Publications by authors named "Olesya Bernikova"

8 Publications

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Prolongation of experimental diabetes mellitus increased susceptibility to reperfusion ventricular tachyarrhythmias.

Can J Physiol Pharmacol 2021 May 5:1-5. Epub 2021 May 5.

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

Diabetes mellitus (DM) is associated with increased risk of sudden cardiac death, but its role in arrhythmogenesis is not clear. We evaluated contributions of DM duration and hyperglycemia level to development of proarrhythmic electrophysiological changes in the experimental ischemia/reperfusion model. Ventricular epicardial 64-lead mapping and arrhythmia susceptibility burst-pacing testing were performed in 43 healthy and 55 diabetic (alloxan model) anesthetized rabbits undergoing 15 min left anterior descending coronary artery occlusion, followed by 15 min reperfusion. During ischemia, arrhythmia inducibility did not differ between the groups, but the number of reperfusion ventricular tachycardias and (or) fibrillations (VT/VFs) were higher in the DM group (14 out of 55) as compared with control (3 out of 43, = 0.017). In the diabetic animals, both DM duration and glucose concentration were associated with reperfusion VT/VF development in univariate logistic regression analysis (odds ratio (OR) 1.058, 95% confidence interval (CI) 1.025-1.092, < 0.001; and OR 1.119, 95% CI 1.045-1.198, = 0.001, respectively). Only the DM duration, however, remained an independent predictor of reperfusion VT/VF in multivariate logistic regression analysis (OR 1.060, 95% CI 1.006-1.117, = 0.029). Among mapping parameters, DM duration was associated with the prolongation of total ventricular activation duration (regression coefficient 0.152, 95% CI 0.049-0.255, = 0.005) and activation-repolarization intervals (ARIs) (regression coefficient 0.900, 95% CI 0.315-1.484, = 0.003). The prolonged ARI was the only mapping characteristic predicting reperfusion VT/VF development (OR 1.028, 95% CI 1.009-1.048, = 0.004). The DM duration-dependent prolongation of ventricular repolarization presents a link between DM development and reperfusion VT/VF inducibility.
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http://dx.doi.org/10.1139/cjpp-2020-0743DOI Listing
May 2021

Melatonin Prevents Early but Not Delayed Ventricular Fibrillation in the Experimental Porcine Model of Acute Ischemia.

Int J Mol Sci 2020 Dec 30;22(1). Epub 2020 Dec 30.

Department of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, 167000 Syktyvkar, Russia.

Antiarrhythmic effects of melatonin have been demonstrated ex vivo and in rodent models, but its action in a clinically relevant large mammalian model remains largely unknown. Objectives of the present study were to evaluate electrophysiological and antiarrhythmic effects of melatonin in a porcine model of acute myocardial infarction. Myocardial ischemia was induced by 40-min coronary occlusion in 25 anesthetized pigs. After ischemia onset, 12 animals received melatonin (4 mg/kg). 48 intramyocardial electrograms were recorded from left ventricular wall and interventricular septum (IVS). In each lead, activation time (AT) and repolarization time (RT) were determined. During ischemia, ATs and dispersion of repolarization (DOR = RTmax - RTmin) increased reaching maximal values by 3-5 and 20-25 min, respectively. Ventricular fibrillation (VF) incidence demonstrated no relations to redox state markers and was associated with increased DOR and delayed ATs (specifically, in an IVS base, an area adjacent to the ischemic zone) ( = 0.031). Melatonin prevented AT increase in the IVS base, ( < 0.001) precluding development of early VF (1-5 min, = 0.016). VF occurrence in the delayed phase (17-40 min) where DOR was maximal was not modified by melatonin. Thus, melatonin-related enhancement of activation prevented development of early VF in the myocardial infarction model.
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http://dx.doi.org/10.3390/ijms22010328DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7795598PMC
December 2020

Contribution of Depolarization and Repolarization Changes to J-Wave Generation and Ventricular Fibrillation in Ischemia.

Front Physiol 2020 30;11:568021. Epub 2020 Sep 30.

Department of Cardiology, Clinical Sciences, Lund University, Lund, Sweden.

: Activation delay in ischemic myocardium has been found to contribute to J-wave appearance and to predict ventricular fibrillation (VF) in experimental myocardial infarction. However, the role of ischemia-related repolarization abnormalities in J-wave generation remains unclear. : The objective of our study was to assess a contribution of myocardial repolarization changes to J-wave generation in the body surface ECG and VF in a porcine acute myocardial infarction model. : In 22 anesthetized pigs, myocardial ischemia was induced by occlusion of the left anterior descending coronary artery (LAD, = 14) and right coronary artery (RCA, = 8). Body surface ECGs were recorded simultaneously with intramyocardial unipolar electrograms led from flexible electrodes positioned across the left ventricular (LV) wall, interventricular septum (IVS), and right ventricular (RV) wall at apical, middle and basal levels of the ventricles (a total of 48 leads). Local activation times (ATs) and activation-repolarization intervals (ARIs, differences between dV/dt maximum during T-wave and dV/dt minimum during QRS) were measured. : J-waves appeared in left precordial leads (in 11 out of 14 animals with LAD occlusion) and right precordial leads (in six out of eight animals with RCA occlusion). During ischemic exposure, ATs prolonged, and the activation delay was associated with J-wave development (OR = 1.108 95% CI 1.072-1.144; < 0.001) and VF incidence (OR = 1.039 95% CI 1.008-1.072; = 0.015). ARIs shortened in the ischemic regions (in the IVS under LAD-occlusion and the lateral RV base under RCA-occlusion). The difference between maximal ARI in normal zones and ARI in the ischemic zones (ΔARI) was associated with J-wave appearance (OR = 1.025 95% CI 1.016-1.033, < 0.001) independently of AT delay in multivariate logistic regression analysis. : Both AT delay and increase of ΔARIs contributed to the development of J-wave in body surface ECG. However, only AT delay was associated with VF occurrence.
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http://dx.doi.org/10.3389/fphys.2020.568021DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7556294PMC
September 2020

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

Multi-lead vs single-lead T -T interval measurements for prediction of reperfusion ventricular tachyarrhythmias.

J Cardiovasc Electrophysiol 2019 10 21;30(10):2090-2097. Epub 2019 Aug 21.

Department of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, Syktyvkar, Russia.

Introduction: Electrocardiographic T -T interval (Tp-Te) is a promising marker for the prediction of ventricular tachycardia and/or ventricular fibrillation (VT/VF). The study was aimed to compare single-lead vs multilead Tp-Te variables as VT/VF predictors in experimental ischemia/reperfusion model.

Methods And Results: Computer simulations were done using the ECGSIM model with an ischemic region set in anterior left ventricular apex. In 18 anesthetized cats, myocardial ischemia was induced by 30-minute ligation of left anterior descending coronary artery followed by reperfusion. Body surface ECGs in limb leads and modified precordial leads were recorded. Tp-Te was detected automatically in individual leads with a custom-designed parametric algorithm. Tp-Te dispersion and total Tp-Te were calculated as a difference between the maximal and minimal value of individual Tp-Te(s) and an interval between the earliest Tpeak and the latest Tend throughout all leads, respectively. Simulations showed that the increase of local, but not total, dispersion of repolarization characteristic for ischemic damage led to nonuniform shortening of T-peak times across 12 standard leads, which in turn resulted in the increase of single-lead Tp-Te(s), total Tp-Te and Tp-Te dispersion. Animals experienced VT/VF showed increased Tp-Te dispersion and total Tp-Te during reperfusion. In univariate logistic regression analysis, only the Tp-Te dispersion at the beginning of reperfusion was associated with the VT/VF incidence. According to ROC curve analysis, the optimal cut-off value of the Tp-Te dispersion was 17 ms (sensitivity 0.71, specificity 0.80).

Conclusions: The reperfusion VT/VFs were independently predicted by increased Tp-Te dispersion, which suggests the importance of multi-lead evaluation of Tp-Te intervals.
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http://dx.doi.org/10.1111/jce.14105DOI Listing
October 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

Effects of echinochrome on ventricular repolarization in acute ischemia.

J Electrocardiol 2015 Mar-Apr;48(2):181-6. Epub 2015 Jan 8.

Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Centre, Ural Branch, Russian Academy of Sciences, 50, Pervomayskaya St, Syktyvkar, Russian Federation; Department of Physiology, Medical Institute of Syktyvkar State University, 11, Babushkin St, Syktyvkar, Russian Federation.

Background: Myocardial ischemic electrophysiological alterations are associated with the generation of reactive oxygen species. However, electrophysiological effects of antioxidants are unclear. Our objective was to determine the effects of the antioxidant echinochrome on ventricular repolarization in a feline model of 30-min ischemia.

Methods And Results: Activation-recovery intervals were measured from 64 ventricular electrograms recorded before and during the LAD ligation in untreated animals (controls, n=5) and animals given echinochrome (1mg/kg, n=5 and 2mg/kg, n=7). In controls, ischemia resulted in the increase of repolarization dispersion, QTc and Tpeak-Tend intervals and precordial T wave amplitude dispersion. Echinochrome attenuated the ischemic increase of repolarization dispersion. The increased dose of echinochrome abolished the ischemic ECG repolarization changes but did not modify the incidence of ventricular arrhythmias.

Conclusion: Echinochrome modified ischemic alterations of repolarization dispersion that were associated with the changes of the body surface T wave amplitude dispersion and Tpeak-Tend interval.
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http://dx.doi.org/10.1016/j.jelectrocard.2015.01.003DOI Listing
November 2015

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
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