Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6-12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 +/- 20 years (range 18-82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 +/- 80 msecs (range 260-580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on beta-adrenergic stimulation are most likely to be terminated by adenosine.
Cardiac device infections are a rare complication of pacing and defibrillator therapy. The number of implanted devices will likely continue to rise with increasing implantation of the cardioverter defibrillator and cardiac resynchronization devices. This report describes a case of an uncommon pathogen for device-associated endocarditis.
Occasional patients have excessive defibrillation energy requirements despite appropriate transvenous defibrillation lead position and modification of defibrillation waveform and configuration. Preliminary data suggest that use of subcutaneous defibrillation electrode arrays with nonthoracotomy systems is associated with a substantial reduction in defibrillation threshold. The current operative approach to subcutaneous lead array implantation involves the use of a separate left chest incision. We present two cases in which implantation of a subcutaneous lead array in combination with a transvenous defibrillation electrode was performed via a single infraclavicular incision and associated with a reduction in defibrillation threshold. Such an approach simplifies implantation and avoids the potential morbidity of the additional incision required of a left lateral chest approach.
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