Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation

Jacob, Andrew S.; Nielsen, David H.; Gianelly, Ralph E.

doi:10.1016/s0196-0644(85)81080-5

Cited by 43 publications

(7 citation statements)

References 6 publications

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“…2). Jacob et al previously reported the case of a young patient presenting with intermittently preexcited AF who subsequently experienced fatal VF after receiving verapamil 5 . However, this case differs from ours in that he was maximally preexcited, and his heart rate was markedly faster (250 bpm vs 120 bpm), prior to the development of VF.…”

Section: Discussioncontrasting

confidence: 50%

“…Second, there are no published case reports, to our knowledge, of diltiazem or metoprolol precipitating VF in a WPW patient presenting with AF. Adenosine and verapamil, whose negative dromotropic effects are more potent than that of diltiazem and possibly even metoprolol, should not be used in such a setting 2,3,5,6,7,8 . One explanation proposed by Gulamhusein et al for the acceleration of preexcited AF by verapamil relates to its direct vasodilator effect, resulting in hypotension and reflex sympathetic activity that can potentially accelerate antegrade AP conduction and induce VF 8 .…”

Section: Discussionmentioning

confidence: 99%

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Precipitation of Ventricular Fibrillation by Intravenous Diltiazem and Metoprolol in a Young Patient with Occult Wolff‐Parkinson‐White Syndrome

Kim

Gerling

Kono

et al. 2008

Pacing Clinical Electrophis

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We report the case of a young man who presented with a rapid, narrow-complex atrial fibrillation. A few hours after being administered intravenous metoprolol and diltiazem for rate control, he developed intermittent ventricular preexcitation on the electrocardiogram (ECG) and experienced ventricular fibrillation, from which he was successfully defibrillated. A subsequent electrocardiogram in sinus rhythm demonstrated previously unknown Wolff-Parkinson-White pattern. A left lateral accessory pathway was successfully ablated. Wolff-Parkinson-White syndrome should be included in the differential diagnosis when a young patient presents with atrial fibrillation, even if the ventricular complexes on the ECG are not preexcited.

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Section: Discussioncontrasting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Precipitation of Ventricular Fibrillation by Intravenous Diltiazem and Metoprolol in a Young Patient with Occult Wolff‐Parkinson‐White Syndrome

Kim

Gerling

Kono

et al. 2008

Pacing Clinical Electrophis

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“…These nondihydropyridine calcium channel blockers should not be used in patients with LV systolic dysfunction and decompensated HF owing to their negative inotropic effects, but they may be used in patients with HF with preserved LV systolic function. In addition, these agents should not be used in patients with pre-excitation and AF due to the potential for shortening bypass tract refractoriness which may accelerate the ventricular rate to precipitate hypotension or ventricular fibrillation (281, 289) (Section 7.8).…”

Section: 1 Specific Pharmacological Agents For Rate Controlmentioning

confidence: 99%

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation

January¹,

Wann²,

Alpert³

et al. 2014

Circulation

3,570

1,139

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“…This is in marked contrast to the effects of intravenous verapamil given under these circumstances, the administration of which frequently results in hemodynamic deterioration and occasionally in death. 31 In addition, the current study has demonstrated that, despite shortening of accessory connection refractoriness by adenosine, the risks associated with inadvertent administration during preexcited atrial flutter are small and should not discourage the use of adenosine as a diagnostic agent in broad complex regular tachycardias of uncertain origin. Although not observed in this study, it is possible that conversion of atrial flutter to sustained atrial fibrillation may occur, and it should be emphasized that, as with administration of all antiarrhythmic agents, continuous electrocardiographic monitoring and availability of DC cardioversion is a necessary precaution during administration of adenosine.…”

Section: Discussionmentioning

confidence: 99%

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections.

et al. 1991

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Background. Several groups have suggested the use of intravenous adenosine or adenosine triphosphate in the diagnosis of regular broad complex tachycardias. However, the short half-life of these agents has precluded assessment of their effects on refractoriness of accessory connections, and their safety in preexcited arrhythmias has not been demonstrated.Methods and Results. We examined the effects of intravenous adenosine on accessory atrioventricular (AV) connections in 30 patients with the Wolff-Parkinson-White syndrome. Intravenous adenosine (12 mg, rapid bolus) was administered to 14 patients (group 1) during continuous atrial pacing at a cycle length 20 msec below that required to cause 2:1 conduction block in the accessory connection (mean pacing cycle length 261+41 msec). After adenosine, transient 1:1 conduction occurred via the accessory connection in 12 of 14 patients, indicating a shortening of antegrade refractoriness. In three of seven patients, this effect was abolished after intravenous propranolol (0.2 mg/kg). Nineteen patients (group 2) received adenosine (0.17±0.04 mg/kg) during induced, preexcited atrial arrhythmias. The minimum RR interval during preexcited atrial fibrillation transiently decreased (252+±44 msec to 224±35 msec, p<0.01) after adenosine, but no change in average RR interval was observed (360± 59 msec to 357±60 msec, NS). The preexcited ventricular response to atrial flutter was transiently accelerated in five of eight patients (415 ±21 msec to 360 ±49 msec, p<0.05) due to shortening of flutter cycle length (207±+10 msec to 180±24 msec, p<0.05). However, 2:1 accessory connection conduction was maintained in all eight patients. All effects were short lived, with the decrease in RR interval during atrial fibrillation occurring for a maximum of two RR intervals only. No patient suffered ventricular arrhythmias or hemodynamic deterioration.Conclusions. Adenosine shortens antegrade refractoriness of accessory AV connections, and in some patients this action is mediated by f3-adrenergic stimulation. Adenosine may cause acceleration of preexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in broad complex, regular tachycardias of uncertain origin. (Circulation 1991;84:1962-1968

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Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation

Cited by 43 publications

References 6 publications

Precipitation of Ventricular Fibrillation by Intravenous Diltiazem and Metoprolol in a Young Patient with Occult Wolff‐Parkinson‐White Syndrome

Precipitation of Ventricular Fibrillation by Intravenous Diltiazem and Metoprolol in a Young Patient with Occult Wolff‐Parkinson‐White Syndrome

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections.

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