Effect of procainamide, propranolol and verapamil on mechanism of tachycardia in patients with chronic recurrent ventricular tachycardia

Wellens, Hein J.J.; Lie, Kong I.; Düren, Donald R.; Dohmen, Henk J.

doi:10.1007/978-94-011-4110-9_16

Cited by 3 publications

(3 citation statements)

References 12 publications

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“…The effects of antiarrhythmic agents have been used to sort out the underlying mechanisms 55–62 . Most important was the recognition that triggered activity due to delayed afterdepolarizations most often occurred in response to catecholamines.…”

Section: Mechanismsmentioning

confidence: 99%

Electrophysiology of Ventricular Tachycardia:

Josephson

2003

Cardiovasc electrophysiol

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Section: Mechanismsmentioning

confidence: 99%

Electrophysiology of Ventricular Tachycardia:

Josephson

2003

Cardiovasc electrophysiol

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“…The effects of antiarrhythmic agents were also used to sort out the underlying mechanisms 55–62 . Most importantly was the recognition that triggered activity due to delayed afterdepolarizations most often occurred in response to catecholamines.…”

Section: Mechanisms (Table Iii)mentioning

confidence: 99%

Electrophysiology of Ventricular Tachycardia:

Josephson

2003

Pacing Clinical Electrophis

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“…By reducing I Na availability over late repolarization, procainamide prolongs myocardial effective refractory period, which contributes to increased excitation wavelength, thus eliminating the arrhythmic substrate. Consequently, in the clinical setting, procainamide is widely used to prevent chronic recurrent ventricular tachycardia (VT) or restore sinus rhythm in patients with atrial fibrillation . Nevertheless, therapeutic effects of procainamide may be often offset by adverse electrophysiological changes that either reduce the clinical efficacy of this agent or even translate to drug‐induced pro‐arrhythmia.…”

Section: Introductionmentioning

confidence: 99%

Procainamide and lidocaine produce dissimilar changes in ventricular repolarization and arrhythmogenicity in guinea‐pig

Osadchii

2013

Fundamemntal Clinical Pharma

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Procainamide is class Ia Na(+) channel blocker that may prolong ventricular repolarization secondary to inhibition of IK r , the rapid component of the delayed rectifier K(+) current. In contrast to selective IN a blockers such as lidocaine, procainamide was shown to produce arrhythmogenic effects in the clinical setting. This study examined whether pro-arrhythmic responses to procainamide may be accounted for by drug-induced repolarization abnormalities including impaired electrical restitution kinetics, spatial gradients in action potential duration (APD), and activation-to-repolarization coupling. In perfused guinea-pig hearts, procainamide was found to prolong the QT interval on ECG and left ventricular (LV) epicardial monophasic APD, increased the maximum slope of electrical restitution, enhanced transepicardial APD variability, and eliminated the inverse correlation between the local APD and activation time values determined at distinct epicardial recording sites prior to drug infusion. In contrast, lidocaine had no effect on electrical restitution, the degree of transepicardial repolarization heterogeneities, and activation-to-repolarization coupling. Spontaneous episodes of monomorphic ventricular tachycardia were observed in 57% of procainamide-treated heart preparations. No arrhythmia was induced by lidocaine. In summary, this study suggests that abnormal changes in repolarization may contribute to pro-arrhythmic effects of procainamide.

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Effect of procainamide, propranolol and verapamil on mechanism of tachycardia in patients with chronic recurrent ventricular tachycardia

Cited by 3 publications

References 12 publications

Electrophysiology of Ventricular Tachycardia:

Electrophysiology of Ventricular Tachycardia:

Electrophysiology of Ventricular Tachycardia:

Procainamide and lidocaine produce dissimilar changes in ventricular repolarization and arrhythmogenicity in guinea‐pig

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