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      Electrocardiographic markers for the prediction of ventricular arrhythmias in patients with systemic sclerosis

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          Abstract

          SSc is an autoimmune disease characterized by microvascular damage, endothelial dysfunction and fibrosis of the skin and the internal organs. Cardiac manifestation in patients with SSc is one of the major organ involvements. Approximately 20% of SSc patients suffer from primary cardiovascular disease and another 20% may have secondary cardiac involvement. Although cardiac arrhythmias are mostly linked to myocardial fibrosis, atrioventricular conduction abnormalities are secondary to the fibrosis of the pulse conduction system. Despite the severe consequences of ventricular rhythm disturbances in patients with SSc, the exact role of electrocardiographic markers in the prediction of these arrhythmias has not yet been clearly elucidated. Therefore, the question is whether certain ECG parameters reflecting ventricular repolarization may help to recognize scleroderma patients with increased risk for ventricular arrhythmias and sudden cardiac death.

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          Mapping and predicting mortality from systemic sclerosis

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            T(p-e)/QT ratio as an index of arrhythmogenesis.

            An increasing number of basic and clinical studies have suggested that the interval from the peak to the end of the electrocardiographic T wave (T(p-e)) may correspond to the transmural dispersion of repolarization and that amplification of the T(p-e) interval is associated with malignant ventricular arrhythmias. In this review, we outline the utility of the T(p-e) interval and the T(p-e)/QT ratio as an electrocardiographic index of arrhythmogenesis for both congenital and acquired ion channel disease leading to ventricular arrhythmias. In healthy individuals, the T(p-e)/QT ratio has a mean value of approximately 0.21 in the precordial leads and it remains relatively constant between the heart rates from 60 to 100 beats per minute. Interestingly, the T(p-e)/QT ratio is significantly greater in the patients at risk for arrhythmic event such as those with long QT syndrome, Brugada syndrome, short QT syndrome, and also in patients with organic heart disease such as acute myocardial infarction. Functional reentry is the underlying mechanism for arrhythmogenesis associated with an increased T(p-e)/QT ratio.
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              T wave peak-to-end interval and QT dispersion in acquired long QT syndrome: a new index for arrhythmogenicity.

              QT dispersion (QTD) on 12-lead ECGs has been proposed as a marker of malignant ventricular tachyarrhythmias, and increased QTD has been reported in long QT syndrome (LQTS). On the other hand, it has been demonstrated that transmural dispersion is associated with ventricular tachyarrhythmias in an experimental model. However, the precise type of QTD or transmural dispersion that contributes most to ventricular tachyarrhythmias in patients with LQTS remains unclear. We evaluated 27 patients with acquired LQTS. These patients were divided into two groups: group A (n =12), patients with polymorphic ventricular tachycardia [torsades de pointes (TdP)], and group B (n =15), patients without TdP. The QT intervals were corrected using Bazett's formula. QTD was measured as the difference between the maximum and the minimum QT intervals, and T wave peak-to-end interval divided by the QT interval (Tpe) in the V5 lead was measured as a new index. Both the corrected QTD (QTDc) and Tpe were significantly larger in group A than in group B. Logistic regression analysis revealed that a reliable predictor for TdP in the QT variables in these patients was not QTDc but Tpe. Cumulative frequency distributions revealed that a Tpe of 0.28 is a good cut-off point for TdP. Tpe did not correlate with the corrected maximum QT interval, whereas the QTDc did correlate with this parameter. In conclusion, Tpe may be the best predictor for TdP in patients with acquired LQTS.
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                Author and article information

                Journal
                Rheumatology (Oxford)
                Rheumatology (Oxford)
                brheum
                Rheumatology (Oxford, England)
                Oxford University Press
                1462-0324
                1462-0332
                March 2020
                14 January 2020
                14 January 2020
                : 59
                : 3
                : 478-486
                Affiliations
                [1 ] Department of Emergency Medicine, Faculty of MedicineUniversity of Debrecen , Debrecen, Hungary
                [2 ] Doctoral School of Health Sciences, Faculty of Public HealthUniversity of Debrecen , Debrecen, Hungary
                [3 ] Department of Rheumatology , Faculty of Medicine, Hungary
                [4 ] Institute of Internal Medicine, Faculty of Medicine , University of Debrecen, Debrecen, Hungary
                Author notes
                Correspondence to: Zoltán Szabó, Department of Emergency Medicine, Faculty of Medicine, University of Debrecen, PO Box 19, Nagyerdei krt. 98, 4032 Debrecen, Hungary. E-mail: szaboz.med@ 123456gmail.com
                Article
                kez644
                10.1093/rheumatology/kez644
                7032033
                31943100
                d2060cee-d0eb-4dfd-85d1-482a756f7625
                © The Author(s) 2020. Published by Oxford University Press on behalf of the British Society for Rheumatology.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 2 August 2019
                : 2 December 2019
                Page count
                Pages: 9
                Funding
                Funded by: Gazdaságfejlesztési és innovációs operatív program (GINOP)
                Award ID: GINOP-2.3.2-15-2016-00062
                Categories
                Reviews

                Rheumatology
                systemic sclerosis,arrhythmias,sudden cardiac death
                Rheumatology
                systemic sclerosis, arrhythmias, sudden cardiac death

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