Increased dispersion of refractoriness in the absence of QT prolongation in patients with mitral valve prolapse and ventricular arrhythmias.

Abstract

Background-The mechanism responsible for the reported high incidence of ventricular arrhythmias in mitral valve prolapse is not clear. Electrocardiographic studies show an increased occurrence of repolarisation abnormalities on the 12 lead surface electrocardiogram, indicating regional differences in ventricular recovery. The purpose of this study was to investigate whether dispersion of refractoriness was an arrhythmogenic mechanism. Methods-QT dispersion was measured in 32 patients with echocardiographically documented mitral valve prolapse and ventricular arrhythmias on 24 hour Holter recordings. QT dispersion was defined as the difference between the maximum and minimum average QT interval in any of the 12 leads of the surface electrocardiogram. QT dispersion corrected for heart rate was calculated by Bazett's formula. The results were compared with the data from 32 matched controls without a history of cardiac disease. Patients taking drugs that influence the QT interval and patients with a QRS duration > 120 ms were excluded. Results-QT dispersion was greater in patients with mitral valve prolapse than in matched controls (60 (20) v 39 (11 ms) respectively, P < 0.001) as was corrected QT (64 (20 ms) v 43 (12 ms) respectively, P < 0 001). There was no significant difference in minimum or maximum QT intervals between the two groups. Conclusions-QT dispersion on the 12 lead surface electrocardiogram was greater in patients with mitral valve prolapse with ventricular arrhythmias than in normal controls, but the maximum QT interval was not increased. The results accord with the hypothesis that regional shortening and lengthening of repolarisation times in patients with mitral valve prolapse may account for the increased dispersion of refractoriness. (Br HeartJ' 1995;73:37-40)

QT Dispersion in Patients with Polycystic Ovary Syndrome.

“…QT dispersion and cardiac disease: Increased QT dispersion reflects electrical inhomogeneity, which may occur as a result of myocardial ischemia, mitral valve prolapse, ventricular hypertrophy or dilatation, autonomic neuropathy, peripheral vascular disease, and hypertension. [9][10][11][12][13][14][15] A recent study, which analyzed the 12-lead electrocardiograms of 1501 healthy adults and 1784 healthy children found that QTd was age and sex independent.…”

Task Force on Sudden Cardiac Death of the European Society of Cardiology

“…Boudoulas et al [412] and Campbell et al [414] found that infero-lateral ST segment changes were associated with the presence of ventricular tachycardia or fibrillation. It was concluded from other studies that prolongation of QT interval and increased QT dispersion might be useful markers of arrhythmic mortality [415,416] . Frequent or complex premature ventricular beats were thought to be a risk factor for SCD but their prognostic role was not proven [417] .…”

Relation Between QT Dispersion and Ventricular Arrhythmias In Uncomplicated Isolated Mitral Valve Prolapse

“…26,31,32 Therefore, increased dispersion of refractoriness may be the arrhythmic mechanism underlying MVP. Tieleman et al 9 and Kulan et al 10 determined that dispersions of QT and QTc were higher than in controls. Kulan et al reported that MVP patients who had a higher incidence of complex ventricular arrhythmias (Lown ≥III) had higher QTd and QTc compared with the those with a lower Lown grade of arrhythmia.…”

“…In fact, we determined neither a significant difference between the patient and control groups from the view-point of QT interval prolongation incidence nor a significant correlation between QTc and ventricular arrhythmia in MVP, which is consistent with previous studies. 9,10 In spite of the contradictory information on the relation between QT prolongation and MVP, it is focused on the link between nonspecific repolarization changes and potentially malign arrhythmia. 22 The inter-lead variability of the QT interval measured in the 12-lead ECG is defined as QTd.…”

“…7,8 Furthermore, there are studies that found that, instead of a prolonged QT interval increase, intrinsic QT dispersion can be related to arrhythmia in these cases. 9,10 In the present study, we aimed to determine the relationship between intrinsic QT dispersion and ventricular Japanese Circulation Journal Vol.63, December 1999 arrhythmias and sudden death in young individuals suffering from uncomplicated isolated MVP (IMVP). In this respect, cases without leaflet thickening (≥5 mm), severe mitral regurgitation or left ventricular systolic dysfunction were included in the study.…”