Publications by authors named "Ksenia A Sedova"

5 Publications

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Terminal T-wave inversion predicts reperfusion tachyarrhythmias in STEMI.

J Electrocardiol 2022 Jan 5;71:28-31. Epub 2022 Jan 5.

Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden; Arrhythmia Clinic, Skåne University Hospital, 22185 Lund, Sweden.

Introduction: A reliable electrocardiographic predictor of ventricular fibrillation (VF) in patients with ST elevation myocardial infarction (STEMI) is lacking so far. Previous experimental/simulation study suggested a terminal T-wave inversion (TTWI) in ischemia-related ECG leads corresponding to anterior infarct localization as an independent predictor of reperfusion VF (rVF). This T-wave characteristic has never been tested as a rVF predictor in clinical settings. The aim of this study was to test if terminal T-wave inversion (TTWI) at admission ECG (before reperfusion) can serve as a predictor of ventricular fibrillation during reperfusion (rVF) in patients with anterior STEMI undergoing primary PCI.

Methods And Results: Study population included consecutive patients with anterior infarct localization admitted for primary PCI (n = 181, age 65 [57; 76] years, 66% male). Of those, 14 patients had rVF (rVF group, age 59 [47; 76] years, 64% male) and patients without rVF comprised the No-rVF group (n = 167, age 65 [57; 76] years, 66% male). Association of TTWI with rVF was analyzed using logistic regression analysis adjusted for relevant clinical and electrocardiographic covariates. The prevalence of TTWI in rVF group was 62% comparing to 23% in the No-rVF group, p = 0.005. TTWI was associated with increased risk of rVF (OR 5.51; 95% CI 1.70-17.89; p = 0.004) and remained a significant predictor after adjustment for age, gender, history of MI prior to index admission, VF before reperfusion, T-T, maximal ST elevation, and QRS duration (OR 23.49; 95% CI 3.14-175.91; p = 0.002).

Conclusions: The terminal T-wave inversion in anterior leads before PCI independently predicted rVF in patients with anterior MI thus confirming the previous experimental/simulation findings.
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http://dx.doi.org/10.1016/j.jelectrocard.2021.12.008DOI Listing
January 2022

Association Between Antiarrhythmic, Electrophysiological, and Antioxidative Effects of Melatonin in Ischemia/Reperfusion.

Int J Mol Sci 2019 Dec 15;20(24). Epub 2019 Dec 15.

Institute of Physiology, Federal Research Centre, Komi Science Centre, Ural Branch of Russian Academy of Sciences, Pervomayskaya st. 50, 167982 Syktyvkar, Russia.

Melatonin is assumed to confer cardioprotective action via antioxidative properties. We evaluated the association between ventricular tachycardia and/or ventricular fibrillation (VT/VF) incidence, oxidative stress, and myocardial electrophysiological parameters in experimental ischemia/reperfusion under melatonin treatment. Melatonin was given to 28 rats (10 mg/kg/day, orally, for 7 days) and 13 animals received placebo. In the anesthetized animals, coronary occlusion was induced for 5 min followed by reperfusion with recording of unipolar electrograms from ventricular epicardium with a 64-lead array. Effects of melatonin on transmembrane potentials were studied in ventricular preparations of 7 rats in normal and "ischemic" conditions. Melatonin treatment was associated with lower VT/VF incidence at reperfusion, shorter baseline activation times (ATs), and activation-repolarization intervals and more complete recovery of repolarization times (RTs) at reperfusion (less baseline-reperfusion difference, ΔRT) ( < 0.05). Superoxide dismutase (SOD) activity was higher in the treated animals and associated with ΔRT ( = 0.001), whereas VT/VF incidence was associated with baseline ATs ( = 0.020). In vitro, melatonin led to a more complete restoration of action potential durations and resting membrane potentials at reoxygenation ( < 0.05). Thus, the antioxidative properties of melatonin were associated with its influence on repolarization duration, whereas the melatonin-related antiarrhythmic effect was associated with its oxidative stress-independent action on ventricular activation.
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http://dx.doi.org/10.3390/ijms20246331DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6941092PMC
December 2019

Repolarization in perfused myocardium predicts reperfusion ventricular tachyarrhythmias.

J Electrocardiol 2018 May - Jun;51(3):542-548. Epub 2017 Dec 6.

Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, Pervomayskaya st., 50, Syktyvkar, Russia; Department of Physiology, Medical Institute of Pitirim Sorokin Syktyvkar State University, Oktyabrskiy pr., 55, Syktyvkar, Russia.

Background: Aim of the study was to find out which myocardial repolarization parameters predict reperfusion ventricular tachycardia and fibrillation (VT/VF) and determine how these parameters express in ECG.

Methods: Coronary occlusion and reperfusion (30/30min) was induced in 24 cats. Local activation and end of repolarization times (RT) were measured in 88 intramyocardial leads. Computer simulations of precordial electrograms were performed.

Results: Reperfusion VT/VF developed in 10 animals. Arrhythmia-susceptible animals had longer RTs in perfused areas [183(177;202) vs 154(140;170) ms in susceptible and resistant animals, respectively, P<0.05]. In logistic regression analysis, VT/VFs were associated with prolonged RTs in the perfused area (OR 1.068; 95% CI 1.012-1.128; P=0.017). Simulations demonstrated that prolonged repolarization in the perfused/border zone caused precordial terminal T-wave inversion.

Conclusions: The reperfusion VT/VFs were independently predicted by the longer RT in the perfused zone, which was reflected in the terminal negative phase of the electrocardiographic T-wave.
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http://dx.doi.org/10.1016/j.jelectrocard.2017.12.003DOI Listing
March 2019

What does the T(peak)-T(end) interval reflect? An experimental and model study.

J Electrocardiol 2013 Jul-Aug;46(4):296.e1-8. Epub 2013 Mar 6.

Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, 50, Pervomayskaya st, Syktyvkar, Russia.

Background: It is unclear whether the Tpeak-Tend interval is an index of the transmural or the total dispersion of repolarization.

Methods: We examined the Tpeak-Tend interval using a computer model of the rabbit heart ventricles based on experimentally measured transmural, apicobasal, and interventricular gradients of action potential duration.

Results: Experimentally measured activation-recovery intervals increased from apex to base, from the left ventricle to the right ventricle, and in the apical portion of the left ventricle from epicardium to endocardium and from the right side of septum to the left side. The simulated Tpeak corresponded to the earliest end of repolarization, whereas the Tend corresponded to the latest end of repolarization. The different components of the global repolarization dispersion were discerned by simulation.

Conclusions: The Tpeak-Tend interval corresponds to the global dispersion of repolarization with distinct contributions of the apicobasal and transmural action potential duration gradients and apicobasal difference in activation times.
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http://dx.doi.org/10.1016/j.jelectrocard.2013.02.001DOI Listing
January 2014

Load-induced changes in ventricular repolarization: evidence of autonomic modulation.

Can J Physiol Pharmacol 2011 Dec 24;89(12):935-44. Epub 2011 Nov 24.

a Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, 50 Pervomayskaya Street, Syktyvkar, 167982 Russia.

Augmented hemodynamic load increases the risk of arrhythmogenesis by modulating cardiac repolarization duration. We hypothesized that the intervention on the autonomic tone may affect the load-dependent changes in ventricular repolarization. Activation-recovery intervals were measured in unipolar electrograms simultaneously recorded from 64 ventricular epicardial leads, in a total of 26 chinchilla rabbits in resting conditions, and after 1 and 10 min of aortic stenosis. Eleven animals were given atropine and propranolol before the loading. The short-term stenosis decreased the activation-recovery intervals in the right ventricle, whereas the prolonged overload increased the repolarization duration in both ventricles. The treatment with the β-adrenergic and M-cholinergic blockers prolonged the activation-recovery intervals, especially at the left ventricle, attenuating the apicobasal and interventricular gradients of repolarization duration seen in the baseline state. Further ventricular loading shortened the repolarization duration in both ventricles in animals with autonomic blockade. Thus, the autonomic tone was shown to be essential for the development of repolarization heterogeneity across the ventricles. The autonomic blockade transformed the biphasic changes of activation-recovery intervals into their monophasic shortening at aortic stenosis.
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http://dx.doi.org/10.1139/y11-098DOI Listing
December 2011
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