This case highlights that incessant ventricular tachycardia in acute Coxsackie B myocarditis can be driven by abnormal automaticity and may be associated with a fatal clinical course due to rapid left ventricular failure.
May signal rapid LV failure in automaticity-driven VT from Coxsackie myocarditis despite amiodarone; leaves open targeted therapies.
A 13-year-old girl presented with incessant ventricular tachycardia complicating acute Coxsackie B3 myocarditis. Electrophysiologic assessment revealed that the tachycardia could not be terminated, overdrive suppressed or accelerated by programmed electrical stimulation, but was transiently slowed by intravenous adenosine triphosphate and had marked spontaneous and sympathoautonomic-mediated fluctuation in the tachycardia cycle length. These features were atypical of reentry and triggered automaticity and suggested that abnormal automaticity was the likely tachycardia mechanism. Intravenous amiodarone slowed the ventricular tachycardia, but the patient eventually succumbed from rapidly progressive left ventricular failure. Postmortem pathohistologic examination confirmed the diagnosis of acute myocarditis.
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Tai et al. (2008) studied this question.
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