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Recurrent AICD shocks in a 60-year-old man
  1. Colin Yeo,
  2. Kelvin CK Wong
  1. Correspondence to Dr Colin Yeo, Department of Cardiology, Changi General Hospital, 2 Simei Street 3, Singapore 529889, Singapore; yeocolin21{at}


Clinical introduction We present the case of a 60-year-old man with history of non-ischaemic cardiomyopathy with left ventricular ejection fraction of 40%. His baseline surface 12-lead ECG shows sinus rhythm with PR interval of 170 ms, no evidence of pre-excitation and a normal QT interval. He had a single-chamber automated implantable cardiac defibrillator (AICD) inserted for sustained wide complex tachycardia associated with palpitations. Subsequently, he presented with recurrent shocks from the AICD coming on at rest despite treatment with amiodarone. He did not experience any significant cardiovascular symptoms except for mild palpitations. There were no reversible causes found for his arrhythmia. Figure 1 shows the device EGM of the event leading to the shock.

Question What is the tachycardia that caused the AICD shock? (figure 1)

  1. Atrial fibrillation (AF) with pre-excitation

  2. Ventricular fibrillation (VF)

  3. Multiform ventricular tachycardia (VT)

  4. Atrial tachycardia (AT) with bundle branch block

  5. Torsades de Pointes (TdP)

Statistics from

Figure 1

Device EGM when patient was shocked by the AICD.

Answer: C

The far-field EGM showed irregularly irregular wide complex tachycardia of slightly variable morphologies, which can be distinguished from the narrow complex EGM immediately following shock delivered by the device. This is not VF because there is too much regularity to the QRS complexes and too much order. TdP is unlikely due to the longer cycle lengths and lack of haemodynamic compromise. Furthermore, TdP has a classic appearance of ‘turning around’ the baseline, which is not present in this instance. AT with bundle-branch block would also be unlikely with the QRS morphology being variable.

On the far-field EGM, the QRS was narrower during beats of shorter cycle lengths (indicated by arrows in see online supplementary Figure), which would be unusual, as pre-excitation usually becomes more apparent as nodal conduction decrements at shorter cycle lengths. These narrow complexes that come early are more likely to represent capture beats during an irregular VT.

After shock delivery by the AID, there were clear narrow complexes initially, interspersed with short runs of broad complex tachycardia, more likely to represent non-sustained VT. These non-sustained runs were documented on a 12-lead ECG (figure 2), which showed irregularly irregular wide complex tachycardia with inferior axis, precordial transition is V1/V2 and absent S wave in V5/V6. The variable QRS morphologies are best appreciated in leads aVL and V1 with changes in axis. This likely represented a left-sided outflow tract VT with an automatic/triggered mechanism and slightly variable exits.1 The variable QRS morphologies would be against pre-excited AF.

Figure 2

12 lead ECG of the non sustained wide complex tachycardia.

Electrophysiology study demonstrated absence of accessory pathway conduction. The origin of the VT was mapped to the left coronary cusp.


We would like to thank the cardiology department of Changi General Hospital for taking care of the patient during his multiple visits to the hospital.



  • Twitter Follow Colin Yeo at @yeocolin

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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