Suppression of refractory recurrent ventricular tachycardia by transvenous rapid cardiac pacing and antiarrhythmic drugs

Friedberg, Charles K.; Lyon, Leonard J.; Donoso, Ephraim

doi:10.1016/0002-8703(70)90392-3

Cited by 43 publications

(3 citation statements)

References 20 publications

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“…Pacing has been used successfully to prevent ventricular arrhythmias associated with the long QT syndromes.`-6 There have also been several reports suggesting that the frequency of spontaneous ventricular ectopic activity and to a lesser extent sustained ventricular arrhythmias can be decreased or completely prevented by atrial and/or right ventricular apical pacing in the setting of acute or chronic coronary artery disease. 16 calize an essential arrhythmogenic area for sustained ventricular tachycardia. 20 The present study demonstrates that pacing at a high current strength (10 to 20 mA) at the site of origin during the drive train prevents ventricular tachycardia induction with right ventricular stimulation in 45% of ventricular tachycardia trials.…”

Section: Discussionmentioning

confidence: 99%

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin.

Marchlinski¹,

Buxton²,

Miller³

et al. 1987

Circulation

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To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with In five of the 1 1 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (> 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: (1) high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, (2) successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.Circulation 76, No. 2, 332-342, 1987. PACING TECHNIQUES in the management of ventricular tachyarrhythmias have been used almost solely as a means for arrhythmia termination.`Only in the management in preventing ventricular tachyarrhythmias of patients with the long QT syndrome has pacing proven effective with any degree of consistency.`The purpose of this study was to determine whether high current strength ventricular pacing at the site of origin

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Section: Discussionmentioning

confidence: 99%

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin.

Marchlinski¹,

Buxton²,

Miller³

et al. 1987

Circulation

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“…[1][2] Immediate defibrillation is the only remedy for arrhythmic sudden death caused by haemodynamically compromising ventricular tachycardia and ventricular fibrillation, 3 although pace termination of ventricular tachycardia may prevent the arrhythmic cascade to ventricular fibrillation. [4][5][6] Immediate defibrillation shock treatment delivery by the implantable cardioverter-defibrillator (ICD) is highly efficacious in preventing sudden cardiac death. 7 8 Though the ICD has been in clinical use for 23 years, 9 indications for its use have broadened in the 1990s as clinical acceptability of ICD treatment has increased (with the advent of small devices capable of pectoral implantation, using per venous defibrillation leads).…”

mentioning

confidence: 99%

The MADIT II and COMPANION studies: will they affect uptake of device treatment?

Morgan¹

2004

Heart

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“…ventricular tachy cardia and other cardiac arrhythmias [5,11). Severe depression of inotropic and chronotropic function of the heart secondary to high dose of antiarhythmic drugs often results in changes in the myocardial contraction, threshold, conductivity and refractoriness [5], A demand pacemaker in this situation may not be able to produce the expected cardiac stimulation. Successful depolarization of the myocardium by pacemaker stimuli would require correction of these electrophysiological changes produced by drug toxicity.…”

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confidence: 99%

Pacemaker Wenckebach Phenomenon Due to Antiarrhythmic Drug Toxicity

Mehta¹,

Khan²

1976

Cardiology

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Two patients with intractable ventricular arrhythmia were managed with ventricular pacing and antiarrhythmic drugs. Toxic levels of these drugs resulted in unusual conduction disturbances at the level of Purkinje ventricular junction which caused pacemaker Wenckebach phenomenon and marked QRS prolongation. Sodium bicarbonate and sodium lactate infusion improved the conduction velocity probably by hyper-polarizing the membrane and reversed the conduction disturbance.

show abstract

Suppression of refractory recurrent ventricular tachycardia by transvenous rapid cardiac pacing and antiarrhythmic drugs

Cited by 43 publications

References 20 publications

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin.

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin.

The MADIT II and COMPANION studies: will they affect uptake of device treatment?

Pacemaker Wenckebach Phenomenon Due to Antiarrhythmic Drug Toxicity

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