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Clinical Arrhythmology and Electrophysiology: A Companion to by Ziad Issa MD, John M. Miller MD

By Ziad Issa MD, John M. Miller MD

With its precise, singular specialise in the scientific element of cardiac arrhythmias, Clinical Arrhythmology and Electrophysiology: A better half to Braunwald's center Disease makes it effortless to use contemporary latest instructions for prognosis and remedy. a professional writer workforce presents clear, clinically targeted guidance on every kind of cardiac arrhythmias, together with practical options for coping with advanced patients.

  • Find the data you wish quickly
  • with a constant association in all chapters, written to a template that indicates each arrhythmia variety in an identical manner.

  • Access the totally searchable contents online
  • at www.expertconsult.com, as well as downloadable photos and dynamic movies.

  • Fully comprehend the reason for therapy of particular arrhythmias
  • with useful concepts which are grounded within the latest uncomplicated technological know-how.

  • Stay modern
  • with new chapters on molecular mechanisms of cardiac electric task, cardiac ion channels, ventricular tachycardia in nonischemic dilated cardiomyopathy, epicardial ventricular tachycardia, ventricular arrhythmias in hypertrophic cardiomyopathy, ventricular arrhythmias in inherited channelopathies, ventricular arrhythmias in congenital middle affliction, atrial arrhythmias in congenital center ailment, and problems of catheter ablation of cardiac arrhythmias.

  • View movies of 27 key concepts online
  • , together with optical mapping of reentrant ventricular arrhythmias, three-d mapping of arrhythmias utilizing assorted mapping and navigation modalities, and fluoroscopy photos illustrating recommendations for electrophysiologic catheter positioning, atrial septal puncture, and pericardial entry.

  • Gain a brand new realizing of sizzling topics
  • equivalent to mechanisms of arrhythmias, electrophysiologic trying out, mapping and navigation modalities, ablation power resources, sinus node disorder, conduction disturbances, atrial tachyarrhythmias, preexcitation syndromes and all kinds of ventricular and supraventricular tachycardias.

Tackle the scientific administration of cardiac arrhythmias with self assurance with the main up to date advice from the specialists you trust.

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Extra resources for Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald's Heart Disease

Example text

1-3). Ca2+ enters the cell during the plateau phase of the action potential through L-type Ca2+ channels that line the sarcolemmal T tubules. However, the rise in intracellular Ca2+ is small and not sufficient to induce contraction. Nonetheless, the small amount of Ca2+ entering the cell via ICaL triggers a rapid mobilization of Ca2+ from the sarcoplasmic reticulum into the cytosol by opening the RyR2 channels in the CICR process. Approximately 75% of Ca2+ present in the cytoplasm during contraction is released from the sarcoplasmic reticulum.

This amplifying process, termed Ca2+-induced Ca2+ release (CICR), causes a rapid increase in intracellular Ca2+ concentration (from approximately 100 nM to approximately 1 µM) to a level required for optimal binding of Ca2+ to troponin C and induction of contraction. 46,49 Cytosolic Ca2+ concentration decreases during diastole: contraction is followed by Ca2+ release from troponin C and its reuptake by the sarcoplasmic reticulum via activation of the sarcoplasmic reticulum Ca2+-ATPase Ca2+ pump, in addition to extrusion across the sarcolemma via the Na+-Ca2+ exchanger.

The increased cAMP levels stimulate cAMP-dependent PKA phosphorylation of the α1C subunit of L-type Ca2+ channels and result in an increase in ICaL amplitude and a shift in activation to a more negative Em. 46,47 The suppression of adenylyl cyclase activity is one of the most common pathways to interrupt PKA-dependent Ca2+ channel stimulation. Adenylyl cyclase is usually suppressed (and cAMP synthesis is blocked) by activation of Gi proteins. , M2 muscarinic receptors, ­adenosine A1 receptors, opiates, and atrial natriuretic peptides) does not change basal ICaL in most cases, but reduces ICaL increased via stimulation of β-adrenergic receptors.

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