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      Weekly Variation of the QT Dispersion in Healthy Subjects and in Patients with Coronary Heart Disease

      ,

      Cardiology

      S. Karger AG

      Healthy individuals, Coronary heart disease, QT dispersion, Weekly variation

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          Abstract

          Background: A circadian and seasonal variation of QT dispersion (QTd) has been shown in healthy individuals. Nevertheless, no data exist regarding the weekly influences on the QTd in healthy individuals and in patients with coronary heart disease (CHD). Design: This study was designed to determine whether there is a weekly variability of QTd in healthy individuals and in patients with CHD. Methods: In this prospective registry study, 53 patients with documented CHD and 57 healthy control subjects were involved. Resting electrocardiograms (ECGs) with double amplitude were recorded at a speed of 50 mm/s on Monday and Friday mornings. QT intervals were measured and QTd were determined by calculating the difference between maximum and minimum QT intervals. Then, rate-corrected QTd (QTcd) were calculated using Bazett’s formula. Results: There was a significant weekly variation of QTd in control subjects (39.3 ± 6.3 vs. 36.2 ±6.1 ms) (p < 0.05) and in patients (56 ± 7.3 vs. 47.4 ± 5.4 ms) (p < 0.0001). There was also a significant weekly variation of QTcd both in control subjects (33 ± 5.3 vs. 30.7 ± 5.6 ms) (p < 0.05) and in patients (47.4 ± 6.4 vs. 41.9 ± 5.4 ms) (p < 0.0001). Conclusions: There is a weekly variation of QTd and QTcd in healthy individuals and in patients with CHD, both with a Monday preference. This fact should be taken into consideration during the chronopharmacological treatment or advisal of primary or secondary preventive measures to these subjects or patients.

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          Most cited references 29

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          Circadian variation in the frequency of onset of acute myocardial infarction.

          To determine whether the onset of myocardial infarction occurs randomly throughout the day, we analyzed the time of onset of pain in 2999 patients admitted with myocardial infarction. A marked circadian rhythm in the frequency of onset was detected, with a peak from 6 a.m. to noon (P less than 0.01). In 703 of the patients, the time of the first elevation in the plasma creatine kinase MB (CK-MB) level could be used to time the onset of myocardial infarction objectively. CK-MB-estimated timing confirmed the existence of a circadian rhythm, with a three-fold increase in the frequency of onset of myocardial infarction at peak (9 a.m.) as compared with trough (11 p.m.) periods. The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents before myocardial infarction but was present in those not receiving such therapy. If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis. If the rhythmic processes that drive the circadian rhythm of myocardial-infarction onset can be identified, their modification may delay or prevent the occurrence of infarction.
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            QT dispersion: an indication of arrhythmia risk in patients with long QT intervals.

            Homogeneity of recovery time protects against arrhythmias whereas dispersion of recovery time is arrhythmogenic. A single surface electrocardiographic QT interval gives no information on recovery time dispersion but the difference between the maximum and minimum body surface QT interval may be relevant. This hypothesis was tested by measuring the dispersion of the corrected QT interval (QTc) in 10 patients with an arrhythmogenic long QT interval (Romano Ward and Jervell and Lange-Nielsen syndromes or drug arrhythmogenicity) and in 14 patients without arrhythmias in whom the QT interval was prolonged by sotalol. QTc dispersion was significantly greater in the arrhythmogenic QT group than in the sotalol QT group. In patients with prolonged QT intervals, QT dispersion distinguished between those with ventricular arrhythmias and those without. This supports the hypothesis that QT dispersion reflects spatial differences in myocardial recovery time. QT dispersion may be useful in the assessment of both arrhythmia risk and the efficacy of antiarrhythmic drugs.
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              Measurement of the QT interval and the risk associated with QTc interval prolongation: a review.

              The accurate measurement of the QT interval and its correction or adjustment for cycle length, age, and gender have been topics of increasing interest over the course of the past 70 years. The availability of digitized electrocardiographic recordings on large normal populations together with statistical adjustment for pertinent covariates has provided useful data for defining QT interval prolongation. Data from the International Long QT Syndrome Registry indicate that the probabilistic risk of developing malignant arrhythmias in patients with QT prolongation is exponentially related to the length of the QTc interval. The risk is further accentuated by the development of T-wave alternans, particularly at very prolonged QTc intervals.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2007
                June 2007
                25 September 2006
                : 108
                : 1
                : 55-61
                Affiliations
                Department of Cardiology, Türkiye Yüksek Ihtisas Hospital, Ankara, Turkey
                Article
                95882 Cardiology 2007;108:55–61
                10.1159/000095882
                17003542
                © 2007 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 2, References: 41, Pages: 7
                Categories
                Original Research

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