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 distinct, singular specialize in the medical point of cardiac arrhythmias, Clinical Arrhythmology and Electrophysiology: A significant other to Braunwald's middle Disease makes it effortless to use modern day most recent directions for prognosis and therapy. a professional writer crew presents clear, clinically concentrated guidance on every kind of cardiac arrhythmias, together with practical options for dealing with advanced patients.

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

  • Access the absolutely searchable contents online
  • at, as well as downloadable photographs and dynamic movies.

  • Fully comprehend the reason for remedy of particular arrhythmias
  • with sensible innovations which are grounded within the most up-to-date simple technological know-how.

  • Stay brand new
  • 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 center disorder, atrial arrhythmias in congenital middle affliction, and issues of catheter ablation of cardiac arrhythmias.

  • View video clips of 27 key ideas online
  • , together with optical mapping of reentrant ventricular arrhythmias, three-dimensional mapping of arrhythmias utilizing assorted mapping and navigation modalities, and fluoroscopy pictures illustrating suggestions for electrophysiologic catheter positioning, atrial septal puncture, and pericardial entry.

  • Gain a brand new knowing of scorching topics
  • akin 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 medical administration of cardiac arrhythmias with self belief with the main updated counsel from the specialists you trust.

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

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44 TREK-1, as an outwardly rectifying current, can potentially participate in balancing the Em and action potential duration. Indeed, on a beat-to-beat basis, it could be involved in a negative feedback loop, hyperpolarizing the Em in response to a stretch stimulus following the stretch activation of nonselective cation channels. The expression of TREK-1 appears to be nonuniform in the heart, with stronger TREK-1 mRNA expression in endocardial cells compared with epicardial cells. This finding possibly reflects different amounts of stretch experienced by muscle cells in different parts of the ventricular wall, leading to differential mechanoelectrical feedback and thereby reducing action potential repolarization in areas of the myocardium where conduction velocity is slower.

Adrenergic receptors, endothelin, angiotensin II, and muscarinic receptors) stimulates phospholipase C, which hydrolyzes PIP2 to inositol 1,4,5-triphosphate (InsP3) and diacylglycerol (DAG). DAG activates PKC, which, in turn, phosphorylates L-type Ca2+ channels. The mechanism of the effect of PKC on the activity of cardiac L-type Ca2+ channels is not exactly known. 46,47 Activation of soluble guanylate cyclase (primarily by nitric oxide) results in the conversion of GTP into cGMP. cGMP activates PKG, which phosphorylates the α1C subunit of the L-type Ca2+ channel, with a resulting inhibition of ICaL.

TASK-1 (KCNK3) and TASK-3 (KCNK9) subunits are functional when associated as homodimers or heterodimers. TASK channels display strong basal currents with very fast activation and inactivation kinetics. 44 Several members of the K2P channel family are expressed in the heart and in the systemic or pulmonary circulations, and some contribute to background K+ currents and the control of Em in vascular smooth muscle cells. The K+ selectivity, voltage-independent gating, and rectification of K2P currents are characteristics that make them strong candidates for mediating background K+ currents.

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