Incessant Automatic Ventricular Tachycardia Complicating Acute Coxsackie B Myocarditis

Tai, Yu‐Tzu; Lau, Chu‐Pak; Fong, Ping-Ching; Li, John Po-Shan; Lee, Kathy Lai‐Fun

doi:10.1159/000175023

Cited by 42 publications

(21 citation statements)

References 11 publications

(12 reference statements)

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“…Cardiac arrhythmias associated with acute myocarditis can range from conduction abnormalities to difficult to suppress lifethreatening ventricular arrhythmias. Death can occur related to HF and arrhythmias including heart block (444,445,(455)(456)(457)(458)(459)(460). Patients with arrhythmias or syncope may require antiarrhythmic drugs and/or device therapy (461).…”

Section: Myocarditismentioning

confidence: 99%

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death

Zipes¹,

Camm²,

Borggrefe³

et al. 2006

Circulation

1,204

671

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Section: Myocarditismentioning

confidence: 99%

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death

Zipes¹,

Camm²,

Borggrefe³

et al. 2006

Circulation

1,204

671

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“…The occurrence of only occasional beats of focus A (Figure 2) where the focus B is continuing in an accelerated rate excludes the possibility of a BVT because of a pingpong effect as there is no consistency in occurrence of focus Triggered activity and abnormal automaticity have been described secondary to myocardial inflammation in myocarditis. 8,22 Incessant nature of the tachycardia, unresponsive to multiple DC cardioversion, antiarrhythmic agents such as β-blockers and lignocaine, suggests that the possible mechanism of VT is enhanced automaticity because arrhythmias either because of reentry or because of delayed after depolarization typically are responsive to these maneuvers. 23 It is possible that local inflammation around the automatic foci could create an entry block in cardiac sarcoidosis, resulting in parasystole.…”

Section: Discussionmentioning

confidence: 99%

Unusual Incessant Ventricular Tachycardia

Shenthar

2015

Circ: Arrhythmia and Electrophysiology

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V entricular tachycardia (VT) is defined as a tachycardia with a rate of >100 per minute, with ≥3 consecutive beats that originates from the ventricles, and is independent of atria or atrioventricular nodal conduction. Of all the VTs, 10% occurs in those with structurally normal heart and these are called as idiopathic VTs, and the rest 90% occurs in patients with structural heart disease. VTs may be classsified based on the clinical characteristic (clinical VT, hemodynamically stable or unstable, repetitive, incessant, etc.), morphology (monomorphic, multiple morphologies, pleomorphic, polymorphic, bidirectional, etc.) or mechanisms (scar-related reentry, automaticity, and triggered activity). Incessant VT is defined as continuous sustained VT during several hours, which recurs promptly despite repeated intervention for termination. VT storm is considered as ≥3 separate episodes of sustained VT within 24 hours, each requiring termination by an intervention. Monomorphic VT has a uniformly similar QRS configuration from beat-to-beat, with either right or left bundle configuration depending on whether the dominant deflection in lead V1 is R or S wave. Multiple monomorphic VTs refer to >1 morphologically distinct monomorphic VT, occurring as different episodes, or induced at different times. Polymorphic VT has continuously changing QRS configuration from beat-to-beat indicating a changing ventricular activation sequence. Pleomorphic VT has >1 morphologically distinct QRS complex occurring during the same episode of VT, but the QRS is not continuously changing. Bidirectional VT (BVT) is characterized by beat-to-beat alternation of the QRS axis on the ECG and is usually regular. Editor's Perspective see p 1512Here, we describe unusual incessant VT in a young male and discuss evaluation, management, and the possible mechanism. Case ReportA 33-year-old male, nondiabetic, nonhypertensive, presented with history of palpitation, chest discomfort, and fatigue of 6 hours duration. He had been otherwise healthy, not on any medications with no history of tobacco, alcohol, or drug use. At presentation, pulse rate was 144 beats per minute, irregular, blood pressure 96/60 mm Hg, and the rest of physical examination was unremarkable. Twelve-lead ECG revealed a wide complex regularly irregular tachycardia at a rate of 144 beats per minute, right bundle morphology, QRS duration of 200 to 220 ms, QRS axis alternating between +160° and −40°, QRS transition alternating from V3 to V6, and evidence of atrioventricular dissociation (Figure 1). Tachycardia was unresponsive to intravenous lignocaine, esmolol, amiodarone (300 mg during 1 hour), and 2 attempts of biphasic direct current (DC) cardioversion of 200 J. Because the tachycardia was incessant, patient was sedated, intubated, ventilated, and continued on intravenous amiodarone (900 mg/24 hours) with further 4 unsuccessful attempts at DC cardioversion. Tachycardia converted to monomorphic VT with occasional VT complexes of the 2nd morphology (Figure 2), which terminated 6 hours late...

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“…Accelerated ventricular rhythms are primarily seen [7,11], although a case of supraventricular tachycardia associated with neonatal Coxsackie B myocarditis has been reported [5]. A child with Coxsackie B4 myocarditis who presented with a tachyarrhythmia originally thought to be supraventricular tachycardia has also been reported [8].…”

Section: Discussionmentioning

confidence: 99%

“…There have been several reports of accelerated ventricular rhythms complicating acute Coxsackie B myocarditis [7,10]; the occurrence of supraventricular tachycardia as a complicating feature is rare [5]. We report a successful outcome in an unusual case of atrial flutter complicating acute neonatal Coxsackie B2 myocarditis.…”

mentioning

confidence: 91%