiV pacing increases transmural repolarization heterogeneity due to epicardial to endocardial wavefront propagation from the LV lead, 9–11 but data are inconsistent on its effect on common ECG markers of ventricular repolarization including QT interval, QT dispersion, JT interval, and Tpeak to Tend interval 12 . Furthermore, while some studies have associated BiV pacing‐induced increases in QT interval with excess ventricular arrhythmia burden, 13–17 others suggest no association 18 . Although QT prolongation is common with BiV pacing, and most patients benefit despite developing transmural repolarization heterogeneity, 19,20 little is known about the complex interaction between concomitant changes in ventricular depolarization and repolarization and their association with long‐term outcomes of BiV pacing.…”

Section: Introductionmentioning

confidence: 99%

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Concomitant changes in ventricular depolarization and repolarization and long‐term outcomes of biventricular pacing

Polcwiartek

Friedman

Emerek

et al. 2020

Pacing Clinical Electrophis

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Background: Biventricular (BiV) pacing increases transmural repolarization heterogeneity due to epicardial to endocardial conduction from the left ventricular (LV) lead. However, limited evidence is available on concomitant changes in ventricular depolarization and repolarization and long-term outcomes of BiV pacing. Therefore, we investigated associations of BiV pacing-induced concomitant changes in ventricular depolarization and repolarization with mortality (i.e., LV assist device, heart transplantation, or all-cause mortality) and sustained ventricular arrhythmia endpoints. Methods: Consecutive BiV-defibrillator recipients with digital preimplantation and postimplantation electrocardiograms recorded between 2006 and 2015 at Duke University Medical Center were included. We calculated changes in QRS duration and corrected JT (JTc) interval and split them by median values. For simplicity, these variables were named QRS decreased (≤ −12 ms), QRS increased (>-12 ms), JTc decreased (≤22 ms), and JTc increased (> 22 ms) and subsequently used to construct four mutually exclusive groups. Results: We included 528 patients (median age, 68 years; male, 69%). No correlation between changes in QRS duration and JTc interval was observed (P = .295). Compared to QRS decreased /JTc increased , increased risk of the composite mortality endpoint was associated with QRS decreased /JTc decreased (hazard ratio [HR] = 1.62; 95% confidence interval [CI] = 1.09-2.43), QRS increased /JTc decreased (HR = 1.86; 95% CI = 1.27-2.71), and QRS increased /JTc increased (HR = 2.25; 95% CI = 1.52-3.35). No QRS/JTc group was associated with excess sustained ventricular arrhythmia risk (P = .400). Conclusion: Among BiV-defibrillator recipients, QRS decreased /JTc increased was associated with the most favorable long-term survival free of LV assist device, heart transplantation, and sustained ventricular arrhythmias. Our findings suggest that improved electrical resynchronization may be achieved by assessing concomitant changes in ventricular depolarization and repolarization.

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Ten-year follow-up of cardiac resynchronization therapy patients with non-ischemic dilated cardiomyopathy assessed by radionuclide angiography: a single-center cohort study

Valzania

Massaro

Spadotto

et al. 2022

J Interv Card Electrophysiol

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Repolarization heterogeneity in patients with cardiac resynchronization therapy and its relation to ventricular tachyarrhythmias

Cited by 20 publications

References 20 publications

Inhalation of printer-emitted particles impairs cardiac conduction, hemodynamics, and autonomic regulation and induces arrhythmia and electrical remodeling in rats

Inhalation of printer-emitted particles impairs cardiac conduction, hemodynamics, and autonomic regulation and induces arrhythmia and electrical remodeling in rats

Concomitant changes in ventricular depolarization and repolarization and long‐term outcomes of biventricular pacing

Ten-year follow-up of cardiac resynchronization therapy patients with non-ischemic dilated cardiomyopathy assessed by radionuclide angiography: a single-center cohort study

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