Marked exercise‐induced T‐wave heterogeneity in symptomatic diabetic patients with nonflow‐limiting coronary artery stenosis

Stocco, Fernando G.; Evaristo, Ederson; Shah, Nishant; Cheezum, Michael K.; Hainer, Jon; Foster, Courtney; Nearing, Bruce D.; Gervino, Ernest V.; Verrier, Richard L.

doi:10.1111/anec.12503

Cited by 5 publications

(1 citation statement)

References 29 publications

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“…Morphologic changes in the T wave are sometimes more immediately remarkable than the mere prolongation of the QT interval; in some cases, the morphology of the T-wave is the only sensitive sign of ventricular repolarization disturbances. 44,45 Gain-of-function mutations of I Na-L I Na-L has also been called steady-state I Na , slow inactivation, persistent current, and late current. Under physiological conditions, the amplitude of I Na-L is larger in midmyocardial cells (M cells) and Purkinje fibers than epicardial and endocardial cells.…”

Section: Gain-of-function Mutations Of I Na-pmentioning

confidence: 99%

Dysfunctional Nav1.5 channels due to SCN5A mutations

Han

Tan

Sun

et al. 2018

Exp Biol Med (Maywood)

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The voltage-gated sodium channel 1.5 (Nav1.5), encoded by the SCN5A gene, is responsible for the rising phase of the action potential of cardiomyocytes. The sodium current mediated by Nav1.5 consists of peak and late components (I and I). Mutant Nav1.5 causes alterations in the peak and late sodium current and is associated with an increasingly wide range of congenital arrhythmias. More than 400 mutations have been identified in the SCN5A gene. Although the mechanisms of SCN5A mutations leading to a variety of arrhythmias can be classified according to the alteration of I and I as gain-of-function, loss-of-function and both, few researchers have summarized the mechanisms in this way before. In this review article, we aim to review the mechanisms underlying dysfunctional Nav1.5 due to SCN5A mutations and to provide some new insights into further approaches in the treatment of arrhythmias. Impact statement The field of ion channelopathy caused by dysfunctional Nav1.5 due to SCN5A mutations is rapidly evolving as novel technologies of electrophysiology are introduced and our understanding of the mechanisms of various arrhythmias develops. In this review, we focus on the dysfunctional Nav1.5 related to arrhythmias and the underlying mechanisms. We update SCN5A mutations in a precise way since 2013 and presents novel classifications of SCN5A mutations responsible for the dysfunction of the peak (I) and late (I) sodium channels based on their phenotypes, including loss-, gain-, and coexistence of gain- and loss-of function mutations in I, I, respectively. We hope this review will provide a new comprehensive way to better understand the electrophysiological mechanisms underlying arrhythmias from cell to bedside, promoting the management of various arrhythmias in practice.

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Section: Gain-of-function Mutations Of I Na-pmentioning

confidence: 99%

Dysfunctional Nav1.5 channels due to SCN5A mutations

Han

Tan

Sun

et al. 2018

Exp Biol Med (Maywood)

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T-Wave Indices and Atherosclerosis

Tse

Bazoukis

Roever

et al. 2018

Curr Atheroscler Rep

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Tpeak-Tend interval, the time difference between the peak and the end of the T-wave, reflects the degree of dispersion of repolarization. Its prolongation has been associated with higher risks of developing ventricular arrhythmias and sudden cardiac death in different pro-arrhythmic conditions such as Brugada and long QT syndromes. In this review, we will provide a comprehensive overview on how Tpeak-Tend is altered in different atherosclerotic conditions such as hypertension, stable coronary artery disease, acute coronary obstruction, and coronary slow flow as well as inflammatory diseases affecting the arterial tree. We will explore its relationship with arterial function and dysfunction, ventricular remodeling, and arrhythmic and mortality outcomes. The published literature shows that patients with coronary atherosclerosis, whether in the form of stable coronary artery disease, chronic total occlusion, slow flow, or acute coronary obstruction, have prolonged Tpeak-Tend intervals and Tpeak-Tend/QT ratios. These can be used to predict the occurrence of ventricular arrhythmias and sudden cardiac death. They also correlate with the extent and severity of arterial stenosis and structural remodeling of the ventricles as well as arterial function and dysfunction. Finally, they can be normalized following revascularization and may therefore be used as a surrogate measure of treatment success.

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Effects of the Antianginal Drugs Ranolazine, Nicorandil, and Ivabradine on Coronary Microvascular Function in Patients With Nonobstructive Coronary Artery Disease: A Meta-analysis of Randomized Controlled Trials

Zhu

Fang

et al. 2019

Clinical Therapeutics

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Marked exercise‐induced T‐wave heterogeneity in symptomatic diabetic patients with nonflow‐limiting coronary artery stenosis

Cited by 5 publications

References 29 publications

Dysfunctional Nav1.5 channels due to SCN5A mutations

Dysfunctional Nav1.5 channels due to SCN5A mutations

T-Wave Indices and Atherosclerosis

Effects of the Antianginal Drugs Ranolazine, Nicorandil, and Ivabradine on Coronary Microvascular Function in Patients With Nonobstructive Coronary Artery Disease: A Meta-analysis of Randomized Controlled Trials

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