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      Increased Short-Term Variability of the QT Interval in Professional Soccer Players: Possible Implications for Arrhythmia Prediction

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          Abstract

          Background

          Sudden cardiac death in competitive athletes is rare but it is significantly more frequent than in the normal population. The exact cause is seldom established and is mostly attributed to ventricular fibrillation. Myocardial hypertrophy and slow heart rate, both characteristic changes in top athletes in response to physical conditioning, could be associated with increased propensity for ventricular arrhythmias. We investigated conventional ECG parameters and temporal short-term beat-to-beat variability of repolarization (STV QT), a presumptive novel parameter for arrhythmia prediction, in professional soccer players.

          Methods

          Five-minute 12-lead electrocardiograms were recorded from professional soccer players (n = 76, all males, age 22.0±0.61 years) and age-matched healthy volunteers who do not participate in competitive sports (n = 76, all males, age 22.0±0.54 years). The ECGs were digitized and evaluated off-line. The temporal instability of beat-to-beat heart rate and repolarization were characterized by the calculation of short-term variability of the RR and QT intervals.

          Results

          Heart rate was significantly lower in professional soccer players at rest (61±1.2 vs. 72±1.5/min in controls). The QT interval was prolonged in players at rest (419±3.1 vs. 390±3.6 in controls, p<0.001). QTc was significantly longer in players compared to controls calculated with Fridericia and Hodges correction formulas. Importantly, STV QT was significantly higher in players both at rest and immediately after the game compared to controls (4.8±0.14 and 4.3±0.14 vs. 3.5±0.10 ms, both p<0.001, respectively).

          Conclusions

          STV QT is significantly higher in professional soccer players compared to age-matched controls, however, further studies are needed to relate this finding to increased arrhythmia propensity in this population.

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          Most cited references53

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          Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles.

          To develop clinical, demographic, and pathological profiles of young competitive athletes who died suddenly. Systematic evaluation of clinical information and circumstances associated with sudden deaths; interviews with family members, witnesses, and coaches; and analyses of postmortem anatomic, microscopic, and toxicologic data. A total of 158 sudden deaths that occurred in trained athletes throughout the United States from 1985 through 1995 were analyzed. MAIN OUTCOME MEASURES--Characteristics and probable cause of death. Of 158 sudden deaths among athletes, 24 (15%) were explained by noncardiovascular causes. Among the 134 athletes who had cardiovascular causes of sudden death, the median age was 17 years (range, 12-40 years), 120 (90%) were male, 70 (52%) were white, and 59 (44%) were black. The most common competitive sports involved were basketball (47 cases) and football (45 cases), together accounting for 68% of sudden deaths. A total of 121 athletes (90%) collapsed during or immediately after a training session (78 cases) or a formal athletic contest (43 cases), with 80 deaths (63%) occurring between 3 PM and 9 PM. The most common structural cardiovascular diseases identified at autopsy as the primary cause of death were hypertrophic cardiomyopathy (48 athletes [36%]), which was disproportionately prevalent in black athletes compared with white athletes (48% vs 26% of deaths; P = .01), and malformations involving anomalous coronary artery origin (17 athletes [13%]). Of 115 athletes who had a standard preparticipation medical evaluation, only 4 (3%) were suspected of having cardiovascular disease, and the cardiovascular abnormality responsible for sudden death was correctly identified in only 1 athlete (0.9%). Sudden death in young competitive athletes usually is precipitated by physical activity and may be due to a heterogeneous spectrum of cardiovascular disease, most commonly hypertrophic cardiomyopathy. Preparticipation screening appeared to be of limited value in identification of underlying cardiovascular abnormalities.
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            Pharmacology of cardiac potassium channels.

            Cardiac K+ channels are membrane-spanning proteins that allow the passive movement of K+ ions across the cell membrane along its electrochemical gradient. They regulate the resting membrane potential, the frequency of pacemaker cells and the shape and duration of the cardiac action potential. Additionally, they have been recognized as potential targets for the actions of neurotransmitters and hormones and class III antiarrhythmic drugs that prolong the action potential duration (APD) and refractoriness and have been found effective to prevent/suppress cardiac arrhythmias. In the human heart, K+ channels include voltage-gated channels, such as the rapidly activating and inactivating transient outward current (Ito1), the ultrarapid (IKur), rapid (IKr) and slow (IKs) components of the delayed rectifier current and the inward rectifier current (IK1), the ligand-gated channels, including the adenosine triphosphate-sensitive (IKATP) and the acetylcholine-activated (IKAch) currents and the leak channels. Changes in the expression of K+ channels explain the regional variations in the morphology and duration of the cardiac action potential among different cardiac regions and are influenced by heart rate, intracellular signalling pathways, drugs and cardiovascular disorders. A progressive number of cardiac and noncardiac drugs block cardiac K+ channels and can cause a marked prolongation of the action potential duration (i.e. an acquired long QT syndrome, LQTS) and a distinct polymorphic ventricular tachycardia termed torsades de pointes. In addition, mutations in the genes encoding IKr (KCNH2/KCNE2) and IKs (KCNQ1/KCNE1) channels have been identified in some types of the congenital long QT syndrome. This review concentrates on the function, molecular determinants, regulation and, particularly, on the mechanism of action of drugs modulating the K+ channels present in the sarcolemma of human cardiac myocytes that contribute to the different phases of the cardiac action potential under physiological and pathological conditions.
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              Increased short-term variability of repolarization predicts d-sotalol-induced torsades de pointes in dogs.

              Identification of patients at risk for drug-induced torsades de pointes arrhythmia (TdP) is difficult. Increased temporal lability of repolarization has been suggested as being valuable to predict proarrhythmia. The predictive value of different repolarization parameters, including beat-to-beat variability of repolarization (BVR), was compared in this serial investigation in dogs with chronic AV block. In anesthetized dogs with electrically remodeled hearts, the dose-dependent difference in drug-induced TdP (d-sotalol, 2 and 4 mg/kg IV over 5 minutes, 25% and 75% TdP, respectively) could not be accounted for by prolongation of QT(c) (410+/-37 to 475+/-60 versus 415+/-47 to 484+/-52 ms, respectively). BVR was quantified by Poincare plots at baseline and immediately before onset of d-sotalol-induced extrasystolic activity. TdP occurrence was associated with an increase in short-term variability (STV) of the left ventricular monophasic action potential duration (3.5+/-1.5 to 5.5+/-1.6 versus 3.0+/-0.7 to 8.6+/-3.8 ms, respectively), which was reversible when TdP was abolished by I(K,ATP) activation. The absence of TdP despite QT(c) prolongation after chronic amiodarone treatment could also be explained by an unchanged STV. In experiments with isolated ventricular myocytes, STV increased after I(Kr) block and was highest in cells that subsequently showed early afterdepolarizations. Proarrhythmia is not related to differences in prolongation of repolarization but corresponds to BVR, here quantified as STV of the left ventricle. STV could be a new parameter to predict drug-induced TdP in patients.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2011
                15 April 2011
                : 6
                : 4
                : e18751
                Affiliations
                [1 ]1st Department of Internal Medicine, Faculty of Medicine, University of Szeged, Szeged, Hungary
                [2 ]Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary
                [3 ]Department of Health Sciences and Sports Medicine, Faculty of Physical Education and Sports Sciences, Semmelweis University, Budapest, Hungary
                [4 ]Division of Cardiovascular Pharmacology, Hungarian Academy of Sciences, Szeged, Hungary
                Tor Vergata University of Rome, Italy
                Author notes

                Conceived and designed the experiments: CL MT TW JGP AV PH. Performed the experiments: CL AO ZsK EB ET AU GP. Analyzed the data: AO ZK AU EB IB. Contributed reagents/materials/analysis tools: GP TW PH AV. Wrote the paper: IB AV CL. Drafted and edited the manuscript: IB CL PH AV JGP.

                Article
                PONE-D-11-02394
                10.1371/journal.pone.0018751
                3078143
                21526208
                a89c70b3-f17f-4d02-b8fb-cac212c40063
                Lengyel et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                : 2 February 2011
                : 17 March 2011
                Page count
                Pages: 10
                Categories
                Research Article
                Biology
                Anatomy and Physiology
                Cardiovascular System
                Electrophysiology
                Medicine
                Anatomy and Physiology
                Cardiovascular System
                Electrophysiology
                Cardiovascular
                Arrhythmias
                Electrophysiology
                Diagnostic Medicine
                Sports and Exercise Medicine

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                Uncategorized

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