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      The Alteration of QT Dispersion in Hemodialysis Subjects

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      Kidney and Blood Pressure Research

      S. Karger AG

      QT dispersion, Hemodialysis, Chronic renal failure

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          Abstract

          Objective: We attempted to observe the alterations in QTd and QTcd in chronic renal failure (CRF) patients before and after hemodialysis (HD) to determine the relevant determinants of QTc duration in HD. Methods: The HD was carried out 2 or 3 times/week in a standard setting for 4–4.5 h. No drug therapy was applied during HD, except for isotonic NaCl infusions and sodium heparin. Maintenance drug therapy, including digitalis, antihypertensive, anti-anginal, and β-blocking agents, was not changed. In the study, we investigated the alterations in QTd and QTcd in 68 CRF patients before and after HD with 12-lead ECG. Plasma Na<sup>+</sup>, K<sup>+</sup>, ionized Ca, creatinine, urea nitrogen, and hemoglobin were also controlled before and after HD. Results: In our study QTd and QTcd significantly increased at the end of HD (p < 0.01). Plasma Na<sup>+</sup> and K<sup>+</sup> decreased, and ionized Ca increased after HD (p < 0.05, 0.01). Plasma Na<sup>+</sup>, K<sup>+</sup>, ionized Ca levels, ultrafiltration volume and myocardial ischemia appear to be the main determinants of QTc duration in HD, not hypertension, gender, patient age, or duration of chronic HD. Conclusion: Changes in plasma Na<sup>+</sup>, K<sup>+</sup> and ionized Ca, the ultrafiltration volume and presence of ischemic heart disease in HD have significant effects on QTcd. ECG data demonstrate that the risk of arrhythmia could be higher with decreased plasma Na<sup>+</sup> and K<sup>+</sup>, increased ionized Ca, the presence of ischemic heart disease and an increased ultrafiltration rate during HD. These results might provide some valuable references for proper HD programs.

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          Most cited references 12

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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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            Transmural electrophysiological heterogeneities underlying arrhythmogenesis in heart failure.

            Although expression of numerous ion channels is altered in heart failure (HF), mechanisms by which dysfunction at the ionic and molecular levels lead to ventricular tachyarrhythmias in HF are unknown. Previously, we found that transmural heterogeneities of repolarization play a critical role in the genesis of polymorphic ventricular tachycardia (PVT) when QT interval was prolonged in LQT2. Because QT interval is also prolonged in HF, we hypothesized that transmural heterogeneities are a mechanism of PVT in HF. Optical action potentials were measured simultaneously from cells spanning the entire transmural wall of arterially perfused canine wedge preparations. Wedges were isolated from dogs without (control, n=5) and with HF (n=8) produced by rapid ventricular pacing. In HF, action potential duration (APD) prolongation was markedly heterogeneous across the transmural wall, and was characterized by disproportionate APD prolongation of midmyocardial (M) cells. APD prolongation of M cells accounted for QT-interval prolongation, and caused significant increases (P<0.01) in spatial gradients of repolarization across the ventricular wall from 4.3+/-2.1 (control) to 12.4+/-3.5 ms/mm (HF). Enhanced gradients were directly responsible for development of functional conduction block, leading to PVT in 63% of HF wedges but in no controls (P<0.03). Moreover, intramural decremental conduction and block of the premature impulse, preceded each episode of PVT, and always occurred at the border between M-cell and subepicardial zones, where repolarization gradients were highest. Selective prolongation of APD within M cells underlies several key features of the HF phenotype, including QT-interval prolongation, transmural heterogeneity of repolarization, and susceptibility to conduction block and reentrant PVT.
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              Comparison of QT dispersion in hypertrophic cardiomyopathy between patients with and without ventricular arrhythmias and sudden death.

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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2006
                November 2006
                17 November 2006
                : 29
                : 4
                : 231-236
                Affiliations
                Department of Nephrology, Jilin Chinese Medical Hospital, Changchun City, Jilin Province, China
                Article
                95738 Kidney Blood Press Res 2006;29:231–236
                10.1159/000095738
                16960462
                © 2006 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: 4, Tables: 4, References: 17, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/95738
                Categories
                Original Paper

                Cardiovascular Medicine, Nephrology

                Chronic renal failure, QT dispersion, Hemodialysis

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