Standard Antiarrhythmic Drugs

Darbar, Dawood

doi:10.1016/b978-1-4557-2856-5.00111-4

Cited by 7 publications

(9 citation statements)

References 89 publications

(58 reference statements)

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“…However, the increases in ERP seen with mexiletine, a pure sodium channel blocker, are probably explained by its preventing re-opening of the sodium channels even after full repolarisation, rather than through effects on the latter. This slowing of the reactivation of sodium channels that normally occurs with repolarisation, prolongs refractoriness independent of action potential duration (APD), which either shortens or remains unchanged with mexiletine (Darbar 2014 ; Tamargo and Delpon 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Tissue-Level Cardiac Electrophysiology Studied in Murine Myocardium Using a Microelectrode Array: Autonomic and Thermal Modulation

2017

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Cardiac electrophysiology is regulated by the autonomic nervous system, and this has both pathophysiological, and possibly therapeutic importance. Furthermore, chamber differences in electrophysiology exist between atria and ventricles, yet there have been few direct comparisons. There is substantial literature on ion channel modulation at the single-cell level but less work on how this affects tissue-level parameters. We used a microelectrode array system to explore these issues using murine atrial and ventricular tissue slices. Activation time, conduction velocity and repolarisation were measured, and their modulation by temperature and pharmacological autonomic agonists were assessed. The system recorded reliable measurements under control conditions in the absence of drug/thermal challenge, and significant baseline differences were found in chamber electrophysiology. The sodium channel blocker mexiletine, produced large magnitude changes in all three measured parameters. Carbachol and isoprenaline induced differing effects in atria and ventricles, whereas temperature produced similar effects on activation and repolarisation.

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Section: Discussionmentioning

confidence: 99%

Tissue-Level Cardiac Electrophysiology Studied in Murine Myocardium Using a Microelectrode Array: Autonomic and Thermal Modulation

2017

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“…Class IC drugs may also cause WCT by slowing atrial rate during atrial flutter until 1:1 AV conduction occurs with a high ventricular rate and wide QRS complex (partly may be due to drug effect, partly to aberrant conduction). Digoxin may cause monomorphic VT as well [1, 2 14, 15]. …”

Section: Patient History and Physical Examination In Wct Differentialmentioning

confidence: 99%

Current Algorithms for the Diagnosis of wide QRS Complex Tachycardias

Vereckei

2014

CCR

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The differential diagnosis of a regular, monomorphic wide QRS complex tachycardia (WCT) mechanism represents a great diagnostic dilemma commonly encountered by the practicing physician, which has important implications for acute arrhythmia management, further work-up, prognosis and chronic management as well. This comprehensive review discusses the causes and differential diagnosis of WCT, and since the ECG remains the cornerstone of WCT differential diagnosis, focuses on the application and diagnostic value of different ECG criteria and algorithms in this setting and also provides a practical clinical approach to patients with WCTs.

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“…1 In cardiac tissues with RMPs positive to −60 mV (i.e., SAN, AVN, and ischemic tissues), I CaL is responsible for AP depolarization (phase 0) and conduction velocity. These blockers stabilize the channel in its inactivated state and prolong its reactivation, so that their effects increase at fast rates (use-dependent block) and at depolarized membrane potentials (voltage-dependent block).…”

Section: Calcium Channel Blockers: Class IV Aadsmentioning

confidence: 99%

“…1 Amiodarone presents a low proarrhythmic risk and is effective against supraventricular and ventricular arrhythmias caused by focal activity or reentry. However, as was mentioned before, amiodarone also inhibits peak I Na (inhibits inactivated Na + channels with fast kinetics [class I]), I NaL , and I CaL (class IV), and antagonizes α-/β-adrenergic receptors (class II).…”

Section: Amiodarone and Dronedaronementioning

confidence: 99%

“…1 Treatment of cardiac arrhythmias with antiarrhythmic drugs (AADs) has two main objectives: relieve symptoms and complications (improve quality of life) and reduce mortality directly related to the arrhythmia. 1 Treatment of cardiac arrhythmias with antiarrhythmic drugs (AADs) has two main objectives: relieve symptoms and complications (improve quality of life) and reduce mortality directly related to the arrhythmia.…”

Section: Antiarrhythmic Drugs: Introductionmentioning

confidence: 99%

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