Assessment of QT dispersion in symptomatic patients with congenital long QT syndromes

Linker, Nicholas J.; Colonna, Paolo; Kekwick, Christopher A.; Till, Janice; Camm, A. John; Ward, David

doi:10.1016/0002-9149(92)90155-r

Cited by 156 publications

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References 26 publications

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“…However, some investigators have proposed that -blockers can effectively prevent TdP without decreasing the QT interval and QT dispersion. 10 In the present study, the addition of a -blocker to bepridil therapy significantly decreased QTc dispersion. Bepridil significantly increased the maximum of QTc, but there was no significant change in the minimum.…”

Section: Effects Of -Blocker On Changes In Qt Interval Qt Dispersionsupporting

confidence: 50%

“…Bepridil is effective for intractable cardiac arrhythmia and does not severe extra-cardiac adverse effects, but can induce torsades de pointes (TdP) associated with QT interval prolongation. [7][8][9] In general, TdP is associated with QT prolongation and/or increase in QT dispersion 10 and/or transmural dispersion of repolarization (TDR). [11][12][13] QT dispersion is a fairly good marker of patients at high risk for serious ventricular arrhythmia and sudden death.…”

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confidence: 99%

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Beta-Blocker Decreases the Increase in QT Dispersion and Transmural Dispersion of Repolarization Induced by Bepridil.

Yoshiga

Shimizu

Yamagata

et al. 2002

Circ J

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Section: Effects Of -Blocker On Changes In Qt Interval Qt Dispersionsupporting

confidence: 50%

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confidence: 99%

Beta-Blocker Decreases the Increase in QT Dispersion and Transmural Dispersion of Repolarization Induced by Bepridil.

Yoshiga

Shimizu

Yamagata

et al. 2002

Circ J

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“…QT dispersion reflects the regional variation in ventricular repolarization, which provides an electrophysiologic substrate for arrhythmias. [20][21][22][23] These findings suggest that glucose-induced insulin secretion is one of the factors that induces or aggravates abnormalities of repolarization in patients with LQTS, which may increase their susceptibility to ventricular arrhythmias.…”

Section: Discussionmentioning

confidence: 93%

Effects of Glucose-Induced Insulin Secretion on Ventricular Repolarization in Patients With Congenital Long QT Syndrome

Nishizaki

Ashikaga

Yamawake

et al. 2002

Circ J

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nsulin modulate ion transport mechanisms in cardiac and skeletal muscles, but has little influence on membrane potential other than hyperpolarization of the resting potential. 1 A recent report suggested that insulin stimulates the L-type calcium current in isolated rat ventricular myocytes in a dose-dependent manner, 2 and we recently reported that QT dispersion was associated with an increased plasma insulin level during an oral glucose tolerance (OGT) test in healthy volunteers. 3 However, it is not known whether glucose-induced insulin secretion plays a functional role in abnormal ventricular repolarization in the human heart.Congenital long QT syndrome (LQTS) caused by mutation of the cardiac potassium-and sodium-channel genes and their associated subunits has distinct ECG abnormalities of ventricular repolarization. The abnormal ST-T wave forms are variously affected by changes in physiological factors including serum electrolyte and catecholamine levels, which may underlie different phenotypes and timedependent fluctuations of the ST-T changes in these patients. [4][5][6][7][8][9][10][11][12][13] However, there has not been an exploration of Circulation Journal Vol.66, January 2002 the effects of plasma insulin level after food intake or glucose load on ventricular repolarization in patients with congenital LQTS. We hypothesized that insulin might exert dose-dependent effects on ventricular repolarization in the human heart and that patients with congenital LQTS would be more sensitive to the insulin action than age-matched control healthy subjects with a normal QT interval. The present study was designed to investigate this hypothesis. Methods Study PatientsThe study included 11 patients with congenital LQTS (4 men, 7 women; mean age, 25±9 years, range 12-44) and 11 healthy age-matched volunteers with normal QT interval as the control group (5 men, 6 women; mean age, 27±8 years, range 17-44). All 11 patients with congenital LQTS had a documented QTc interval (corrected QT interval with a modification of Bazzett's formula 14 ) greater than 480 ms (498±40 ms) on 12-lead ECG before receiving medication. Ten patients had a history of stress-induced syncope, and one had a history of cardiac arrest. Torsades de pointes was documented in 8 patients: it was familial in 7 and sporadic in 4 patients.Three patients with congenital LQTS were taking propranolol, one was taking propranolol and mexiletine, and 7 were not receiving any medication at the time of OGT test. The control group had a mean QT interval of 401±27 ms. Both groups had normal results on physical examination and no overt diabetes mellitus, renal disease or endocrine disorders. Excluded were subjects with a systolic blood pressure greater than 140 mmHg, diastolic blood pressure greater than 85 mmHg, total cholesterol greater than 12. To assess the role of insulin in ventricular repolarization in patients with congenital long QT syndrome (LQTS), an oral glucose tolerance (OGT) test was performed in 11 patients with LQTS and in 11 control cases without...

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“…[1][2][3] Previous clinical studies of QT dispersion have shown that it is increased in patients with hypertrophic cardiomyopathy, 4 5 and also in patients with the long QT syndrome 6 and those with myocardial infarction. 1 7 In patients with hypertrophic cardiomyopathy, prolonged QT dispersion has been related to an increased risk of serious ventricular arrhythmias or sudden death.…”

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confidence: 99%

Iatrogenic left coronary artery dissection

Hobbs¹

2003

Heart

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Objective: To evaluate the relation between QT variables and disproportion of left ventricular wall hypertrophy in patients with hypertrophic cardiomyopathy. Design: Retrospective analysis of the results of echocardiography and electrocardiography. Setting: University hospital (tertiary referral centre). Patients: 70 patients with hypertrophic cardiomyopathy were divided into four groups according to the distribution of left ventricular wall hypertrophy on cross sectional echocardiography: group A-hypertrophy confined to the interventricular septum; group B-hypertrophy confined to the interventricular septum and left ventricular anterior wall; group C-hypertrophy confined to the interventricular septum, left ventricular anterior wall, and lateral free wall; group D-hypertrophy involving all portions of the left ventricle. Main outcome measures: QT intervals and QT dispersion in precordial six lead ECGs. Results: There were no significant differences in the maximum left ventricular wall thickness among the four groups, and maximum and minimum QTc intervals also did not differ. QTc dispersion was increased significantly in groups A and B compared with groups C and D. Dispersions of the interval from the J point to the end of the T wave (JTc dispersions) in groups A and B were also increased significantly compared with groups C and D. By linear regression analysis, QTc and JTc dispersions correlated with the ratio of the interventricular septal thickness to left ventricular posterior wall thickness (p = 0.0152 and p = 0.0075, respectively). Conclusions: QT dispersion may be affected by not only electrical inhomogeneity but also by morphological inhomogeneity of the left ventricle in patients with hypertrophic cardiomyopathy.

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Assessment of QT dispersion in symptomatic patients with congenital long QT syndromes

Cited by 156 publications

References 26 publications

Beta-Blocker Decreases the Increase in QT Dispersion and Transmural Dispersion of Repolarization Induced by Bepridil.

Beta-Blocker Decreases the Increase in QT Dispersion and Transmural Dispersion of Repolarization Induced by Bepridil.

Effects of Glucose-Induced Insulin Secretion on Ventricular Repolarization in Patients With Congenital Long QT Syndrome

Iatrogenic left coronary artery dissection

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