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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 3, May/June 2015

AFRICA

145

who develop QT prolongation and TdP have an underlying

genetic predisposition, resulting in prolongation of the action

potential duration, which is exacerbated by the bradycardia.

Conclusion

Our case re-emphasises the risks involved in administering

erythromycin to patients. In particular, patients with AV block

should not receive this drug. The timing of the TdP is interesting

because it coincided with the insertion of the temporary pacing

lead. It is very likely that the ventricular ectopics induced by

the temporary lead in the right ventricular apex precipitated the

short–long cycle that led to the TdP. Instead of repeated DC

cardioversion, we could have temporarily paced the patient at

a more rapid rate to prevent the recurrence of the bradycardia-

induced TdP. Based on data from Kurita

et al.

,

9

a rate above 60

bpm would have been sufficient to prevent further episodes of

TdP.

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