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Sökning: WFRF:(Pyotr Platonov)

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1.
  • Abdollahpur, Mostafa, et al. (författare)
  • A subspace projection approach to quantify respiratory variations in the f-wave frequency trend
  • 2022
  • Ingår i: Frontiers in Physiology. - : Frontiers Media SA. - 1664-042X. ; 13
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The autonomic nervous system (ANS) is known as a potent modulator of the initiation and perpetuation of atrial fibrillation (AF), hence information about ANS activity during AF may improve treatment strategy. Respiratory induced ANS variation in the f-waves of the ECG may provide such information. Objective: This paper proposes a novel approach for improved estimation of such respiratory induced variations and investigates the impact of deep breathing on the f-wave frequency in AF patients. Methods: A harmonic model is fitted to the f-wave signal to estimate a high-resolution f-wave frequency trend, and an orthogonal subspace projection approach is employed to quantify variations in the frequency trend that are linearly related to respiration using an ECG-derived respiration signal. The performance of the proposed approach is evaluated and compared to that of a previously proposed bandpass filtering approach using simulated f-wave signals. Further, the proposed approach is applied to analyze ECG data recorded for 5 min during baseline and 1 min deep breathing from 28 AF patients from the Swedish cardiopulmonary bioimage study (SCAPIS). Results: The simulation results show that the estimates of respiratory variations obtained using the proposed approach are more accurate than estimates obtained using the previous approach. Results from the analysis of SCAPIS data show no significant differences between baseline and deep breathing in heart rate (75.5 ± 22.9 vs. 74 ± 22.3) bpm, atrial fibrillation rate (6.93 ± 1.18 vs. 6.94 ± 0.66) Hz and respiratory f-wave frequency variations (0.130 ± 0.042 vs. 0.130 ± 0.034) Hz. However, individual variations are large with changes in heart rate and atrial fibrillatory rate in response to deep breathing ranging from -9% to +5% and -8% to +6%, respectively and there is a weak correlation between changes in heart rate and changes in atrial fibrillatory rate ( r = 0.38, p < 0.03). Conclusion: Respiratory induced f-wave frequency variations were observed at baseline and during deep breathing. No significant changes in the magnitude of these variations in response to deep breathing was observed in the present study population.
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2.
  • Abdollahpur, Mostafa, et al. (författare)
  • Respiratory Induced Modulation in f-Wave Characteristics During Atrial Fibrillation
  • 2021
  • Ingår i: Frontiers in Physiology. - : Frontiers Media SA. - 1664-042X. ; 12
  • Tidskriftsartikel (refereegranskat)abstract
    • The autonomic nervous system (ANS) is an important factor in cardiac arrhythmia, and information about ANS activity during atrial fibrillation (AF) may contribute to personalized treatment. In this study we aim to quantify respiratory modulation in the f-wave frequency trend from resting ECG. First, an f-wave signal is extracted from the ECG by QRST cancelation. Second, an f-wave model is fitted to the f-wave signal to obtain a high resolution f-wave frequency trend and an index for signal quality control ((Formula presented.)). Third, respiratory modulation in the f-wave frequency trend is extracted by applying a narrow band-pass filter. The center frequency of the band-pass filter is determined by the respiration rate. Respiration rate is estimated from a surrogate respiration signal, obtained from the ECG using homomorphic filtering. Peak conditioned spectral averaging, where spectra of sufficient quality from different leads are averaged, is employed to obtain a robust estimate of the respiration rate. The envelope of the filtered f-wave frequency trend is used to quantify the magnitude of respiratory induced f-wave frequency modulation. The proposed methodology is evaluated using simulated f-wave signals obtained using a sinusoidal harmonic model. Results from simulated signals show that the magnitude of the respiratory modulation is accurately estimated, quantified by an error below 0.01 Hz, if the signal quality is sufficient ((Formula presented.)). The proposed method was applied to analyze ECG data from eight pacemaker patients with permanent AF recorded at baseline, during controlled respiration, and during controlled respiration after injection of atropine, respectively. The magnitude of the respiratory induce f-wave frequency modulation was 0.15 ± 0.01, 0.18 ± 0.02, and 0.17 ± 0.03 Hz during baseline, controlled respiration, and post-atropine, respectively. Our results suggest that parasympathetic regulation affects the magnitude of respiratory induced f-wave frequency modulation.
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3.
  • Abdollahpur, Mostafa, et al. (författare)
  • Respiratory Modulation in Permanent Atrial Fibrillation
  • 2020
  • Ingår i: 2020 Computing in Cardiology, CinC 2020. - 2325-8861 .- 2325-887X. - 9781728173825 ; 2020-September
  • Konferensbidrag (refereegranskat)abstract
    • Several studies have shown that the autonomic nervous system (ANS) can induce changes during atrial fibrillation (AF). There is currently a lack of methods for quantifying ANS induced variations during AF. The purpose of this study is to quantify respiratory induced modulation in the f-wave frequency trend. Following qrst-cancellation, the local f-wave frequency is estimated by fitting a harmonic f-wave model signal and a quality index (SQI) is computed based on the model fit. The resulting frequency trend is filtered using a narrow bandpass filter with a center frequency corresponding to the local respiration rate. The magnitude of the respiratory induced f-wave frequency modulation is estimated by the envelope of the filtered frequency trend. The performance of the method is validated using simulations and the method is applied to analyze ECG data from eight patients with permanent AF recorded during 0.125 Hz frequency controlled respiration before and after the full vagal blockade, respectively. Results from simulated data show the magnitude of the respiratory induced f-wave frequency modulation can be estimated with an error of less than = 0.005Hz if the SQI is above 0.45. The signal quality was sufficient for analysis in 7 out of 8 patients. In 4 patients the magnitude decreased and in 3 patients there was no change.
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4.
  • Andlauer, Robin, et al. (författare)
  • Influence of left atrial size on P-wave morphology : differential effects of dilation and hypertrophy
  • 2018
  • Ingår i: Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology. - : Oxford University Press (OUP). - 1532-2092. ; 20:3, s. 36-44
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims: Chronic left atrial enlargement (LAE) increases the risk of atrial fibrillation. Electrocardiogram (ECG) criteria might provide a means to diagnose LAE and identify patients at risk; however, current criteria perform poorly. We seek to characterize the potentially differential effects of atrial dilation vs. hypertrophy on the ECG P-wave. Methods and results: We predict effects on the P-wave of (i) left atrial dilation (LAD), i.e. an increase of LA cavity volume without an increase in myocardial volume, (ii) left atrial concentric hypertrophy (LACH), i.e. a thickened myocardial wall, and (iii) a combination of the two. We performed a computational study in a cohort of 72 anatomical variants, derived from four human atrial anatomies. To model LAD, pressure was applied to the LA endocardium increasing cavity volume by up to 100%. For LACH, the LA wall was thickened by up to 3.3 mm. P-waves were derived by simulating atrial excitation propagation and computing the body surface ECG. The sensitivity regarding changes beyond purely anatomical effects was analysed by altering conduction velocity by 25% in 96 additional model variants. Left atrial dilation prolonged P-wave duration (PWd) in two of four subjects; in one subject a shortening, and in the other a variable change were seen. Left atrial concentric hypertrophy, in contrast, consistently increased P-wave terminal force in lead V1 (PTF-V1) in all subjects through an enlarged amplitude while PWd was unaffected. Combined hypertrophy and dilation generally enhanced the effect of hypertrophy on PTF-V1. Conclusion: Isolated LAD has moderate effects on the currently used P-wave criteria, explaining the limited utility of PWd and PTF-V1 in detecting LAE in clinical practice. In contrast, PTF-V1 may be a more sensitive indicator of LA myocardial hypertrophy.
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5.
  • Andreasen, Laura, et al. (författare)
  • Brugada syndrome-associated genetic loci are associated with J-point elevation and an increased risk of cardiac arrest
  • 2018
  • Ingår i: Frontiers in Physiology. - : Frontiers Media SA. - 1664-042X. ; 9:JUL
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: A previous genome-wide association study found three genetic loci, rs9388451, rs10428132, and rs11708996, to increase the risk of Brugada Syndrome (BrS). Since the effect of these loci in the general population is unknown, we aimed to investigate the effect on electrocardiogram (ECG) parameters and outcomes in the general population. Materials and Methods: A cohort of 6,161 individuals (median age 45 [interquartile range (IQR) 40-50] years, 49% males), with available digital ECGs, was genotyped and subsequently followed for a median period of 13 [IQR 12.6-13.4] years. Data on outcomes were collected from Danish administrative healthcare registries. Furthermore, ~400,000 persons from UK Biobank were investigated for associations between the three loci and cardiac arrest/ventricular fibrillation (VF). Results: Homozygote carriers of the C allele in rs6800541 intronic to SCN10A had a significantly larger J-point elevation (JPE) compared with wildtype carriers (11 vs. 6 μV, P < 0.001). There was an additive effect of carrying multiple BrS-associated risk alleles with an increased JPE in lead V1. None of the BrS-associated genetic loci predisposed to syncope, atrial fibrillation, or total mortality in the general Danish population. The rs9388451 genetic locus adjacent to the HEY2 gene was associated with cardiac arrest/VF in an analysis using the UK Biobank study (odds ratio = 1.13 (95% confidence interval: 1.08-1.18), P = 0.006). Conclusions: BrS-associated risk alleles increase the JPE in lead V1 in an additive manner, but was not associated with increased mortality or syncope in the general population of Denmark. However, the HEY2 risk allele increased the risk of cardiac arrest/VF in the larger population study of UK Biobank indicating an important role of this common genetic locus.
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6.
  • Attia, Zachi I., et al. (författare)
  • Rapid Exclusion of COVID Infection With the Artificial Intelligence Electrocardiogram
  • 2021
  • Ingår i: Mayo Clinic proceedings. - : ELSEVIER SCIENCE INC. - 0025-6196 .- 1942-5546. ; 96:8, s. 2081-2094
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To rapidly exclude severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection using artificial intelligence applied to the electrocardiogram (ECG). Methods: A global, volunteer consortium from 4 continents identified patients with ECGs obtained around the time of polymerase chain reaction-confirmed COVID-19 diagnosis and age- and sex-matched controls from the same sites. Clinical characteristics, polymerase chain reaction results, and raw electrocardiographic data were collected. A convolutional neural network was trained using 26,153 ECGs (33.2% COVID positive), validated with 3826 ECGs (33.3% positive), and tested on 7870 ECGs not included in other sets (32.7% positive). Performance under different prevalence values was tested by adding control ECGs from a single high-volume site. Results: The area under the curve for detection of acute COVID-19 infection in the test group was 0.767 (95% CI, 0.756 to 0.778; sensitivity, 98%; specificity, 10%; positive predictive value, 37%; negative predictive value, 91%). To more accurately reflect a real-world population, 50,905 normal controls were added to adjust the COVID prevalence to approximately 5% (2657/58,555), resulting in an area under the curve of 0.780 (95% CI, 0.771 to 0.790) with a specificity of 12.1% and a negative predictive value of 99.2%. Conclusion: Infection with SARS-CoV-2 results in electrocardiographic changes that permit the artificial intelligence-enhanced ECG to be used as a rapid screening test with a high negative predictive value (99.2%). This may permit the development of electrocardiography-based tools to rapidly screen individuals for pandemic control. (C) 2021 Mayo Foundation Medical Education and Research
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7.
  • Axelsson, Jimmy, et al. (författare)
  • Ejection fraction in left bundle branch block is disproportionately reduced in relation to amount of myocardial scar
  • 2018
  • Ingår i: Journal of Electrocardiology. - : Elsevier BV. - 0022-0736 .- 1532-8430. ; 51:6, s. 1071-1076
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: The relationship between left ventricular (LV) ejection fraction (EF) and LV myocardial scar can identify potentially reversible causes of LV dysfunction. Left bundle branch block (LBBB) alters the electrical and mechanical activation of the LV. We hypothesized that the relationship between LVEF and scar extent is different in LBBB compared to controls. Methods: We compared the relationship between LVEF and scar burden between patients with LBBB and scar (n = 83), and patients with chronic ischemic heart disease and scar but no electrocardiographic conduction abnormality (controls, n = 90), who had undergone cardiovascular magnetic resonance (CMR) imaging at one of three centers. LVEF (%) was measured in CMR cine images. Scar burden was quantified by CMR late gadolinium enhancement (LGE) and expressed as % of LV mass (%LVM). Maximum possible LVEF (LVEFmax) was defined as the function describing the hypotenuse in the LVEF versus myocardial scar extent scatter plot. Dysfunction index was defined as LVEFmax derived from the control cohort minus the measured LVEF. Results: Compared to controls with scar, LBBB with scar had a lower LVEF (median [interquartile range] 27 [19–38] vs 36 [25–50] %, p < 0.001), smaller scar (4 [1–9] vs 11 [6–20] %LVM, p < 0.001), and greater dysfunction index (39 [30–52] vs 21 [12–35] % points, p < 0.001). Conclusions: Among LBBB patients referred for CMR, LVEF is disproportionately reduced in relation to the amount of scar. Dyssynchrony in LBBB may thus impair compensation for loss of contractile myocardium.
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8.
  • Azarov, Jan E., et al. (författare)
  • Progressive increase of the Tpeak-Tend interval is associated with ischaemia-induced ventricular fibrillation in a porcine myocardial infarction model
  • 2018
  • Ingår i: Europace. - : Oxford University Press (OUP). - 1099-5129. ; 20:5, s. 880-886
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims:Repolarization indices of ECG have been widely assessed as predictors of ventricular arrhythmias. However, little is known of the dynamic changes of these parameters during continuous monitoring in acute ischaemic episodes. The objective of the study was to evaluate repolarization-related predictors of ventricular fibrillation (VF) during progression of experimental myocardial infarction. Methods and results: Myocardial infarction was induced in 27 pigs by 40-min balloon inflation in the left anterior descending coronary artery, and 12-lead ECG was continuously recorded. Rate-corrected durations of the total Tpeak-Tend intervals measured from the earliest T-wave peak to the latest T-wave end in any lead were determined at baseline and at minute 1, 2, 5, and then every 5th minute of occlusion. There were 7 early (1-3 min) and 10 delayed (15-30 min) VFs in 16 pigs. Baseline Tpeak-Tend did not differ between animals with and without VF. Tpeak-Tend interval rapidly increased immediately after balloon inflation and was greater in VF-susceptible animals at 2-15 min compared with the animals that never developed VF (P < 0.05). Tpeak-Tend was tested as a predictor of delayed VFs. Median Tpeak-Tend at 10th min of occlusion was higher in delayed VF group (n = 10) than in animals without VF (n = 11): 138 [IQR 121-148] ms vs. 111 [IQR 106-127] ms, P = 0.02. Tpeak-Tend ≥123 ms (10th min) predicted delayed VF episodes with HR = 4.5 95% CI 1.1-17.8, P = 0.031.
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9.
  • Azarov, Jan E., et al. (författare)
  • Prolongation of The Activation Time in Ischemic Myocardium is Associated with J-wave Generation in ECG and Ventricular Fibrillation
  • 2019
  • Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 9:1
  • Tidskriftsartikel (refereegranskat)abstract
    • 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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10.
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