Europace Advance Access originally published online on May 1, 2008
Europace 2008 10(6):767-768; doi:10.1093/europace/eun105
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VENTRICULAR TACHYCARDIA
Bidirectional ventricular tachycardia in fulminant myocarditis
1 Cardiology, UZ Gasthuisberg, University of Leuven, Herestraat 49, 3000 Leuven, Belgium; 2 Pediatric Cardiology, UZ Gasthuisberg, University of Leuven, Herestraat 49, 3000 Leuven, Belgium; 3 Intensive care, UZ Gasthuisberg, University of Leuven, Herestraat 49, 3000 Leuven, Belgium
Manuscript submitted 19 February 2008. Accepted after revision 2 April 2008.
* Corresponding author. Tel: +32 495 99 26 59; fax: +32 3 666 49 87. E-mail address: benjamin.berte{at}uz.kuleuven.ac.be
Key Words: Bidirectional ventricular tachycardia, myocarditis, Ecg
A 14-year-old girl (176 cm, 60 kg) was referred to our hospital with acute heart failure. She had a history of dyspnoea during a week. She developed orthopnoea and palpitations on the day of admission. The ECG of the referring hospital showed a bidirectional ventricular tachycardia (VT) (Figure 1A). She was transferred to our intensive care unit. After administration of amiodarone (300 mg/2 h followed by 900 mg/24 h iv), sinus rhythm was restored. Marked ST elevation became apparent in all leads (Figure 1B). After stabilization another ECG showed ventricular bigeminy (Figure 1C). Echocardiography was suggestive for acute myocarditis. Fulminant myocarditis was proven by endomyocardial biopsy. No aetiological agents could be withheld. After 4 days, our patient developed cardiogenic shock and an assist device was placed. She was successfully transplanted 58 days after the diagnosis.
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Distinction between acute and fulminant acute myocarditis is important in view of the difference in presentation and outcome. Fulminant myocarditis is associated with critical illness and rapid deterioration to cardiovascular collapse.1
Ventricular arrhythmias are common. Bidirectional VT is a rare rhythm disorder that is usually described in digitalis intoxication, but is also seen in ischaemic heart disease, hypokalaemia, myocarditis, and familial catecholaminergic polymorphic VT.2,3 Experimental data in a canine ventricular wedge preparation suggest that the underlying mechanism of VT in these cases is ectopic discharges by triggered activity mainly in the epicardium.4 In these experiments, bidirectional VT and polymorphic VT are preceded by multiple ectopic beats, increasing transmural dispersion and creating a substrate for VT. In view of the presence of multiple ventricular extrasystoles, our case is illustrative for this pathophysiological mechanism. Distinction between bidirectional VT (Figure 1A) and ventricular bigeminy (Figure 1C) can be difficult. In Figure 1C, QRS complexes identical to the ones in sinus rhythm (Figure 1B) with a normal PR can be clearly distinguished from other QRS complexes with a very short PR suggestive of ventricular extrasystoles. In contrast, in Figure 1A, none of the QRS complexes resemble sinus rhythm and there might in some complexes be a suggestion of a retrograde P-wave shortly after the QRS, both indicative for bidirectional VT. Conflict of interest: none declared.
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[1] Amabile N, Fraisse A, Bouvenot J, Chetaille B, Ovaert C. Outcome of acute fulminant myocarditis in children. Heart (2006) 92:1269–73.
[2] Grimard C, De Labriolle A, Charbonnier B, Babuty D. Bidirectional ventricular tachycardia resulting from digoxin toxicity. J Cardiovasc Electrophysiol (2005) 16:807–8.[CrossRef][Web of Science][Medline]
[3] Francis J, Sankar V, Nair VK, Priori S. Catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm (2005) 2:550–4.[CrossRef][Web of Science][Medline]
[4] Gi-Byoung Nam, Burashnikov A, Antzelevitch C. Cellular mechanisms underlying the development of catecholaminergic ventricular tachycardia. Circulation (2005) 111:2727–33.
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