BACKGROUND--Idiopathic ventricular tachycardia (VT) occurs in a small but important subset of patients without clinically overt heart disease. The mechanism of the arrhythmogenesis remains unclear in these patients. This study examines modulation of the QT interval by the autonomic nervous system in a group of patients with idiopathic ventricular tachycardia. METHODS--Cardiac autonomic activity and ventricular repolarisation were studied in 27 patients with VT associated with a clinically normal heart (NHVT) and in 20 normal subjects. All the patients were in sinus rhythm, had normal atrioventricular conduction, and were in a drug free state. Cardiac efferent autonomic activity was measured by spectral analysis of heart rate variability from 24 hour ambulatory electrocardiograms on a Holter analysis system (Marquette). Ventricular repolarisation was evaluated by measuring the QT intervals from the same 24 hour Holter tapes at one hour intervals. RESULTS--There was no difference in any of the QT interval variables including the maximum, minimum, and mean of both the QT interval and its corrected value (Bazett's formula) between patients with NHVT and normal subjects. The high frequency component (0.04-0.15 Hz) of heart rate variability was significantly decreased in patients with NHVT compared with normal subjects (16 (8) v 21 (12) ms, p < 0.05). There was a significant correlation between the spectral variables of heart rate variability and the mean, maximal, and minimal QT intervals in normal subjects, whereas the relation was lost in patients with NHVT. No difference was found in mean heart rate between normal subjects and patients with NHVT (70 (9) v 72 (13) beats/min, NS). CONCLUSIONS--The high frequency component of heart rate variability is significantly decreased and the relation of QT interval to heart rate variability is significantly altered in patients with NHVT as compared with normal subjects. These findings suggest that abnormal modulation of the QT interval by the autonomic nervous system may play an important part in the arrhythmogenesis of NHVT. This might result from impaired vagal efferent cardiac activity in these patients.
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