Key points are not available for this paper at this time.
Design
Review
Answers are grounded in this paper and cite their sources.
This article reviews the physiological, pharmacological, and clinical implications of electrical heterogeneity in the heart, including its role in arrhythmias such as Brugada syndrome and Long QT syndrome.
The sections in this article are: Action Potential and Ionic Distinctions Methodological Considerations in the Assessment of Electrical Heterogeneity Pharmacological Distinctions Epicardium versus Endocardium M‐cells versus Epicardium and Endocardium M‐Cells versus Purkinje Cells Molecular Distinctions Potassium Channels Sodium Channels Gap Junctions Chloride Conductances Calcium Channels Pumps and Exchangers Simulation of Action Potential Heterogeneity Developmental Aspects Physiological and Clinical Implications Transmural Distribution of I to and the J Wave Phase 2 Re‐entry as a Mechanism of Extrasystolic Activity Phase 2 Re‐entry as a Trigger for VT / VF : The Brugada Syndrome Early Repolarization Syndrome Ischemia Role of Transmural Heterogeneity in Inscription of the Electrocardiographic T Wave Role of Transmural Heterogeneity in Inscription of the U Wave Role of Transmural Heterogeneity in the Long QT Syndrome Torsade de Pointes Pharmacological Therapy for LQTS : Reducing Transmural Dispersion of Repolarization Summary
No takes yet. Share an insight, caveat, or question.
Antzelevitch et al. (2002) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: