Read e-book online Electrical Diseases of the Heart: Genetics, Mechanisms, PDF

By A. A. M. Wilde, P. A. Friedman, M. J. Ackerman, W.-K. Shen, Ihor Gussak, Charles Antzelevitch

ISBN-10: 1846288533

ISBN-13: 9781846288531

ISBN-10: 1846288541

ISBN-13: 9781846288548

This publication offers a special modern and succinct distillation of the present prestige of lately delineated electric illnesses of the center, emphasizing their universal and numerous medical positive factors. the most recent advancements within the box of experimental and scientific cardiac electrophysiology, genetics, pharmacology and interventional cures of varied scientific arrhythmogenic entities are featured and mentioned when it comes to contemporary advances in easy and medical technological know-how. The booklet is split into seven significant components. each one half contains chapters (total of sixty four) facing similar themes.

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Extra resources for Electrical Diseases of the Heart: Genetics, Mechanisms, Treatment, Prevention

Example text

Consequently, their action potential has a different shape and characteristics (Figure 1–6). Automatic cells from the sinus node or from the atrioventricular node have a less polarized membrane potential because they express less background K+ channels. Because of a less negative membrane potential, their Na+ current is permanently inactivated and the depolarizing phase of their action potential relies on the activation of slow Ca2+ currents. As a consequence, the kinetics of the rising phase (a parameter 16 I.

The local intracellular Ca2+ concentration ([Ca2+]i) increase activates Ca2+-dependent channels localized on the sarcoplasmic reticulum (SR) membrane (ryanodine receptors),which liberate further Ca2+ into the cytoplasm. A chain reaction induces a general [Ca2+]i increase, which induces sarcomeric contraction. At the same time, it induces (1) the Ca2+-dependent inactivation of the sarcolemmal L-type Ca2+ channels and (2) the repumping of the intracellular Ca2+ toward the sarcoplasmic reticulum (Ca2+-ATPase) and outward to the myocyte (Na–Ca exchanger), resulting in a decrease in [Ca2+]I.

Basic Res Cardiol 2001; 96:517–527. 44. Rosati B, Pan Z, Lypen S, et al. Regulation of KChIP2 potassium channel beta subunit gene expression underlies the gradient of transient outward current in canine and human ventricle. J Physiol 2001;533: 119–125. 45. Shi W, Wymore R, Yu H, et al. Distribution and prevalence of hyperpolarization-activated cation channel (HCN) mRNA expression in cardiac tissues. Circ Res 1999;85:e1–6. 46. Marionneau C, Couette B, Liu J, et al. Specific pattern of ionic channel gene expression associated with pacemaker activity in the mouse heart.

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Electrical Diseases of the Heart: Genetics, Mechanisms, Treatment, Prevention by A. A. M. Wilde, P. A. Friedman, M. J. Ackerman, W.-K. Shen, Ihor Gussak, Charles Antzelevitch

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