Precordial QT interval dispersion as a marker of torsade de pointes. Disparate effects of class Ia antiarrhythmic drugs and amiodarone.

Hii, John T.Y.; Wyse, D. George; Gillis, Anne M.; Duff, Henry J.; Solylo, Michale; Mitchell, L. Brent

doi:10.1161/01.cir.86.5.1376

Cited by 356 publications

(111 citation statements)

References 28 publications

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“…Prior studies showed that heterogeneity in repolarization probably predisposes to such life-threatening arrhythmias as ventricular tachycardia and ventricular fibrillation (15,16). Electrical instability of the heart muscle can be detected via QTd using surface ECG (17).…”

Section: Discussionmentioning

confidence: 99%

Short-term effect of transcatheter aortic valve implantation on QT dispersion

Kasapkara¹,

Ayhan²,

Durmaz³

et al. 2015

Turk J Med Sci

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Background/aim: Electrophysiological changes are observed following mechanical stretches due to pressure overload in patients with severe aortic stenosis (AS). The electrical instability occurs after depolarization and dispersion of repolarization. The aim of this study was to evaluate changes in ventricular repolarization following transcatheter aortic valve implantation (TAVI). Materials and methods:The study population included 100 consecutive patients with severe AS that underwent TAVI. Electrocardiography (ECG) was performed at baseline, immediately after TAVI, and 1 week after TAVI. Results:The mean age of the patients was 78.2 ± 7.2 years. Thirty-four (34%) of the patients were male and 66 (66%) were female. Compared to the baseline, mean QT dispersion (QTd) immediately after TAVI and 1 week after TAVI decreased significantly (

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Section: Discussionmentioning

confidence: 99%

Short-term effect of transcatheter aortic valve implantation on QT dispersion

Kasapkara¹,

Ayhan²,

Durmaz³

et al. 2015

Turk J Med Sci

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“…'7-'923 Recently, an association has been reported between ventricular arrhythmias and QTc dispersion. 24 Therefore the increased dispersion of refractoriness could well be the arrhythmogenic mechanism in mitral valve prolapse. However, the present study did not detect a direct correlation between the increased dispersion of refractoriness in mitral valve prolapse and the number of spontaneously occurring ventricular arrhythmias or the incidence of complaints such as palpitation, presyncope, or syncope.…”

Section: Discussionmentioning

confidence: 99%

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

Tieleman

Crijns

Wiesfeld

et al. 1995

Heart

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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)

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“…Increased QT dispersion is believed to be a risk factor for cardiac arrhythmias and sudden death. 5,6) We have searched English Medline on the internet (National Library of Medicine Gateway Search, http://gateway.nlm.nih.gov/gw/Cmd), but could not find any study regarding cardiac arrhythmias or QT interval dispersion in this syndrome. Thus, our aim in this study was to investigate QT dispersion in patients with PCOS.…”

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confidence: 99%

QT Dispersion in Patients with Polycystic Ovary Syndrome.

et al. 2002

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SUMMARYCardiac risk factors are observed more frequently in patients with polycystic ovary syndrome (PCOS). On the other hand, increased QT dispersion, which is a risk factor for cardiac arrhythmias and sudden death, has not been investigated in this syndrome. In this study, we evaluated QT dispersion in PCOS patients without overt heart disease. Thirtysix consecutive women with PCOS (mean age 24±5 years) and 36 healthy women of similar ages (mean age 24±4 years) participated in this study. PCOS was diagnosed if there were polycystic ovaries by ultrasound (enlarged ovaries with ≥8 cysts 2-8 mm in diameter), oligoamenorrhea (intermenstrual interval >35 days), hirsutism (Ferriman-Gallwey score, ≥7) and elevated serum levels of testosterone (≥2.7 nmol/L). Electrocardiograms were recorded at a paper speed of 50 mm/s. QT intervals were manually measured by a cardiologist. All intervals were corrected for heart rate according to Bazett's formula: QTc interval=QT interval/square root of the RR interval. Mean values of body mass index, heart rate, and blood pressure were not significantly different between the two groups (P>0.05). No significant differences in QT intervals (maximum QT, minimum QT, QT dispersion, minimum corrected QT, maximum corrected QT, and corrected QT dispersion) were observed between the two groups (P>0.05). Our results suggest that the risk of ventricular arrhythmias or sudden cardiac death is not increased in PCOS patients. (Jpn Heart J 2002; 43: 487-493) Key words: Electrocardiography, Polycystic ovary syndrome, QT dispersion POLYCYSTIC ovary syndrome (PCOS) is a disorder of chronic anovulation, hyperandrogenism, hirsutism, obesity, subfertility, hyperlipidemia, and insulin resistance. Infertility is not the only important component of this syndrome, since the risks of cardiac disease and hypertension also increase in women with PCOS.1-3) Insulin resistance and hyperinsulinemia appear central to the pathophysiology of PCOS. Glucose intolerance, abnormally high fasting serum lipid concentrations, and high blood pressure are the three cardiac risk factors that have From the

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Precordial QT interval dispersion as a marker of torsade de pointes. Disparate effects of class Ia antiarrhythmic drugs and amiodarone.

Cited by 356 publications

References 28 publications

Short-term effect of transcatheter aortic valve implantation on QT dispersion

Short-term effect of transcatheter aortic valve implantation on QT dispersion

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

QT Dispersion in Patients with Polycystic Ovary Syndrome.

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