Nonsustained polymorphous ventricular tachycardia during amiodarone therapy for atrial fibrillation complicating cardiomyopathy. Management with intravenous magnesium sulfate.

A case is presented in which amiodarone was administered to suppress paroxysmal atrial fibrillation in a patient with an idiopathic cardiomyopathy. Eleven days after initiation of therapy with amiodarone, the patient experienced syncope and was noted to have recurrent episodes of polymorphous ventricular tachycardia. The patient was hospitalized and treated with a bolus as well as continuous infusion of intravenous magnesium sulfate. When the infusion was transiently discontinued, recurrences of polymorphous ventricular tachycardia were noted. The probable proarrhythmic action of amiodarone, although rare, is reviewed along with a discussion of the novel use of intravenous magnesium sulfate therapy.

Setting of relatively low energy outputs may permit implantation of a nonthoracotomy automatic cardioverter defibrillator system when high energy outputs prove ineffective.

At intraoperative testing of defibrillation thresholds during implantation of internal cardioverter defibrillators, standard step-down approaches of energy outputs are used. If relatively high energy outputs are not successful at defibrillating the heart, the electrodes are frequently reconfigured. When attempting implantation of a nonthoracotomy lead system, high defibrillation thresholds may warrant opening of the chest cavity to place one or more epicardial electrodes. A case is presented where a nonthoracotomy system was able to be implanted using relatively low energy outputs which were reproducibly successful at terminating ventricular fibrillation when higher energy outputs were unsuccessful. Mechanisms for this phenomenon and alternate recommendations for defibrillation testing are presented.

Inhibition of bradycardia pacing caused by far-field atrial sensing in a third-generation cardioverter defibrillator with an automatic gain feature.

The diagnostic accuracy of implantable cardioverter defibrillators may be improved by automatically adjusting gain algorithms, which in general reduce the likelihood of oversensing while maintaining the ability to detect the low amplitude signals associated with ventricular fibrillation. We present a patient with a third-generation device who developed prolonged ventricular asystole arising as a complication of the automatic gain feature. During asystole the device automatically increased sensitivity in order to prevent undersensing of ventricular fibrillation, which in this case resulted in far-field sensing of atrial activity and inhibition of ventricular pacing.

Sustained ventricular tachycardia associated with sarcoidosis: assessment of the underlying cardiac anatomy and the prospective utility of programmed ventricular stimulation, drug therapy and an implantable antitachycardia device.

The presentation, cardiac anatomy and utility of programmed ventricular stimulation in seven patients with sustained ventricular tachycardia associated with sarcoidosis are described. The mean patient age was 38 +/- 8 years. Pulmonary involvement was apparent in three patients and no systemic manifestations of sarcoidosis were present in one patient. All patients had electrocardiographic abnormalities at rest and six had a left ventricular ejection fraction less than 45%. All seven patients had left ventricular wall motion abnormalities and five had mitral valve dysfunction. Sustained ventricular tachycardia was easily induced in all patients. Spontaneous sustained ventricular tachycardia was not prevented with corticosteroid administration. Despite antiarrhythmic drug therapy, two patients had sudden cardiac death and an additional four had recurrence of ventricular tachycardia. Four patients had an automatic cardioverter-defibrillator implanted and received drug therapy; all four received appropriate shocks. This report represents the largest descriptive series of consecutive patients with sustained ventricular tachycardia associated with sarcoidosis. Antiarrhythmic drug therapy of ventricular tachycardia in patients with sarcoidosis, even when guided with programmed ventricular stimulation, is associated with a high rate of arrhythmia recurrence or sudden death, or both. Thus, implantation of an automatic antitachycardia device (cardioverter-defibrillator) should be considered as primary therapy in such patients. Furthermore, sarcoidosis should be excluded, with Kveim skin testing if necessary, in any patient with sustained ventricular tachycardia of unknown origin.