The Experts below are selected from a list of 33 Experts worldwide ranked by ideXlab platform
E John M D Madias - One of the best experts on this subject based on the ideXlab platform.
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decrease disappearance of pacemaker stimulus spikes due to anasarca further proof that the mechanism of attenuation of ecg voltage with anasarca is extracardiac in origin
Annals of Noninvasive Electrocardiology, 2004Co-Authors: E John M D MadiasAbstract:BACKGROUND: Recent work showed that AN leads to a decrement of the potentials of QRS complexes. Although the mechanism has been thought to be extracardiac in origin, and due to a decrease of the electrical impedance of the volume conductor from water overload, more proof on this will be welcome. It is hypothesized that the pacemaker "spikes" (PS) are independent of Heart Depolarization, and thus their change at the body surface with AN would be reflective of extracardiac influences. This study was designed to explore the impact of anasarca (AN) on the amplitude of PSs, and to further delineate the mechanism of ECG attenuation with AN. METHODS: The sum of PS measurements in millimeters in the 6 limb leads (SigmaPS6), and 12 ECG leads (SigmaPS12), and the sum of QRS complexes in the 6 limb leads (SigmaQRS6), and 12 ECG leads (SigmaQRS12) were computed in six patients fitted with a pacemaker (3 with AN and 3 "controls"), and these variables were correlated with weight change. RESULTS: Correlation of percentage change in weight and SigmaPS12 was excellent (r = -0.88, P = 0.02), but not for SigmaPS6 (r = -0.73, P = 0.1). Also, the percentage weight correlated well with SigmaQRS6 (r = -0.82, P = 0.046), but not SigmaQRS12 (r = -0.61, P = 0.2). Correlation of percentage change in SigmaQRS6 and SigmaPS6 was excellent (r = 0.91, P = 0.01), but not the percentage change in SigmaQRS12 and SigmaPS12 (r = 0.72, P = 0.11). CONCLUSIONS: PSs undergo amplitude attenuation in patients developing AN, similar to the one noted in the QRS complexes. Since these changes are independent of the cardiac activation, and are similar in extent to those impacting the QRS complexes, the attenuation of the voltage of the entire ECG curve in AN appears to be extracardiac in origin.
John E. Madias - One of the best experts on this subject based on the ideXlab platform.
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Decrease/disappearance of pacemaker stimulus "spikes" due to anasarca: further proof that the mechanism of attenuation of ECG voltage with anasarca is extracardiac in origin.
Annals of Noninvasive Electrocardiology, 2004Co-Authors: John E. MadiasAbstract:BACKGROUND: Recent work showed that AN leads to a decrement of the potentials of QRS complexes. Although the mechanism has been thought to be extracardiac in origin, and due to a decrease of the electrical impedance of the volume conductor from water overload, more proof on this will be welcome. It is hypothesized that the pacemaker "spikes" (PS) are independent of Heart Depolarization, and thus their change at the body surface with AN would be reflective of extracardiac influences. This study was designed to explore the impact of anasarca (AN) on the amplitude of PSs, and to further delineate the mechanism of ECG attenuation with AN. METHODS: The sum of PS measurements in millimeters in the 6 limb leads (SigmaPS6), and 12 ECG leads (SigmaPS12), and the sum of QRS complexes in the 6 limb leads (SigmaQRS6), and 12 ECG leads (SigmaQRS12) were computed in six patients fitted with a pacemaker (3 with AN and 3 "controls"), and these variables were correlated with weight change. RESULTS: Correlation of percentage change in weight and SigmaPS12 was excellent (r = -0.88, P = 0.02), but not for SigmaPS6 (r = -0.73, P = 0.1). Also, the percentage weight correlated well with SigmaQRS6 (r = -0.82, P = 0.046), but not SigmaQRS12 (r = -0.61, P = 0.2). Correlation of percentage change in SigmaQRS6 and SigmaPS6 was excellent (r = 0.91, P = 0.01), but not the percentage change in SigmaQRS12 and SigmaPS12 (r = 0.72, P = 0.11). CONCLUSIONS: PSs undergo amplitude attenuation in patients developing AN, similar to the one noted in the QRS complexes. Since these changes are independent of the cardiac activation, and are similar in extent to those impacting the QRS complexes, the attenuation of the voltage of the entire ECG curve in AN appears to be extracardiac in origin.
T. Nagenthiran - One of the best experts on this subject based on the ideXlab platform.
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Heart Depolarization VECTOR LOCUS CARDIOGRAM AND ITS CLINICAL DIAGNOSTIC APPLICATIONS
Journal of Mechanics in Medicine and Biology, 2012Co-Authors: T. Nagenthiran, Dhanjoo N. Ghista, V. Ramanan PrasadAbstract:This study demonstrates the development of the Heart Depolarization vector locus cardiogram (HPVLC, from limb leads and a modified Einthoven's triangle) as a diagnostic measure of the left ventricular Depolarization strength. Our work involves the reconstruction of the "equivalent Heart electrical-activity vector (HAV)" for the QRS complex from limb leads voltages of a sample ECG recording, and plotting the progression of the cardiac vector during the QRS complex. A realistic visualization of the progression of the equivalent-dipole HAV during the QRS complex is possible by staging the HPVLC of the QRS complex from the onset of the QRS till the end of the Depolarization stage. This can enable the characterization of the HPVLC by means of an analytical function. By studying the HPVLC for various electro-cardiological disorders, it is possible to determine the ranges of the analytical function's parameters for normal and disordered electro-cardiological states, for diagnostic purpose. We have seen that the monitored ECG is theoretically derived from HAV components on the sides of the Einthoven triangle. Nevertheless, in cardiac practice, the monitored ECG is employed in diagnosis of Heart diseases. From the ECG, we can obtain the Heart rate, and therefrom the Heart rate variability, which too has diagnostic applications. Many nonlinear methods have been proposed to analyze ECG and HRV for detection of cardiac abnormalities, using linear and nonlinear methods. Herein, we have shown how HRV signal can be analyzed in terms of four recurrence quantification analysis (RQA) features, which are then combined into an Integrated Index to enable better separation of normal and diabetic subjects.
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Frontal Plane Vectorcardiograms: Theory and Graphics Visualization of Cardiac Health Status
Journal of Medical Systems, 2010Co-Authors: Dhanjoo N. Ghista, U. Rajendra Acharya, T. NagenthiranAbstract:The electrocardiogram (ECG) is a representative signal containing information about the condition of the Heart. The shape and size of the P-QRS-T wave, the time intervals between its various peaks, may contain useful information about the nature of disease afflicting the Heart. However, these subtle details cannot be directly monitored by the human observer. Besides, these signals are highly subjective, and the symptoms may appear at random in the time scale. It is very taxing and time-consuming to decipher cardiac abnormalities based on these ECG signals. The Vectorcardiogram (VCG) is the vector loop in the 2-D frontal plane, indicating the magnitude and direction of the instantaneous Heart electrical activity vector (HAV), which represents the sum of the dipole vectors located along the instantaneous Depolarization wavefront. The HAV is constructed from the monitored 3-lead ECG signals, placed at the three vertices of the modified Einthoven triangle formed by the 3-lead system in the frontal plane of the torso. The VCG examines the electrical activities within the Heart, using the ECG signals along the three sides of the modified Einthoven triangle, and displays electrical events in the 2-dimensional frontal plane. This study demonstrates the development of the Heart-depolarisation vector-locus cardiogram (using modified Einthoven’s triangle), as a diagnostic measure of the left ventricular depolarisation strength. Our work involves the reconstruction of the “equivalent Heart vector” for the QRS complex from limb lead voltages of a sample ECG, and plotting the progression of the cardiac vector during the QRS complex. We have demonstrated the construction of the frontal plane Heart-Depolarization vector cardiogram (HDVC), as the path of the locus of the tip of the Heart electrical activity vector, with initial and terminal points at the origin. In this work, we have shown characteristic patterns of HDVC for cardiac states namely, normal, bundle branch block, ventricular hypertrophy and myocardial infarction. We have demonstrated how HDVC can be diagnostically employed to characterize cardiac disorders, such as ventricular hypertrophy bundle branch block and inferior myocardial infarction.
Dhanjoo N. Ghista - One of the best experts on this subject based on the ideXlab platform.
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Heart Depolarization VECTOR LOCUS CARDIOGRAM AND ITS CLINICAL DIAGNOSTIC APPLICATIONS
Journal of Mechanics in Medicine and Biology, 2012Co-Authors: T. Nagenthiran, Dhanjoo N. Ghista, V. Ramanan PrasadAbstract:This study demonstrates the development of the Heart Depolarization vector locus cardiogram (HPVLC, from limb leads and a modified Einthoven's triangle) as a diagnostic measure of the left ventricular Depolarization strength. Our work involves the reconstruction of the "equivalent Heart electrical-activity vector (HAV)" for the QRS complex from limb leads voltages of a sample ECG recording, and plotting the progression of the cardiac vector during the QRS complex. A realistic visualization of the progression of the equivalent-dipole HAV during the QRS complex is possible by staging the HPVLC of the QRS complex from the onset of the QRS till the end of the Depolarization stage. This can enable the characterization of the HPVLC by means of an analytical function. By studying the HPVLC for various electro-cardiological disorders, it is possible to determine the ranges of the analytical function's parameters for normal and disordered electro-cardiological states, for diagnostic purpose. We have seen that the monitored ECG is theoretically derived from HAV components on the sides of the Einthoven triangle. Nevertheless, in cardiac practice, the monitored ECG is employed in diagnosis of Heart diseases. From the ECG, we can obtain the Heart rate, and therefrom the Heart rate variability, which too has diagnostic applications. Many nonlinear methods have been proposed to analyze ECG and HRV for detection of cardiac abnormalities, using linear and nonlinear methods. Herein, we have shown how HRV signal can be analyzed in terms of four recurrence quantification analysis (RQA) features, which are then combined into an Integrated Index to enable better separation of normal and diabetic subjects.
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Frontal Plane Vectorcardiograms: Theory and Graphics Visualization of Cardiac Health Status
Journal of Medical Systems, 2010Co-Authors: Dhanjoo N. Ghista, U. Rajendra Acharya, T. NagenthiranAbstract:The electrocardiogram (ECG) is a representative signal containing information about the condition of the Heart. The shape and size of the P-QRS-T wave, the time intervals between its various peaks, may contain useful information about the nature of disease afflicting the Heart. However, these subtle details cannot be directly monitored by the human observer. Besides, these signals are highly subjective, and the symptoms may appear at random in the time scale. It is very taxing and time-consuming to decipher cardiac abnormalities based on these ECG signals. The Vectorcardiogram (VCG) is the vector loop in the 2-D frontal plane, indicating the magnitude and direction of the instantaneous Heart electrical activity vector (HAV), which represents the sum of the dipole vectors located along the instantaneous Depolarization wavefront. The HAV is constructed from the monitored 3-lead ECG signals, placed at the three vertices of the modified Einthoven triangle formed by the 3-lead system in the frontal plane of the torso. The VCG examines the electrical activities within the Heart, using the ECG signals along the three sides of the modified Einthoven triangle, and displays electrical events in the 2-dimensional frontal plane. This study demonstrates the development of the Heart-depolarisation vector-locus cardiogram (using modified Einthoven’s triangle), as a diagnostic measure of the left ventricular depolarisation strength. Our work involves the reconstruction of the “equivalent Heart vector” for the QRS complex from limb lead voltages of a sample ECG, and plotting the progression of the cardiac vector during the QRS complex. We have demonstrated the construction of the frontal plane Heart-Depolarization vector cardiogram (HDVC), as the path of the locus of the tip of the Heart electrical activity vector, with initial and terminal points at the origin. In this work, we have shown characteristic patterns of HDVC for cardiac states namely, normal, bundle branch block, ventricular hypertrophy and myocardial infarction. We have demonstrated how HDVC can be diagnostically employed to characterize cardiac disorders, such as ventricular hypertrophy bundle branch block and inferior myocardial infarction.
Luiz Belardinelli - One of the best experts on this subject based on the ideXlab platform.
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Pathological Roles of the Cardiac Sodium Channel Late Current (Late INa)
Electrical Diseases of the Heart, 2013Co-Authors: Sridharan Rajamani, John C. Shryock, Luiz BelardinelliAbstract:The causes, consequences, and potential therapeutic benefit of inhibiting cardiac late sodium current are reviewed. Myocardial sodium channels enable electrical excitability and impulse conduction in the Heart. Depolarization induces sodium channel openings and a large inward Na+ current that forms the upstroke of the cardiac action potential (AP). The cardiac AP is characterized by a long plateau phase during which Na+ channels are inactivated. Disruption of the process of Na+ channel inactivation, even when it affects only a small fraction of Na+ channels, results in a late or persistent inward Na+ current (late INa) that flows throughout the AP plateau. The magnitude of late INa is normally small but an increase can have pathological consequences. Both inherited (congenital) and acquired diseases may cause late INa to be enhanced. Mutations in genes encoding Na+ channel alpha and beta subunits and channel-associated proteins are causes of an enhanced late INa and LQT3 syndrome. Ischemia, Heart failure, oxidative stress, and increased activities of certain protein kinases are associated with an increase of late INa. The consequences of an increased late INa include prolongation of the duration of the AP and facilitation of early after-Depolarizations, and increased loading of myocytes with Na+. Myocyte Na+ loading leads to Ca2+ loading via Na+/Ca2+ exchange, delayed after-Depolarizations, and activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). CaMKII activation is associated with phosphorylation of the Na+ channel that further increases late INa, creating a potential positive feedback loop. Inhibition of late INa ameliorates electrical and mechanical dysfunction caused by LQT3 syndrome, ischemia, Heart failure, and Na+/Ca2+ overload. In these settings, the advantages of reducing an enhanced late INa may include: increased repolarization reserve associated with decreased AP duration and variability; decreased occurrences of early and delayed after-Depolarizations and triggered arrhythmias; improvements of myocardial Ca2+ handling, ventricular diastolic relaxation, and contractile efficiency.
