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Journal ArticleDOI

Cellular Basis for the Electrocardiographic J Wave

Gan-Xin Yan, +1 more
- 15 Jan 1996 - 
- Vol. 93, Iss: 2, pp 372-379
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TLDR
The results provide the first direct evidence in support of the hypothesis that heterogeneous distribution of a transient outward current-mediated spike-and-dome morphology of the action potential across the ventricular wall underlies the manifestation of the electrocardiographic J wave.
Abstract
Background The J wave is a deflection that appears in the ECG as a late delta wave following the QRS or as a small secondary R wave (R′). Also referred to as an Osborn wave, the J wave has been observed in the ECG of animals and humans for more than four decades, yet the mechanism underlying its manifestation is poorly understood. The present study investigates the cellular basis for the J wave using an isolated arterially perfused preparation consisting of a wedge of canine right or left ventricle. Methods and Results A 12-lead ECG was initially recorded in vivo. After isolation and arterial perfusion of the right or left ventricular wedge, transmembrane action potentials were simultaneously recorded from epicardial, M region, and endocardial transmural sites with three floating microelectrodes. A transmural ECG was recorded concurrently. A J wave was observed at the R-ST junction of the ECG in 17 of 20 adult dogs, usually in leads II, III, aVR, and aVF and the mid to lateral precordial leads. The J wave...

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Citations
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Intracellular Ca2+ release underlies the development of phase 2 in mouse ventricular action potentials.

TL;DR: It is concluded that mouse ventricular APs display a phase 2; however, changes in Ca(2+) dynamics and thermodynamic parameters also diminish phase 2, mostly by impairing the Na(+)/Ca( 2+) exchanger.
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Brugada syndrome: clinical, genetic, molecular, cellular and ionic aspects.

TL;DR: A brief review summarizes the key clinical and experimental milestones that have brought us to the current understanding and approach to therapy of the Brugada syndrome.
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Lambda-like ST segment elevation in acute myocardial infarction - a new risk marker for ventricular fibrillation? Three case reports.

TL;DR: In this paper, the authors present three cases with acute myocardial infarction (AMI) and atypical ST segment elevation, complicated with episodes of ventricular fibrilation (VF) or SCD.
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Postprandial augmentation of bradycardia-dependent ST elevation in patients with Brugada syndrome.

TL;DR: The effects of taking meals on the ST‐RR relationship in the daily life of patients with Brugada syndrome and the effects of glucose‐induced insulin secretion were assessed.
References
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Journal ArticleDOI

Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report.

TL;DR: Common clinical and ECG features define a distinct syndrome in this group of patients with recurrent episodes of aborted sudden death unexplainable by currently known diseases, not explainable by electrolyte disturbances, ischemia or structural heart disease.
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Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells.

TL;DR: In spite of important advances in cardiology in recent years, pharmacological control of cardiac arrhythmias in the clinic remains an experiment conducted on a patient-by-patient basis using a trial and error approach tempered by good clinical judgment.
Journal ArticleDOI

Inward current channels activated by intracellular Ca in cultured cardiac cells.

TL;DR: Researchers report here studies on single channel currents recorded from heart muscle cells, in which they have found a channel, abundant in cardiac membrane, which does not seem to belong in any of the familiar categories.
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Characteristics of the Delayed Rectifier Current (IKr and IKs) in Canine Ventricular Epicardial, Midmyocardial, and Endocardial Myocytes A Weaker IKs Contributes to the Longer Action Potential of the M Cell

TL;DR: The results suggest that the distinctive phase-3 repolarization features of M cells are due in part to a lesser contribution of IKs and that this distinction may also explain why M Cells are the main targets for agents that prolong APD in ventricular myocardium.
Journal ArticleDOI

Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts.

TL;DR: It is proposed that the parallel orientation of the muscle bundles in the epicardial border zone is an important cause of ventricular tachycardia because activation transverse to myocardial fibers is sufficiently slow to permit the occurrence of reentry.
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