Download e-book for kindle: Clinical Arrhythmology and Electrophysiology: A Companion to by Ziad Issa MD, John M. Miller MD

By Ziad Issa MD, John M. Miller MD

ISBN-10: 1455712744

ISBN-13: 9781455712748

With its exact, singular specialise in the medical point of cardiac arrhythmias, Clinical Arrhythmology and Electrophysiology: A significant other to Braunwald's middle Disease makes it effortless to use present day newest directions for prognosis and therapy. knowledgeable writer staff presents clear, clinically concentrated guidance on every kind of cardiac arrhythmias, together with practical ideas for handling advanced patients.

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

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

  • Fully comprehend the explanation for remedy of particular arrhythmias
  • with sensible thoughts which are grounded within the newest easy technology.

  • 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 middle disorder, atrial arrhythmias in congenital middle ailment, and problems 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 diverse mapping and navigation modalities, and fluoroscopy photographs illustrating recommendations for electrophysiologic catheter positioning, atrial septal puncture, and pericardial entry.

  • Gain a brand new realizing of sizzling topics
  • similar to mechanisms of arrhythmias, electrophysiologic checking out, mapping and navigation modalities, ablation strength resources, sinus node disorder, conduction disturbances, atrial tachyarrhythmias, preexcitation syndromes and every kind of ventricular and supraventricular tachycardias.

Tackle the medical administration of cardiac arrhythmias with self belief with the main updated tips from the specialists you trust.

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

Example text

It is believed that the differential origin of the triggering beat is responsible for the observed discrepancy in arrhythmogenesis and the clinical features compared with other types of LQTS. 8,35,36 Catecholaminergic Polymorphic Ventricular Tachycardia Three novel loss-of-function mutations of KCNJ2 have been found in patients with catecholaminergic polymorphic VT (CPVT). 34 IK1 reduction can trigger arrhythmia by allowing inward currents, which are no longer counterbalanced by the strong outward IK1, to depolarize the Em gradually during phase 4.

Further studies are necessary to clarify CARDIAC ION CHANNELS α1C subunit. The combined use of Ca2+ channel blockers can enhance or weaken the block effect because, at least in part, of the different binding sites for those drugs. It is noteworthy that increased extracellular Ca2+ concentrations inhibit the binding of phenylalkylamines and dihydropyridines to their receptors on the Ca2+ channel. Verapamil and diltiazem preferentially block open and inactivated states of the channel. The more frequently the Ca2+ channel opens, the better is the penetration of the drug to the binding site; hence, these drugs cause use-dependent block of conduction in cells with Ca2+-dependent action potentials such as those in the sinus node and AVN.

Channels with properties similar to the steady-state noninactivating K+ current [Iss] that is well characterized in rodent myocytes). 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.

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Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald's Heart Disease by Ziad Issa MD, John M. Miller MD

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