Ventricular fibrillation induced by transesophageal atrial pacing in hypertrophic cardiomyopathy
S Favale1, M Di Biase, U Rizzo
1Division of Cardiology, University of Bari, Italy.
Insights
Sudden death in hypertrophic cardiomyopathy may stem from atrial tachyarrhythmias triggering ventricular fibrillation. Electrophysiological properties of the myocardium appear crucial, not just high heart rates.
Area of Science:
- Cardiology
- Electrophysiology
- Genetics
Background:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart condition associated with a high risk of sudden cardiac death.
- The precise mechanisms underlying sudden death in HCM remain incompletely understood.
- Family history of HCM and sudden death is a significant risk factor.
Observation:
- An 18-year-old patient with a family history of HCM and sudden death experienced inducible ventricular fibrillation (VF).
- VF was repeatedly induced via transesophageal atrial stimulation with 1:1 atrioventricular (AV) conduction at a rapid ventricular rate (200 beats/min).
- Pharmacological depression of the AV node successfully prevented VF induction.
Findings:
- The induction of VF occurred at a ventricular rate not considered exceptionally high.
- This suggests that the intrinsic electrophysiological properties of the hypertrophic myocardium play a critical role in facilitating VF.
- Atrial tachyarrhythmias may precipitate life-threatening ventricular arrhythmias in HCM patients.
Implications:
- Understanding the electrophysiological basis of VF in HCM is vital for risk stratification.
- Targeting AV node conduction could be a potential therapeutic strategy to prevent sudden death.
- Further research into the role of atrial tachyarrhythmias in HCM-related sudden cardiac death is warranted.
Abstract:
Sudden death is a rather frequent occurrence in patients with hypertrophic cardiomyopathy, yet the mechanism is uncertain in most cases. We describe a case of an 18 years old patient with a family history of hypertrophic cardiomyopathy and sudden death in whom ventricular fibrillation could be repeatedly induced by means of transesophageal atrial stimulation with 1:1 AV conduction at a rate of 200 beats min-1 and prevented by pharmacological depression of AV node. The not particularly high ventricular rate at which VF occurred could suggest that in hypertrophic cardiomyopathy a major role in favouring VF induction is played by the electrophysiological properties of the myocardium and that sudden death can occur as a consequence of different atrial tachyarrhythmias.
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