Dynamics of the QT interval in patients with exercise-induced ventricular tachycardia in normal and abnormal hearts

Abstract

Inhomogeneity of ventricular repolarization reflected in prolongation of the QT interval of the surface electrocardiogram can predispose patients to ventricular arrhythmia. This study examines whether an abnormality of QT adaptation to changes in heart rate is likely to be of importance in the pathogenesis of ventricular tachycardia (VT) in patients with and without underlying structural heart disease. The QT-R-R relationship during exercise was studied in 52 patients. Forty-two patients had VT associated with a “clinically normal” heart (idiopathic VT), of which 23 had no VT on exercise and 19 had exercise-induced VT. These patients were compared to 10 subjects with exercise-induced VT related to ischemic heart disease. The QT interval was measured manually from computer-averaged QRS complexes recorded at 1- to 3-minute intervals during treadmill exercise tests. An approximately linear association existed between the QT and R-R intervals within the range of heart rates observed. The slope of the QT-R-R relation was lower in patients with structural heart disease (0.23 ± 0.06) than in patients with normal hearts with (0.29 ± 0.12) and without (0.29 ± 0.12) exercise-induced VT ( p < 0.05). The intercept of the regression line was higher in patients with structurally abnormal hearts (209.2 ± 55.3 msec) than in patients with idiopathic VT with (155.6 ± 49.7 msec) and without (157.7 ± 69.0 msec) exercise-induced VT ( p < 0.02). The corrected QT (Bazett's formula) was similar in all three groups at rest, but was higher in patients with structurally abnormal hearts at peak exercise, 449.6 ± 28.0 versus 425.8 ± 27.4 msec (idiopathic VT, exercise induced) versus 427.3 ± 26.6 msec (idiopathic VT, not exercise induced) ( p < 0.05). There was no statistically significant difference in any of these parameters between patients with and without exercise-induced VT in structurally normal hearts. The results suggest that rate adaptation of the QT interval is abnormal in patients with structural heart disease and may be involved in the pathogenesis of the VT. QT adaptation is normal in patients with idiopathic VT and exercise-induced arrhythmia in which the mechanism is less likely to be dependent on an abnormality of repolarization dynamics.