Publications by authors named "Marina A Vaykshnorayte"

6 Publications

  • Page 1 of 1

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

Prolongation of The Activation Time in Ischemic Myocardium is Associated with J-wave Generation in ECG and Ventricular Fibrillation.

Sci Rep 2019 08 21;9(1):12202. Epub 2019 Aug 21.

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

J-wave pattern has been recognized as an arrhythmic risk marker, particularly in myocardial infarction patients. Mechanisms underlying J-wave development in ischemia remain unknown. In myocardial infarction model, we evaluated activation time delay as a prerequisite of J-wave appearance and predictor of ventricular fibrillation. Body surface ECGs and myocardial unipolar electrograms were recorded in 14 anesthetized pigs. 48 intramural leads were positioned across ventricular free walls and interventricular septum. Myocardial ischemia was induced by ligation of the left anterior descending coronary artery and the recordings were done during 40-minute coronary occlusion. The local activation times were determined as instants of dV/dt minimum during QRS complex in unipolar electrograms. During occlusion, ventricular local activation time prolonged in the middle portion of the left ventricular free wall, and basal and middle portions of septum, while J-waves appeared in precordial leads in 11 animals. In logistic regression and ROC curve analyses, activation time delay at a given time-point was associated with J-wave development, and a longer activation time was associated with ventricular fibrillation appearance. In experimental coronary occlusion, activation delay in ischemic myocardium was associated with generation of the J waves in the body surface ECG and predicted ventricular fibrillation.
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http://dx.doi.org/10.1038/s41598-019-48710-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6704253PMC
August 2019

Functional role of myocardial electrical remodeling in diabetic rabbits.

Can J Physiol Pharmacol 2015 Apr 22;93(4):245-52. Epub 2014 Dec 22.

Laboratory of Cardiac Physiology, Institute of Physiology, Komi Science Center, Ural Branch, Russian Academy of Sciences, 50 Pervomayskaya Street, 167982 Syktyvkar, Russia., First Department of Internal Diseases of Komi Branch of Kirov State Medical Academy, 11 Babushkin Street, Syktyvkar 167000, Russia., Department of Physiology, Medical Institute of Syktyvkar State University, 11 Babushkin Street, Syktyvkar 167000, Russia.

The objective of the study was to investigate the role of electrical remodeling of the ventricular myocardium in hemodynamic impairment and the development of arrhythmogenic substrate. Experiments were conducted with 11 healthy and 12 diabetic (alloxan model, 4 weeks) rabbits. Left ventricular pressure was monitored and unipolar electrograms were recorded from 64 epicardial leads. Aortic banding was used to provoke arrhythmia. The diabetic rabbits had prolonged QTc, with activation-recovery intervals (surrogates for repolarization durations) being relatively short on the left ventricular base and long on the anterior apical portions of both ventricles (P < 0.05). In the diabetic rabbits, a negative correlation (-0.726 to -0.817) was observed between dP/dt(max), dP/dt(min), and repolarization dispersions. Under conditions of systolic overload (5 min), tachyarrhythmias were equally rare and the QTc and activation-recovery intervals were shortened in both groups (P < 0.05), whereas QRS was prolonged in the diabetic rabbits only. The repolarization shortening was more pronounced on the apex, which led to the development of apicobasal and interventricular end of repolarization gradients in the healthy animals, and to the flattening of the repolarization profile in the diabetic group. Thus, the diabetes-related pattern of ventricular repolarization was associated with inotropic and lusitropic impairment of the cardiac pump function.
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http://dx.doi.org/10.1139/cjpp-2014-0293DOI Listing
April 2015

The contribution of ventricular apicobasal and transmural repolarization patterns to the development of the T wave body surface potentials in frogs (Rana temporaria) and pike (Esox lucius).

Comp Biochem Physiol A Mol Integr Physiol 2011 May 31;159(1):39-45. Epub 2011 Jan 31.

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

The study aimed at the simultaneous determination of the transmural and apicobasal differences in the repolarization timing and the comparison of the contributions of these two repolarization gradients to the development of the body surface T wave potentials in animals with the single heart ventricle (fishes and amphibians). Unipolar potentials were measured on the body surface, epicardium and in the intramural (subepicardial, Epi; midmyocardial; and subendocardial, Endo) ventricular layers of 9 pike and 8 frogs. Activation times, repolarization times and activation-recovery intervals were determined. A transmural gradient in repolarization durations in frogs (Endo>Epi, P<0.024) corresponds to the gradient in repolarization times. No significant transmural difference in repolarization duration is observed in pike that produces a repolarization sequence from Endo to Epi (Endo
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http://dx.doi.org/10.1016/j.cbpa.2011.01.016DOI Listing
May 2011

Epicardial activation-to-repolarization coupling differs in the local areas and on the entire ventricular surface.

J Electrocardiol 2011 Mar-Apr;44(2):131-7. Epub 2011 Jan 8.

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

Hypothesis: Local and global activation-to-repolarization coupling differ from each other. Experiments were done in 12 dogs and 7 frogs. Activation times (ATs), end of repolarization times (RTs), and activation-recovery intervals (ARIs) were measured in 24 or 64 leads on the entire ventricular surface and on the epicardial patch 5 × 5 mm. The ARI and RT dispersions were greater than AT dispersion on the entire ventricular epicardium but not in the local patch. Both ATs and ARIs were inversely related to each other in the patch but not necessarily on the entire epicardium. The RT sequence depended on the AT sequence within the local patch but not on the entire surface. The contributions of the AT sequence and ARI distribution to the RT sequence was determined by the AT/ARI dispersion ratio. Thus, the AT sequence strongly influenced the RT sequence of the local epicardial fragment but not of the entire ventricular surface.
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http://dx.doi.org/10.1016/j.jelectrocard.2010.11.007DOI Listing
July 2011
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