Anton Mateasik

International Laser Centre, Presburg, Bratislavský, Slovakia

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Publications (48)59.19 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Acute myocardial infarction creates regions of altered electrical properties of myocardium resulting in typical QRS patterns (pathological Q waves) and ST segment deviations observed in leads related to the MI location. The aim of this study was to present a graphical method for imaging the changes in the sequence of depolarization and the ST segment deviations in myocardial infarction using the Dipolar ElectroCARdioTOpography (DECARTO) method. Material and Methods Simulated ECG data corresponding to intramural, electrically inactive areas encircled by transmural areas with slowed impulse propagation velocity in anteroseptal and inferior locations were used for imaging the altered sequence of depolarization and the ST vector. The ECGs were transformed to areas projected on the image surface so as to image the process of ventricular depolarization based on the orientation and magnitude of the instantaneous QRS vectors, and the estimated “myocardium at risk” based on the ST segment deviation. Results The images are presented as Mercator projections with the texture of anatomical segments of the heart and the corresponding coronary artery distribution. The changes in depolarization sequence were visible as dislocations of activated areas circumventing the affected areas, while the “myocardium at risk” estimated from the ST segment deviation pointed to the affected area. Conclusion The presented method of imaging ECG allows visualizing changes in sequence of depolarization as well as the ST segment deviations in myocardial infarction and they can be visually compared with non-ECG imaging methods.
    Journal of Electrocardiology. 01/2014;
  • Laser Physics Letters 12/2013; 10(12):5703-. · 7.71 Impact Factor
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    ABSTRACT: Reduction or interruption of the blood supply to myocardium due to occlusion of coronary artery and consequent ischemia leads to changes of electrogenesis: changes in morphology and duration of action potentials and slowing of conduction velocity in the affected area. In this study we simulated the effects of localized changes in depolarization sequence on the QRS and ST segment patterns, using computer modeling. The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows changing the velocity of impulse propagation in the myocardium. An intramural electrically inactive area encircled by a transmural area with slowed impulse propagation velocity was introduced in anteroseptal and inferior locations. The effects on the QRS complex and the ST segment of the 12-lead electrocardiogram are presented. The intramural electrically inactive area caused QRS changes typical for corresponding locations of a myocardial infarction observed in patients, which were further considerably modified by slowed impulse propagation velocity in the surrounding area. Additionally, areas of slowed impulse propagation velocity led to ST segment deviations in the "reciprocal" leads, shifting the ST segment towards the affected areas. Using computer modeling we showed that the localized alteration of impulse propagation not only modified the QRS complex, but produced also changes in the ST segment consistent with changes which are usually interpreted as the effect of "injury current".
    Journal of electrocardiology 09/2013; · 1.08 Impact Factor
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    ABSTRACT: Lipid peroxidation is a major biochemical consequence of the oxidative deterioration of polyunsaturated lipids in cell membranes and causes damage to membrane integrity and loss of protein function. 4-hydroxy-2-nonenal (HNE), one of the most reactive products of n-6 polyunsaturated fatty acid peroxidation of membrane phospholipids, has been shown to be capable of affecting both nicotinamide adenine dinucleotide (phosphate) reduced [NAD(P)H] as well as NADH production. However, the understanding of its effects in living cardiac cells is still lacking. Our goal was to therefore investigate HNE effects on NAD(P)H noninvasively in living cardiomyocytes. Spectrally resolved lifetime detection of endogenous fluorescence, an innovative noninvasive technique, was employed. Individual fluorescence components were resolved by spectral linear unmixing approach. Gathered results revealed that HNE reduced the amplitude of both resolved NAD(P)H components in a concentration-dependent manner. In addition, HNE increased flavoprotein fluorescence and responsiveness of the NAD(P)H component ratio to glutathione reductase (GR) inhibitor. HNE also increased the percentage of oxidized nucleotides and decreased maximal NADH production. Presented data indicate that HNE provoked an important cell oxidation by acting on NAD(P)H regulating systems in cardiomyocytes. Understanding the precise role of oxidative processes and their products in living cells is crucial for finding new noninvasive tools for biomedical diagnostics of pathophysiological states.
    Journal of Biomedical Optics 06/2013; 18(6):67009. · 2.88 Impact Factor
  • A. Mateasik, D. Chorvat, A. Chorvatova
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    ABSTRACT: Spectral analysis of the autofluorescence images of isolated cardiac cells was performed to evaluate and to classify the metabolic state of the cells in respect to the responses to metabolic modulators. The classification was done using machine learning approach based on support vector machine with the set of the automatically calculated features from recorded spectral profile of spectral autofluorescence images. This classification method was compared with the classical approach where the individual spectral components contributing to cell autofluorescence were estimated by spectral analysis, namely by blind source separation using non-negative matrix factorization. Comparison of both methods showed that machine learning can effectively classify the spectrally resolved autofluorescence images without the need of detailed knowledge about the sources of autofluorescence and their spectral properties.
    Proc SPIE 02/2013;
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    ABSTRACT: The genus Gluconobacter is frequently used for biotechnological and/or nanotechnological applications. We studied endogenous fluorescence of nicotinamide adenine dinucleotide (phosphate) (NAD(P)H), indicator of the oxidative metabolic state in mammalian cells, in Gluconobacter oxydans (G. oxydans). Time-resolved measurements (excitation by 375nm pulsed diode laser) were employed to record the bacterial fluorescence intensity, as well as its modifications by metabolic modulation. Results were gathered on fresh bacteria, on de-frozen ones, as well as on bacteria encapsulated in alginate beads. NAD(P)H fluorescence increased linearly with the concentration of bacteria. Freezing, which has little effect on the viability of bacteria or the concentration-dependent fluorescence rise, affected the temperature-dependence of NAD(P)H fluorescence. Sodium cyanide (10 mM) provoked significant rise in the NAD(P)H fluorescence, while dinitrophenol (200 μM) induced its decrease, confirming the bacterial NAD(P)H fluorescence sensitivity to modulators of electron transport chain. Gathered results demonstrate that endogenous NAD(P)H fluorescence can be successfully recorded in the bacterial strain G. oxydans using time-resolved measurements.
    Proc SPIE 01/2013; 8588:85880V1-11.
  • Journal of electrocardiology 01/2013; 46(6):616-617. · 1.08 Impact Factor
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    ABSTRACT: Time-resolved spectrometry of endogenous nicotinamide dinucleotide phosphate [NAD(P)H] fluorescence is a useful method to evaluate metabolic oxidative state in living cells. Ouabain is a well-known pharmaceutical drug used in the treatment of cardiovascular disease, the effects of which on myocardial metabolism were recently demonstrated. Mechanisms implicated in these actions are still poorly understood. We investigate the effect of ouabain on the metabolic oxidative state of living cardiac cells identified by time-resolved fluorescence spectroscopy of mitochondrial NAD(P)H. Spectral unmixing is used to resolve individual NAD(P)H fluorescence components. Ouabain decreased the integral intensity of NAD(P)H fluorescence, leading to a reduced component amplitudes ratio corresponding to a change in metabolic state. We also noted that lactate/pyruvate, affecting the cytosolic NADH gradient, increased the effect of ouabain on the component amplitudes ratio. Cell oxidation levels, evaluated as the percentage of oxidized NAD(P)H, decreased exponentially with rising concentrations of the cardiac glycoside. Ouabain also stimulated the mitochondrial NADH production. Our study sheds a new light on the role that ouabain plays in the regulation of metabolic state, and presents perspective on a noninvasive, pharmaceutical approach for testing the effect of drugs on the mitochondrial metabolism by means of time-resolved fluorescence spectroscopy in living cells.
    Journal of Biomedical Optics 10/2012; 17(10):101505-1. · 2.88 Impact Factor
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    ABSTRACT: An increased QRS voltage is considered to be specific for the electrocardiogram (ECG) diagnosis of left ventricular hypertrophy (LVH). However, the QRS-complex patterns in patients with LVH cover a broader spectrum: increased QRS voltage, prolonged QRS duration, left axis deviation, and left anterior fascicular block- and left bundle branch block-like patterns, as well as pseudo-normal QRS patterns. The classical interpretation of the QRS patterns in LVH relates these changes to increased left ventricular mass (LVM) per se, while tending to neglect the modified active and passive electrical properties of the myocardium. However, it has been well documented that both active and passive electrical properties in LVH are altered. Using computer simulations, we have shown that an increased LVM is not the only determinant of QRS complex changes in LVH, as these changes could also be produced without changing the left ventricular mass, implying that these QRS patterns can be present in patients before their LVM exceeds the arbitrary upper normal limits. Our results link the experimental evidence on electrical remodeling with clinical interpretation of ECG changes in patients with LVH and stress the necessity of a complex interpretation of the QRS patterns considering both spatial and nonspatial determinants in terms of the spatial angle theory. We assume that hypertrophic electrical remodeling in combination with changes in left ventricular size and shape explains the variety of ECG patterns as well as the discrepancies between ECG and left ventricular mass.
    Journal of electrocardiology 09/2012; · 1.08 Impact Factor
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    ABSTRACT: Cardiac cells are highly structured with a non-uniform morphology. Although precise estimation of their volume is essential for correct evaluation of hypertrophic changes of the heart, simple and unified techniques that allow determination of the single cardiomyocyte volume with sufficient precision are still limited. Here, we describe a novel approach to assess the cell volume from confocal microscopy 3D images of living cardiac myocytes. We propose a fast procedure based on segementation using active deformable contours. This technique is independent on laser gain and/or pinhole settings and it is also applicable on images of cells stained with low fluorescence markers. Presented approach is a promising new tool to investigate changes in the cell volume during normal, as well as pathological growth, as we demonstrate in the case of cell enlargement during hypertension in rats.
    Proc SPIE 05/2012; 8427:2-.
  • P Mlkvý, I Cavarga, A Mateásik
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    ABSTRACT: Endoscopic mucosal resection and piece meal polypectomy are methods of choice in broad based unifocal rectosigmoideal lesions. Thermal ablative modalities are indicated for flat adenomas, lateral spreading tumors and as an adjunct therapeutic modality for incomplete polypectomy. Photodynamic therapy using ALA photosensitiser is effective in the treatment of multifocal lesions either alone or in a combination with thermal ablative techniques. At present "tailored suite" combination of these techniques for each patient according the character of the lesion is considered to be the most effective treatment for rectosigmoideal praecancerous lesions and early cancer.
    Vnitr̆ní lékar̆ství 12/2011; 57(12):1034-7.
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    ABSTRACT: The electrocardiographic (ECG) diagnosis of left ventricular hypertrophy (LVH) is based on the assumption that QRS voltage increases with left ventricular mass. However, most of patients with echocardiographically detected LVH do not have increased QRS voltage. Reduced intercellular coupling has been observed in LVH patients and animal models. The purpose of this study was to show that this uncoupling can explain relatively low QRS voltage in LVH patients. Electrocardiograms and vectorcardiograms (VCG) were simulated with a realistic large-scale computer model of the human heart and torso that reliably represented the effects of reduced coupling on both propagation and ECG voltage. Uncoupling reduced QRS voltage in all leads except aVL, reflecting a decrease in vector amplitude as well as a leftward axis deviation that suggested left anterior fascicular block. Low QRS voltage does not necessarily contradict a diagnosis of LVH but may be an indication for electrical uncoupling. The diagnostic value of this "relative voltage deficit" needs to be demonstrated in clinical studies.
    Journal of electrocardiology 07/2011; 44(5):571-6. · 1.08 Impact Factor
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    ABSTRACT: By definition, the electrocardiographic (ECG) patterns of left bundle-branch block (LBBB) represent distinctive changes in duration and shape of the QRS complex caused by intraventricular conduction delay in the left ventricle (LV) due to structural abnormalities in the His-Purkinje conduction system and/or ventricular myocardium. However, impaired conduction in the working myocardium is not taken into consideration in the practical ECG diagnosis. Because the degree of LV myocardium impairment could be of importance for clinical evaluation of patients, we studied the effects of blocked and of delayed onsets of activation in the LV to simulate complete and incomplete LBBBs and slowed conduction in the LV myocardium by applying an analytical computer model. We demonstrated that typical LBBB patterns were caused both by block or delay in the onset of the LV activation, as well as by impaired conduction in the myocardium itself while maintaining the location and onset of the LV activation. The most important difference was the absence of initial anteriorly oriented electrical forces in cases of the simulated complete LBBB and of incomplete LBBB if the onset of LV activation was delayed (≥ 6 milliseconds). Under the conditions defined in this model that did not consider myocardial infarction, the presence of initial anteriorly oriented electrical forces was indicative of preserved conduction in the left bundle and of impaired conduction in LV working myocardium. CONCLUSION: The elucidation of the participation of working myocardium impairment in the intraventricular conduction delay in the LV could be of vital significance for the clinical management of patients with LBBB patterns, for example, indicated for resynchronization therapy.
    Journal of electrocardiology 06/2011; 44(6):768-78. · 1.08 Impact Factor
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    ABSTRACT: NAD(P)H fluorescence was investigated by spectrally-resolved lifetime detection, while individual NAD(P)H fluorescence components were resolved by spectral linear unmixing approach. Photobleaching was induced by excitation of a defocused elliptical spot with a 375nm picosecond laser for 30s repeated every 60s for 7min. Our data indicate presence of three individual components in cardiac cell autofluorescence (AF), and we recorded comparable photobleaching of the two resolved NAD(P)H components ("bound" and "free"). Decrease in photon counts during photobleaching was induced by lowering of the component amplitudes, without modification in the fluorescence lifetimes, while the ratio of the two amplitudes remained unchanged. Gathered results are crucial for choosing appropriate light excitation and fluorescence acquisition for prolonged studies of endogenous fluorescence aiming to investigate changes in metabolic oxidative state in living cardiac cells during their contraction.
    Proc SPIE 02/2011;
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    ABSTRACT: The contributions of reduced conduction velocity (CV) and prolonged action potential duration (APD) to QT interval prolongation and T wave and T vector loop morphology in left ventricular hypertrophy (LVH) were studied using an analytical computer model. Three types of anatomic LVH were simulated: concentric and eccentric hypertrophy, and left ventricular dilatation. In each LVH type, depolarization changes were simulated by CV slowing and primary repolarization changes by APD prolongation. Both CV slowing and APD prolongation prolonged the QT interval; however, the secondary and primary repolarization changes differed in additional electrocardiogram (ECG) characteristics creating specific vectorcardiographic/ECG patterns. The secondary repolarization changes were characterized by prolonged QT interval, accompanied by pronounced QRS changes, including increased maximum spatial QRS vector magnitude, prolonged QRS duration, QRS morphology consistent with intraventricular conduction delay, lower values of the T/QRS duration ratio, increased maximum spatial T vector magnitude, narrow and prolonged discordant T vector loops, and discordant tall T waves creating a pattern of ST strain in the precordial ECG leads. QT prolongation in primary repolarization changes was accompanied with inconsiderable changes of QRS amplitude and duration, higher values of the T/QRS duration ratio, widened rounded T loops, and notched or bifid T waves in left precordial leads of the 12-lead ECG. These simulation data are consistent with the accumulated evidence suggesting that LVH induces changes in CV and APD. Our results emphasize the need for simultaneous consideration of morphologic QRS and T wave patterns together with QT prolongation in clinical evaluation of LVH.
    Journal of electrocardiology 01/2011; 43(6):624-33. · 1.08 Impact Factor
  • Photodiagnosis and Photodynamic Therapy - PHOTODIAGNOSIS PHOTODYN THER. 01/2011; 8(2):174-174.
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    ABSTRACT: Rejection of transplanted hearts remains one of the principal reasons for death of paediatric patients, but an appropriate diagnostic tool for the mild rejection in early stages is still missing. Tissue autofluorescence (AF) is one of the most versatile non-invasive tools for mapping the metabolic state in living tissues. Increasing interest in the imaging and diagnosis of living cells and tissues based on their intrinsic fluorescence rather than fluorescence labelling is closely connected to the latest developments in high-performance spectroscopy and microscopy techniques. In this contribution, we investigate individual components in spectrally- and time-resolved NAD(P)H fluorescence, revealed by linear unmixing, responsible for increased fluorescence in patients presenting mild rejection of transplanted hearts. Application of such approach has the potential to improve the diagnostics of the cardiac transplant rejection by helping currently used histological analysis.
    Journal of Biophotonics 10/2010; 3(10-11):646-52. · 3.10 Impact Factor
  • Journal of Electrocardiology - J ELECTROCARDIOL. 01/2010; 43(6):640-640.
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    ABSTRACT: The increased QRS voltage is considered to be a specific electrocardiogram (ECG) sign of left ventricular hypertrophy (LVH), and it is expected that the QRS voltage reflects the increase in left ventricular mass (LVM). However, the increased QRS voltage is only one of QRS patterns observed in patients with LVH. According to the solid angle theory, the resultant QRS voltage is influenced not only by spatial (anatomic) but also by nonspatial (electrophysiologic) determinants. In this study, we used a computer model to evaluate the effect of changes in anatomy and conduction velocity of the left ventricle on QRS complex characteristics. The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows to change dimensions of the ventricles, as well as the conduction velocity in the individual layers of myocardium. Three types of anatomic changes were simulated: concentric hypertrophy, eccentric hypertrophy, and dilatation. The conduction velocity was slowed in the inner layer of the left ventricle representing the Purkinje fiber mesh and in the layers representing the working myocardium. The outcomes of the model are presented as the time course of the spatial QRS vector magnitude, the vectorcardiographic QRS loops (VCGs) in horizontal, left sagittal, and frontal planes, as well as derived 12-lead ECGs. The following indicators of the 12-lead ECG were evaluated: the left axis deviation, the intrinsicoid deflection in V6, Cornell voltage, Cornell voltage-duration product, and Sokolow-Lyon index. The increase in LVM did not affect the QRS voltage proportionally, and the LVM and type of hypertrophy were not the only determinants of the QRS patterns. The conduction velocity slowing resulted in a spectrum of QRS patterns including increased QRS voltage and duration, left axis deviation, prolonged intrinsicoid deflection, VCG patterns of left bundle branch block, as well as pseudo-normal VCG/ECG patterns. The anatomic changes and conduction velocity slowing affected differently Sokolow-Lyon index and Cornell criteria. We showed that the LVM is not the only determinant of the QRS complex changes in LVH, but it is rather a combination of anatomic and electric remodeling that creates the whole spectrum of the QRS complex changes seen in LVH patients. The slowed conduction velocity in the model heart produced QRS patterns consistent with changes described in LVH, even if the LVM was not changed.
    Journal of electrocardiology 09/2009; 43(3):200-8. · 1.08 Impact Factor
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    ABSTRACT: A graphic method was developed for presentation of the location and extent of the myocardium at risk in patients with acute myocardial infarction (AMI). This method is based on a mathematical processing of ST-segment deviations of standard 12-lead electrocardiogram following the concept of Titomir and Ruttkay-Nedecky in their dipolar electrocardiotopographic method. The center of the location of the area at risk is given by the spatial orientation of the resultant spatial ST vector, and the extent of the area at risk is derived from the Aldrich score. The areas at risk are projected on a spherical image surface, on which a texture of the anatomical quadrants of the ventricular surface and its coronary artery supply are projected. The method was tested in 10 patients with AMI with single-vessel disease, including 6 patients with an occlusion in the proximal left anterior descending coronary artery (LAD), 3 patients with an occlusion in the right coronary artery, and one patient with occlusion in the left circumflex coronary artery. The estimated areas at risk were compared with myocardial perfusion single photon emission computed tomography. Eight (80%) patients of 10 were correctly localized according to the Aldrich decision rules for the location of AMI. The areas at risk in patients with LAD occlusion correctly localized by the Aldrich score were situated in the anteroseptal and anterosuperior quadrants. In the inferior AMI group, the area at risk was localized in the posterolateral and inferior quadrants. The visual comparison with myocardial perfusion single photon emission computed tomography (SPECT) showed best agreement in patients with LAD involvement. The initial testing showed that this method allows a graphic presentation of estimated area at risk using clinically defined diagnostic rules. The area at risk can be displayed in images that are familiar for clinicians and can be compared with or superimposed on results of other imaging methods used in cardiology.
    Journal of electrocardiology 02/2009; 42(2):172-80. · 1.08 Impact Factor

Publication Stats

131 Citations
59.19 Total Impact Points

Institutions

  • 2001–2014
    • International Laser Centre
      Presburg, Bratislavský, Slovakia
  • 2012–2013
    • Comenius University in Bratislava
      Presburg, Bratislavský, Slovakia
  • 2011
    • St. Elizabeth Cancer Institute Hospital - Onkologický ústav sv. Alžbety, s.r.o
      Slovakia
  • 2007
    • CHU Sainte-Justine
      Montréal, Quebec, Canada