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• A case of sudden cardiac arrest: Is it truly idiopathic?
  Michael Papadakis
  Published on: 13 July 2009
• Correct management, Incorrect rationale.
  Ralph G. Oriscello
  Published on: 22 June 2009

• Published on: 13 July 2009

  A case of sudden cardiac arrest: Is it truly idiopathic?

  • Michael Papadakis, Research Fellow in Cardiology
  • Other Contributors:
    • Sanjay Sharma

  To the editor: We read with great interest the case of a sudden cardiac arrest associated with early repolarisation by Magapu et al.1 Early repolarisation pattern on the 12-lead electrocardiogram has been linked to an increased risk of malignant arrhythmias although intense debate exists as to the causal effect, given the high frequency of such repolarisation patterns in the general and athletic population. Our experien...

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  To the editor: We read with great interest the case of a sudden cardiac arrest associated with early repolarisation by Magapu et al.1 Early repolarisation pattern on the 12-lead electrocardiogram has been linked to an increased risk of malignant arrhythmias although intense debate exists as to the causal effect, given the high frequency of such repolarisation patterns in the general and athletic population. Our experience with screening of young athletes in the UK confirms the high frequency of early repolarisation pattern in this group.

  Having examined meticulously both electrocardiograms presented we would suggest an alternative diagnosis of Brugada syndrome that should be explored. Although the authors discuss the need to exclude ion channelopathies as a cause of the cardiac arrest, it is unclear from the investigations section whether the possibility of Brugada syndrome was fully explored. ECG A exhibits a partial right bundle branch block pattern with 1mm ST-segment elevation and a negative T-wave in V1 and a J-point elevation with < 1mm saddle-shaped ST-segment elevation in V2 and V3, which could represent type-3 Brugada pattern. Supporting evidence to a diagnosis of Brugada syndrome would include the timing of the cardiac arrest since most patients with Brugada syndrome exhibit malignant arrhythmias at rest, especially during sleep and increased parasympathetic activity appears to play an important role in exacerbating the electrical imbalance and triggering arrhythmias.2 Furthermore although repolarisation changes in Brugada syndrome are usually manifested in the anterior pre- cordial leads (V1-V3), similar changes in the inferior and lateral leads have been reported and therefore one should be cautious when interpreting the early repolarisation patterns.3 Finally, there are reports in the literature of normalisation of the ST-segment elevation with increased sympathetic activity during exercise and unmasking of the syndrome with increased parasympathetic activity in the recovery phase, which may partly explain the phenomenon observed by the authors.4

  It would be helpful for the authors to clarify; 1) whether a provocation test with a sodium ion channel blocker such as Ajmaline or Flecainide was performed to unmask the Brugada phenotype and 2) whether the electrocardiographic changes were accentuated on recovery immediately post exercise testing.

  References: 1. Magapu P, Newall N. A case of sudden cardiac arrest associated with early repolarisation. Heart 2009;95:930.

  2. Yan GX, Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. Circulation 1999;100:1660-1666.

  3. Ogawa M, Kumagai K, Yamanouchi Y, Saku K. Spontaneous onset of ventricular fibrillation in Brugada syndrome with J wave and ST segment elevation in the inferior leads. Heart rhythm 2005;2:97-99.

  4. Esperer HD, Hoos O, Hottenroft K. Syncope due to Brugada syndrome in a young athlete. Br J Sports Med 2007;41:180-181.

  Competing intersts: None

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  Conflict of Interest:
  None declared.

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• Published on: 22 June 2009

  Correct management, Incorrect rationale.

  • Ralph G. Oriscello, Chief, Cardiology
  • Other Contributors:
    • Brijesh Patel, Steve C. Tsai

  It was with great interest and enthusiasm that we read the recent "Images in Cardiology" presentation of Drs. Magapu and Newall. Without commenting on the eventual neurologic status of their patient, resuscitated for 45 minutes, followed by a prolonged stay in the Intensive Care Unit, most likely tethered to a ventilator, they concluded that the final therapy to prevent a recurrence was the insertion of an implantable c...

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  It was with great interest and enthusiasm that we read the recent "Images in Cardiology" presentation of Drs. Magapu and Newall. Without commenting on the eventual neurologic status of their patient, resuscitated for 45 minutes, followed by a prolonged stay in the Intensive Care Unit, most likely tethered to a ventilator, they concluded that the final therapy to prevent a recurrence was the insertion of an implantable cardioverter-defibrillator. We agree.

  We do not agree with their final diagnosis. While acknowledging correctly that the usual causes of sudden cardiac death must be considered, including the Brugada syndrome, arrhythmogenic right ventricular dysplasia/cardiomyopathy, catecholamine-induced ventricular tachycardia, and the long QT syndromes, they concentrated on an early repolarization wave as the potential cause of the sudden ventricular arrhythmia.

  The initial electrocardiogram they present shows an unmistakable Brugada syndrome variant, a type 3 with a saddle-back morphology. Leads V1 and V2 are diagnostic. This electrocardiogram possibly would have converted to the more classic variety (type 1) had a sodium channel blocking agent been administered.

  The literature is punctuated with similar cases of an arrest during sleep. None have been published in attribution to early repolarization. They have been published in documentation of the Brugada syndrome.

  Respectfully,

  Ralph G. Oriscello, MD, FACC, Steve C. Tsai, MD, Brijesh Patel, MD

  (This is solely the opinion of the above physicians and does not reflect the opinion of the Department of Veterans Affairs).

  References:

  Wellen HJ. Early repolariztion revisited. N Engl J Med 2008;358:2063- 5.

  Marill KA, Ellinor PT. Case 37-2005: A 35-year-old man with cardiac arrest while sleeping. N Engl J Med 2005;353:2492-501.

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  Conflict of Interest:
  None declared.

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