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Journal Article
Research Support, Non-U.S. Gov't
The mode of onset of ventricular tachycardia. A patient-specific phenomenon.
European Heart Journal 1997 December
AIMS: The purpose of our study was to investigate the electrical trigger modes of monomorphic ventricular tachycardia, by analysing stored intracardiac electrograms, and to identify haemodynamic or electrocardiographic predictors in patients with cardioverter-defribrillators.
METHODS: We recorded 286 episodes of monomorphic ventricular tachycardia in 38 patients with at least three events. The electrical triggers were characterized by the morphology number, complexity, and coupling interval of premature depolarizations preceding the ventricular tachycardia. We also evaluated clinical and electrocardiographic data.
RESULTS: We found two basic electrical trigger modes. Two hundred and sixteen events (75%) were observed to have no RR-interval variations before onset, while 70 episodes (25%) had a short-long-short sequence. These episodes invariably featured increased QT disperson. In 31 of 38 patients (82%), the ventricular tachycardias were always initiated by the same mode of onset. In eight patients, the monomorphic ventricular tachycardias were always triggered by short-long-short sequences. In seven patients, more than one onset mechanism was observed.
CONCLUSIONS: Two basic modes of onset were responsible for monomorphic ventricular tachycardia: one without RR-interval variations immediately prior to onset and another characterized by short-long-short sequences and increased QT dispersion. The mechanisms were largely patient-specific and not related to cardiac diagnosis or left ventricular function.
METHODS: We recorded 286 episodes of monomorphic ventricular tachycardia in 38 patients with at least three events. The electrical triggers were characterized by the morphology number, complexity, and coupling interval of premature depolarizations preceding the ventricular tachycardia. We also evaluated clinical and electrocardiographic data.
RESULTS: We found two basic electrical trigger modes. Two hundred and sixteen events (75%) were observed to have no RR-interval variations before onset, while 70 episodes (25%) had a short-long-short sequence. These episodes invariably featured increased QT disperson. In 31 of 38 patients (82%), the ventricular tachycardias were always initiated by the same mode of onset. In eight patients, the monomorphic ventricular tachycardias were always triggered by short-long-short sequences. In seven patients, more than one onset mechanism was observed.
CONCLUSIONS: Two basic modes of onset were responsible for monomorphic ventricular tachycardia: one without RR-interval variations immediately prior to onset and another characterized by short-long-short sequences and increased QT dispersion. The mechanisms were largely patient-specific and not related to cardiac diagnosis or left ventricular function.
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