A digital computer model of the vectorcardiogram with distance and boundary effects: Simulated myocardial infarction

Selvester, Ronald H.; Kalaba, Robert E.; Collier, Clarence R.; Bellman, Richard; Kagiwada, H.

doi:10.1016/0002-8703(67)90098-1

Cited by 68 publications

(16 citation statements)

References 13 publications

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“…Moreover, it can be demonstrated that the results for the spherical cell are very similar to those obtained when the cell is modeled as an elongated cylinder. 2 Although the mechanism of the activation process in the heart is not yet fully understood in many of its details (13), it is clear from the studies of Durrer et al (14) and Scher (15) that the direction of signal propagation (as defined earlier in the present paper) does not generally proceed in the direction of the cell cylinder axis. For instance, in the left ventricular wall the direction is more nearly in a plane normal to the cylinder axis, and in the right ventricle and the septum it appears in some locations to be neither normal to nor along the axis.…”

Section: The Myocardial Cellmentioning

confidence: 73%

“…Among the most successful are those of Selvester and his group (2)(3)(4)(5), which have become successively more sophisticated with regard to modeling of the heart and the body; they have also been utilized to simulate infarction (4,5) and hypertrophy (2). Direct comparison of their results with ours is difficult, because Selvester and his group have concentrated their efforts on ventricular depolarization and the QRS complex and our interest has been centered on repolarization and the S-T, T effects as well.…”

mentioning

confidence: 99%

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A mechanism for the electrocardiogram response to left ventricular hypertrophy and acute ischemia.

Thiry¹,

Rosenberg²,

Abbott³

1975

Circulation Research

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A proposed mechanism for explaining the electrocardiographic response in left ventricular hypertrophy and in subendocardial and epicardial acute ischemia was incorporated in a mathematical model of electrical heart activity. The model of hypertrophy was simply an increase in cell size, and the principal effect on the computer-generated 12-lead electrocardiograms (ECGs) was an increase in R-wave amplitude and ventricular activation time and a flattening or polarity reversal of the T wave. The model of acute ischemia was a reduction between plateau and resting potential of the transmembrane action potential. The principal effect on the computer-generated 12-lead ECGs was an S-T segment displacement up or down depending on the location of the lesion. This shift was linearly proportional to the severity of the ischemia, i.e., the reduction in electrical activity of the ischemic cell, and for a lesion of given severity the S-T segment shift was a measure of the area, not the volume, of ischemic tissue. Therefore, this model suggests that a direct correlation does not necessarily exist between volume-measuring tests such as serum enzyme values in the case of necrosis and S-T segment shifts.

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Section: The Myocardial Cellmentioning

confidence: 73%

mentioning

confidence: 99%

A mechanism for the electrocardiogram response to left ventricular hypertrophy and acute ischemia.

Thiry¹,

Rosenberg²,

Abbott³

1975

Circulation Research

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“…In situations where the scar is located in the ventricles, a typical scenario after an MI episode, scar-related VT/VF can spontaneously occur, leading to hemodynamic collapse and SCD. It has been long established that these conduction abnormalities cause characteristic alterations on the ECG trace, such as prolonged R-waves, change of the value of the QRS-angle, fractionations (notches, slurs) in the QRS-complex, elevation/depression of the ST-segment [9]- [11]. In addition there have been studies suggesting that the morphology of the T-wave (T-wave alternans) is affected by the presence of scar since it represents the repolarization of the ventricles [12].…”

Section: Introductionmentioning

confidence: 99%

On the Detection of Myocadial Scar Based on ECG/VCG Analysis

Dima

Panagiotou

Mazomenos

et al. 2013

IEEE Trans. Biomed. Eng.

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Abstract-In this paper, we address the problem of detecting the presence of myocardial scar from standard ECG/VCG recordings, giving effort to develop a screening system for the early detection of scar in the point-of-care. Based on the pathophysiological implications of scarred myocardium, which results in disordered electrical conduction, we have implemented four distinct ECG signal processing methodologies in order to obtain a set of features that can capture the presence of myocardial scar. Two of these methodologies: a.) the use of a template ECG heartbeat, from records with scar absence coupled with Wavelet coherence analysis and b.) the utilization of the VCG are novel approaches for detecting scar presence. Following, the pool of extracted features is utilized to formulate an SVM classification model through supervised learning. Feature selection is also employed to remove redundant features and maximize the classifier's performance. Classification experiments using 260 records from three different databases reveal that the proposed system achieves 89.22% accuracy when applying 10-fold cross validation, and 82.07% success rate when testing it on databases with different inherent characteristics with similar levels of sensitivity (76%) and specificity (87.5%).

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“…Beginning in the 1960s, Selvester and colleagues developed a computer simulation of the electrical activation of the heart and studied the effect of scar, hypertrophy and conduction defects on the body surface vectorcardiogram (VCG) and ECG 15, 16. They showed that myocardial scar in all parts of the LV produced characteristic and quantifiable changes in the VCG and ECG and developed scores that considered Q- and R-wave durations, R/Q and R/S amplitude ratios, R- and S-wave amplitudes and R-wave notches 17, 18.…”

Section: Introductionmentioning

confidence: 99%

ECG Quantification of Myocardial Scar in Cardiomyopathy Patients With or Without Conduction Defects

Strauss

Selvester

Lima

et al. 2008

Circ: Arrhythmia and Electrophysiology

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138

128

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Background-Myocardial scarring from infarction or nonischemic fibrosis forms an arrhythmogenic substrate. The Selvester QRS score has been extensively validated for estimating myocardial infarction scar size in the absence of ECG confounders, but has not been tested to quantify scar in patients with hypertrophy, bundle branch/fascicular blocks, or nonischemic cardiomyopathy. We assessed the hypotheses that (1) QRS scores (modified for each ECG confounder) correctly identify and quantify scar in ischemic and nonischemic patients when compared with the reference standard of cardiac magnetic resonance using late-gadolinium enhancement, and (2)

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A digital computer model of the vectorcardiogram with distance and boundary effects: Simulated myocardial infarction

Cited by 68 publications

References 13 publications

A mechanism for the electrocardiogram response to left ventricular hypertrophy and acute ischemia.

A mechanism for the electrocardiogram response to left ventricular hypertrophy and acute ischemia.

On the Detection of Myocadial Scar Based on ECG/VCG Analysis

ECG Quantification of Myocardial Scar in Cardiomyopathy Patients With or Without Conduction Defects

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