Determination of Human Ventricular Repolarization by Noncontact Mapping

Yue, Arthur M.; Paisey, John; Robinson, S W; Betts, Timothy R.; Roberts, Paul R.; Morgan, John M.

doi:10.1161/01.cir.0000141734.43393.be

Cited by 75 publications

(70 citation statements)

References 30 publications

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“…In humans with preserved ventricular function, TRT is also dependent on activation-repolarization coupling, such that reduced coupling increases TRT dispersion when measured during steady-state pacing (7,9,24,25). We evaluated coupling by measuring the slope of the AT-ARI relationship, and a slope deviating from Ϫ1 indicated less coupling (7,26). During the basic drive in our patients, the AT-ARI slope at early sites (Ϫ0.5) deviated to the same extent from Ϫ1 as the AT-ARI slope of late sites (Ϫ1.5), thereby producing similar TRT dispersion.…”

Section: Discussionmentioning

confidence: 99%

“…For biphasic T waves, local repolarization was computed from the midpoint between the two phases of the T wave (20,24,25). Although Coronel et al (5) have argued that the original Wyatt method more accurately measures the end of local repolarization in isolated pig hearts, in vivo human studies (4,26) have consistently shown significant underestimation with this method when the T wave is positive. In these studies, the modified Wyatt method provided better correlation with monophasic action potential duration (MAP 90) than the original Wyatt method, so the former approach continues to be implemented to define the local repolarization in humans (10).…”

Section: Study Populationmentioning

confidence: 99%

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Modulated dispersion of activation and repolarization by premature beats in patients with cardiomyopathy at risk of sudden death

Subramanian

Suszko

Selvaraj

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Subramanian A, Suszko A, Selvaraj RJ, Nanthakumar K, Ivanov J, Chauhan VS. Modulated dispersion of activation and repolarization by premature beats in patients with cardiomyopathy at risk of sudden death. Am J Physiol Heart Circ Physiol 300: H2221-H2229, 2011. First published March 25, 2011; doi:10.1152/ajpheart.01050.2010.-Premature beats can trigger ventricular arrhythmias in heart disease, but the mechanisms are not well defined. We studied the effect of premature beats on activation and repolarization dispersion in seven patients with cardiomyopathy (57 Ϯ 10 yr, left ventricular ejection fraction 31 Ϯ 7%). Activation time (AT), activation-recovery interval (ARI), and total repolarization time (TRT) were measured from 26 unipolar electrograms during right ventricle (RV) endocardial (early) to left ventricle epicardial (late) activation in response to RV apical extrastimulation (S1S2). Early TRT dispersion increased significantly with shorter S1S2 (1.0 Ϯ 0.2 to 2.3 Ϯ 0.4 ms/mm, P Ͻ 0.0001), with minimal change in late TRT dispersion (0.8 Ϯ 0.1 to 1.0 Ϯ 0.3 ms, P ϭ 0.02). This was associated with an increase in early AT dispersion (1.0 Ϯ 0.1 to 1.5 Ϯ 0.2 ms/mm, P ϭ 0.05) but no change in late AT dispersion (0.6 Ϯ 0.1 to 0.7 Ϯ 0.2 ms/mm, P ϭ 0.4). Early and late ARI dispersion did not change with shorter S1S2. AT restitution slopes were similar between early and late sites, as was slope heterogeneity. ARI restitution slope was greater in early vs. late sites (1.3 Ϯ 0.6 vs. 0.8 Ϯ 0.6, P ϭ 0.03), but slope heterogeneity was similar. With shorter S1S2, AT-ARI slopes became less negative (flattened) at both early (Ϫ0.4 Ϯ 0.1 to ϩ0.04 Ϯ 0.2) and late (Ϫ1.5 Ϯ 0.2 to ϩ0.3 Ϯ 0.2) sites, implying less activation-repolarization coupling. There was no difference in AT-ARI slopes between early and late sites at short S1S2. In conclusion, high-risk patients with cardiomyopathy have greater TRT dispersion at tightly coupled S1S2 due to greater AT dispersion and activation-repolarization uncoupling. Modulated dispersion is more pronounced at early vs. late activated sites, which may predispose to reentrant ventricular arrhythmias. restitution; congestive heart failure FREQUENT PREMATURE VENTRICULAR beats are associated with an increased risk of sudden cardiac death in patients with left ventricular dysfunction (18). Critically timed premature beats can initiate ventricular tachycardia and fibrillation by providing a depolarizing trigger during the vulnerable period of cardiac repolarization. Premature beats can also modulate activation and repolarization gradients, creating zones of slow conduction and prolonged refractoriness, leading to unidirectional conduction block and reentry (8, 11). These gradients have been evaluated in response to programmed ventricular extrastimulation in patients with preserved ventricular function along the endocardium during percutaneous intervention (9,15,24,25) and the epicardium during intraoperative mapping (7, 17). Based on these clinical studies, repolarization heterogeneity is minimized by...

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Section: Discussionmentioning

confidence: 99%

Section: Study Populationmentioning

confidence: 99%

Modulated dispersion of activation and repolarization by premature beats in patients with cardiomyopathy at risk of sudden death

Subramanian

Suszko

Selvaraj

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…ARI was calculated by subtracting activation time from repolarization time. ARI has been previously validated and shown to correlate well with local action potential duration (56)(57)(58)(59). In addition, it serves as a method of recording action potential duration without causing myocardial injury.…”

Section: Methodsmentioning

confidence: 99%

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction

Vaseghi¹,

Salavatian²,

Rajendran³

et al. 2017

JCI Insight

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“…The methodology has been described extensively and validated previously. 18,21,22 A multielectrode basket catheter 23 was used to record 32 unipolar contact electrograms from the RV simultaneously with the noncontact mapping signals. In addition to the endocardial mapping signals from the RV and LV, wide bipole signals were recorded between the distal electrodes of the standard EP catheters each placed in the RV free wall and left atrial free wall.…”

Section: Mapping Of Vfmentioning

confidence: 99%

Mechanisms of Ventricular Fibrillation in Canine Models of Congestive Heart Failure and Ischemia Assessed by In Vivo Noncontact Mapping

et al. 2005

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Background-Much of the research performed studying the mechanism of ventricular fibrillation (VF) has been in normal ventricles rather than under a pathological condition predisposing to VF. We hypothesized that different ventricular substrates would alter the mechanism and characteristics of VF. Methods and Results-Three groups of dogs were studied: (1) control (nϭ8), (2) pacing-induced congestive heart failure (nϭ7), and (3) acute ischemia produced by 30 minutes of mid left anterior descending artery ligation (nϭ5). A noncontact mapping catheter (Ensite 3000, ESI) was placed via transseptal into the left ventricle (LV), along with an electrophysiology catheter. A multielectrode basket catheter (EP Technologies) was placed in the right ventricle, along with an electrophysiology catheter. Several episodes of VF were recorded in each animal. In addition to constructing isopotential and isochronal maps of the VF episodes, signals underwent frequency domain analysis as a fast Fourier transform was performed over a 2-second window every 1 second. From the fast Fourier transform, the dominant frequency was determined, and the organization was calculated. In control dogs, meandering, reentrant spiral wave activity was the main feature of the VF. The congestive heart failure group showed evidence of a stable rotor (nϭ3), evidence of a focal source (nϭ3), or no evidence of a driver in the LV (nϭ1). The ischemic group showed evidence of an initial focal mechanism that transitioned into reentry. In the control and ischemic groups, the LV always had higher dominant frequencies than the right ventricle. Conclusions-Different ventricular substrates produced by the different animal models altered the characteristics of VF.Thus, different mechanisms of VF may be present in the LV, depending on the animal model.

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Determination of Human Ventricular Repolarization by Noncontact Mapping

Cited by 75 publications

References 30 publications

Modulated dispersion of activation and repolarization by premature beats in patients with cardiomyopathy at risk of sudden death

Modulated dispersion of activation and repolarization by premature beats in patients with cardiomyopathy at risk of sudden death

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction

Mechanisms of Ventricular Fibrillation in Canine Models of Congestive Heart Failure and Ischemia Assessed by In Vivo Noncontact Mapping

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