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QRS complex waveform indicators of ventricular activation slowing: Simulation studies
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ScienceDirect Journal of Electrocardiology xx (2016) xxx – xxx www.jecgonline.com
QRS complex waveform indicators of ventricular activation slowing: Simulation studies Ljuba Bacharova, MD, DSc, MBA, a, b,⁎ Vavrinec Szathmary, RNDr, PhD, c Jana Svehlikova, RNDr, PhD, d Anton Mateasik, RNDr, PhD, a Milan Tysler, Ing, PhD d a International Laser Center, Bratislava, Slovakia Institute of Pathological Physiology, Medical Faculty, Comenius University, Bratislava, Slovakia Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic d Institute of Measurement Science, Slovak Academy of Sciences, Bratislava, Slovak Republic b
c
Abstract
Diffuse or regional activation slowing in ventricular myocardium can result from different cardiac pathologies, such as left ventricular hypertrophy, ischemia or fibrosis. Altered ventricular activation sequence leads to deformations of the activation front and consequently to the changes in the QRS complex. Using a computer model we simulated the effect of slowed ventricular activation on the QRS waveform with a special interest in ECG changes which reproduce the ECG criteria of left ventricular hypertrophy (ECG-LVH). This paper describes results of a set of computer modeling experiments and discusses visual QRS patterns. Slowed ventricular activation in the whole left ventricle resulted in the prolongation of QRS duration, leftward shift of electrical axis, and increase in the QRS amplitude mainly in the precordial leads, having thus their main impact on simulated Sokolow–Lyon index and Cornell voltage. Slowed ventricular activation in the anteroseptal region resulted in a leftward shift of the electrical axis and increased values of ECG-LVH criteria seen in limb leads or in a combination with precordial leads (Gubner criterion, Cornell voltage). Transmural slowing and midwall slowing in two layers in the anteroseptal area led also to the QRS duration prolongation. Changes in QRS complex were more pronounced in the cases of transmural slowing as compared to the left ventricular midwall slowing. Using computer modeling, we showed that slowed ventricular activation is a potent determinant of QRS complex morphology and can mimic ECG patterns that are usually interpreted as the effect of left ventricular hypertrophy, i.e., increased left ventricular mass. These results contribute to understanding the variety of ECG finding documented in patients with LVH, considering not only anatomical enlargement but also the altered electrical properties of hypertrophied myocardium. © 2016 Elsevier Inc. All rights reserved.
Keywords:
QRS complex waveform; Left ventricular hypertrophy; Left ventricular mass; Ventricular activation slowing; Simulation studies
Introduction Electrocardiographic signs of left ventricular hypertrophy (ECG-LVH) are documented as significant cardiovascular risk factor [1] and they are defined as indicators of target organ damage in hypertensive patients [2]. However, this adverse prognosis is independent on the increased left ventricular mass (LVM) [1,3]. A fundamental theory, accepted for over a half century as an explanation of QRS amplitude changes in the ECG with ⁎ Corresponding author at: International Laser Center, Ilkovicova 3, 841 04 Bratislava, Slovak Republic. E-mail address: [email protected] http://dx.doi.org/10.1016/j.jelectrocard.2016.07.032 0022-0736/© 2016 Elsevier Inc. All rights reserved.
increased myocardial mass, is the solid angle theorem. This postulates that QRS voltage is influenced by spatial determinants, such as the extent of the activation front and the distance of the recording electrode from this wave front, as well as by non-spatial characteristics—the electrophysiological properties of myocardium. Both animal and human studies have documented that there are nonspatial (electrophysiologic) changes in hypertrophied myocardial cells which might contribute to the ECG changes seen in this state, causing changes in the wave form and the speed of conduction of the process through the myocardium [4]. However, our ability to detect and measure these electrical alterations in patients is limited. We can partially
2
L. Bacharova et al. / Journal of Electrocardiology xx (2016) xxx–xxx
overcome this limitation by using computer simulation/ modeling, which allows the study of situations under explicitly defined conditions that are otherwise difficult to investigate. This paper describes results of a set of computer modeling experiments [5–9] addressing anatomical changes of the left ventricle, as well as the effect of diffuse and localized slowing of ventricular activation, on the QRS morphology and duration, and discusses visual QRS patterns.
Diffuse transmural activation propagation slowing in the whole left ventricle The first simulation studies [5,6] demonstrated the effect of different anatomical patterns of cardiac enlargement: concentric hypertrophy, eccentric hypertrophy, and dilatation without increased mass. We showed that myocardial mass and type of hypertrophy were neither the only nor the principal determinants of the QRS patterns. It was the combination of anatomic changes and the transmural slowing of ventricular activation (slowing in all ventricular wall layers of the model heart) which resulted in maximal changes. As is presented in Figs. 1 and 2, various combinations resulted in a spectrum of QRS patterns similar to those seen in patients with LVH, from pseudo-normal ECG findings, thorough increased QRS voltage and duration, prolonged intrinsicoid deflection, left axis deviation, to a QRS pattern of left bundle branch block [5,6]. Diffuse transmural slowing of conduction velocity in the simulated normal-sized left ventricle also produced a remarkable alteration in the QRS complex, mimicking the ECG abnormalities with LVH, but without a change in left ventricular size (Fig. 3A).
Regional activation propagation slowing The QRS changes consistent with classical ECG-LVH criteria were also observed with a localized transmural or intramural slowing in conduction velocity in the simulated “non-hypertrophied” (normal-sized) hearts (Fig. 3B, C)
[7,8]. (“Intramural slowing” was defined as slowing in the mid wall layers of the model left ventricle as oppose to the “transmural slowing.”) In classical ECG interpretation of left ventricular hypertrophy, the effect of localized impairment of myocardium is not considered (it is considered in unique entities such as myocardial infarction). However, local ischemic changes (regional slowing) can occur in LVH due to the disproportionate increase in myocardial mass and its blood supply, as well as concomitant ischemic heart disease. The simulation studies [7,8] showed that the local slowing in ventricular activation either transmural or mid wall, can mimic ECG-LVH QRS changes, producing left axis deviation. These changes mimic ECG changes in the limb leads such as a leftward shift of the electrical axis, an increase in RaVL amplitude, the pattern of a fascicular block, increased QRS voltage in precordial leads, all of which could result in a diagnosis of LVH with commonly used ECG criteria.
The effect of reduced intercellular coupling Using a different model – a realistic large-scale computer model of the human heart and torso [9] – the effect of reduced intercellular coupling was studied, an alteration that has been documented in LVH patients and animal models. It was shown that 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.
Lessons learned These simulation findings contribute to our understanding and interpretation of increased QRS voltage in patients with an actual increase in left ventricular mass by raising the possibility that this can result from mechanisms unrelated to the extent of the wave front or proximity to the recording electrodes. It can also result from slowed ventricular activation, both generalized and localized, and with and without an increase in left ventricular mass.
Fig. 1. Simulated 12-lead electrocardiograms: The effect of the anatomical type of left ventricular hypertrophy on the QRS complex. A: concentric hypertrophy, B: eccentric hypertrophy, C: dilatation. Blue: reference ECG, red: pathological ECG.
L. Bacharova et al. / Journal of Electrocardiology xx (2016) xxx–xxx
3
Fig. 2. Simulated 12-leaed electrocardiograms: The effect of transmural slowing in ventricular activation on the QRS complex in different anatomical types of left ventricular hypertrophy. A: concentric hypertrophy, B: eccentric hypertrophy, C: dilatation. Blue: reference ECG, red: pathological ECG.
They can also help us understand the so-called false positive examples in which various ECG criteria are positive, yet the LV mass is not increased. They can also explain the more frequent problem of a false negative ECG in patients who have a definite increase in heart weight, yet the ECG does not meet the usual criteria for this diagnosis. Our overall observations suggest that there is no direct correlation between QRS amplitude or QRS morphology and left ventricular mass. The complexity of this relationship underscores the conclusions of The Working Group in its earlier reports [10,11]. Seeking a more specific and sensitive ECG method of detecting increased left ventricular mass is not likely to succeed, nor is it necessary given the superior ability of direct methods for this task (echocardiography and cardiac magnetic resonance imaging). Our research efforts would be more productively deployed in exploring the cellular origin of ECG changes, and in their usefulness in predicting adverse clinical outcomes. The QRS voltage is influenced by complex and multifactorial cardiac and extracardiac processes, both structural and electrophysiological, that can have opposite effects on the QRS voltage and morphology. Additionally,
diffuse or regional impulse propagation slowing in ventricular myocardium can result from different cardiac pathologies, such as left ventricular hypertrophy, ischemia or fibrosis.
Limitations The general limitation of any modeling study is the required simplification of complicated processes. The limitations of the model used in these studies [12] include, also, an analytically defined ventricular shape, defined areas of impaired conduction velocity, and a defined 50% slowing in ventricular activation. Slowing by 50% theoretically corresponds to an advanced clinical stage of pathology, probably also including critical gap junctional uncoupling, ischemia, and the replacement of myocardial cells with fibrotic tissue. The presented simulation studies are focused on QRS complex morphology. However, the electrical remodeling of the heart in LVH is a more complex process affecting depolarization and repolarization of ventricles as well as of
Fig. 3. Simulated 12-leaed electrocardiograms: The effect of ventricular activation slowing in the normal-sized model heart. A: transmural slowing of ventricular activation in the whole left ventricle, B: transmural slowing of ventricular activation in the anteroseptal region of the left ventricle, C: ventricular activation slowing in the midwall of the left ventricle. Blue: reference ECG, red: pathological ECG.
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L. Bacharova et al. / Journal of Electrocardiology xx (2016) xxx–xxx
atria, as illustrated by the six components of the Romhilt-Estes LVH score [13]. The presented results are a part of the effort of The Working Group on ECG Diagnosis of Left Ventricular Hypertrophy [10,11,14]. The Working Group is now preparing a new report. In addition to the simulation studies reported today, it will include new research on the predictive ability of ECG abnormalities once ascribed to LVH [15–17]. Each of the six ECG abnormalities comprising the Romhilt– Estes score is independently predictive of cardiovascular disease, and each is different from the other five in their pattern of prediction of specific cardiovascular outcomes, and their overlap with other risk factors [16,17]. The report will also include new research linking MRI evidence of mid-wall ventricular alterations in hypertrophy and the presence of electrical abnormalities [18]. Conclusions Both the simulation studies and the other studies which are encompassed in The Working Group reports demonstrate that the electrical alterations seen with heart disease are much more complex and more interrelated with the fundamental physiological processes that lead to human disease than previously suspected. Some ECG abnormalities may be able to predict a specific pathophysiological state. We look forward to a more varied and interdisciplinary research agenda, clarifying the complex chain of electrical events seen in the ECG, and linking them to the genetic, chemical, and mechanical components of heart disease. The ECG may be predictive of specific types of myocardial disease, specific pathological processes, and other information that could be used to control or reverse abnormal physiology. This is the ultimate “added value” which could evolve from a fresh look at the venerable ECG. Acknowledgment This paper was partly supported by Grant VEGA 2/0071/ 16 from the VEGA Grant Agency, Slovak Republic. References [1] Kannel WB. Left ventricular hypertrophy as a risk factor: the Framingham experience. J Hypertens Suppl 1991;9:S3–8. [2] Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, Böhm M, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2013;31:1281–357.
[3] Sundström J, Lind L, Arnlöv J, Zethelius B, Andrén B, Lithell HO. Echocardiographic and electrocardiographic diagnoses of left ventricular hypertrophy predict mortality independently of each other in a population of elderly men. Circulation 2001;103:2346–51. [4] Hill JA. Hypertrophic reprogramming of the left ventricle: translation to the ECG. J Electrocardiol 2012;45:624–9. [5] Bacharova L, Szathmary V, Kovalcik M, Mateasik A. Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study. J Electrocardiol 2010;43:200–8. [6] Bacharova L, Szathmary V, Mateasik A. ECG patterns of left bundle branch block caused by intraventricular conduction impairment in working myocardium: a model study. J Electrocardiol 2011;44:768–78. [7] Bacharova L, Szathmary V, Mateasik A. QRS complex and ST segment manifestations of ventricular ischemia: the effect of regional slowing of ventricular activation. J Electrocardiol 2013;46:497–504. [8] Bacharova L, Szathmary V, Svehlikova J, Mateasik A, Gyhagen J, Tysler M. The effect of conduction velocity slowing in left ventricular midwall on the QRS complex morphology: a simulation study. J Electrocardiol 2016;49:164–70. [9] Bacharova L, Mateasik A, Krause R, Prinzen F, Auricchio A, Potse M. The effect of reduced intercellular coupling on electrocardiographic signs of left ventricular hypertrophy. J Electrocardiol 2011;44:571–6. [10] Bacharova L, Estes EH, Bang L, Rowlandson I, Schillaci G, Verdecchia P, et al. The first statement of the Working Group on ECG Diagnosis of Left Ventricular Hypertrophy. J Electrocardiol 2010;43:197–9. [11] Bacharova L, Estes EH, Bang LE, Hill JA, Macfarlane PW, Rowlandson I, et al. Second statement of the Working Group on Electrocardiographic Diagnosis of Left Ventricular Hypertrophy. J Electrocardiol 2011;44:568–70. [12] Szathmáry V, Osvald R. An interactive computer model of propagated activation with analytically defined geometry of ventricles. Comput Biomed Res 1994;27:27–38. [13] Romhilt DW, Estes Jr EH. A point-score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J 1968;75:752–8. [14] Bacharova L, Schocken D, Estes H, Strauss D. The role of ECG in the diagnosis of left ventricular hypertrophy (in the 21st century). Curr Cardiol Rev 2014;10:257–61. [15] Bacharova L, Chen H, Estes EH, Mateasik A, Bluemke D, Lima J, et al. Determinants of discrepancies in detection and comparison of the prognostic significance of left ventricular hypertrophy by electrocardiogram and cardiac magnetic resonance imaging. Cardiol 2015;115:515–22. [16] Estes EH, Zhang Z-M, Li Y, Tereshchenko LG, Soliman EZ. The Romhilt-Estes left ventricular hypertrophy score and its components predict all-cause mortality in the general population. Am Heart J 2015;170:104–9. [17] Estes EH, Zhang Z-M, Li Y, Tereshchenko LG, Soliman EZ. Individual components of the Romhilt–Estes left ventricular hypertrophy score differ in their prediction of cardiovascular events: the Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J 2015;170:1220–6. [18] Bacharova L, Ugander M. Left ventricular hypertrophy: the relationship between the electrocardiogram and cardiovascular magnetic resonance imaging. Ann Noninvasive Electrocardiol 2014;9:524–33.
ScienceDirect Journal of Electrocardiology xx (2016) xxx – xxx www.jecgonline.com
QRS complex waveform indicators of ventricular activation slowing: Simulation studies Ljuba Bacharova, MD, DSc, MBA, a, b,⁎ Vavrinec Szathmary, RNDr, PhD, c Jana Svehlikova, RNDr, PhD, d Anton Mateasik, RNDr, PhD, a Milan Tysler, Ing, PhD d a International Laser Center, Bratislava, Slovakia Institute of Pathological Physiology, Medical Faculty, Comenius University, Bratislava, Slovakia Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic d Institute of Measurement Science, Slovak Academy of Sciences, Bratislava, Slovak Republic b
c
Abstract
Diffuse or regional activation slowing in ventricular myocardium can result from different cardiac pathologies, such as left ventricular hypertrophy, ischemia or fibrosis. Altered ventricular activation sequence leads to deformations of the activation front and consequently to the changes in the QRS complex. Using a computer model we simulated the effect of slowed ventricular activation on the QRS waveform with a special interest in ECG changes which reproduce the ECG criteria of left ventricular hypertrophy (ECG-LVH). This paper describes results of a set of computer modeling experiments and discusses visual QRS patterns. Slowed ventricular activation in the whole left ventricle resulted in the prolongation of QRS duration, leftward shift of electrical axis, and increase in the QRS amplitude mainly in the precordial leads, having thus their main impact on simulated Sokolow–Lyon index and Cornell voltage. Slowed ventricular activation in the anteroseptal region resulted in a leftward shift of the electrical axis and increased values of ECG-LVH criteria seen in limb leads or in a combination with precordial leads (Gubner criterion, Cornell voltage). Transmural slowing and midwall slowing in two layers in the anteroseptal area led also to the QRS duration prolongation. Changes in QRS complex were more pronounced in the cases of transmural slowing as compared to the left ventricular midwall slowing. Using computer modeling, we showed that slowed ventricular activation is a potent determinant of QRS complex morphology and can mimic ECG patterns that are usually interpreted as the effect of left ventricular hypertrophy, i.e., increased left ventricular mass. These results contribute to understanding the variety of ECG finding documented in patients with LVH, considering not only anatomical enlargement but also the altered electrical properties of hypertrophied myocardium. © 2016 Elsevier Inc. All rights reserved.
Keywords:
QRS complex waveform; Left ventricular hypertrophy; Left ventricular mass; Ventricular activation slowing; Simulation studies
Introduction Electrocardiographic signs of left ventricular hypertrophy (ECG-LVH) are documented as significant cardiovascular risk factor [1] and they are defined as indicators of target organ damage in hypertensive patients [2]. However, this adverse prognosis is independent on the increased left ventricular mass (LVM) [1,3]. A fundamental theory, accepted for over a half century as an explanation of QRS amplitude changes in the ECG with ⁎ Corresponding author at: International Laser Center, Ilkovicova 3, 841 04 Bratislava, Slovak Republic. E-mail address: [email protected] http://dx.doi.org/10.1016/j.jelectrocard.2016.07.032 0022-0736/© 2016 Elsevier Inc. All rights reserved.
increased myocardial mass, is the solid angle theorem. This postulates that QRS voltage is influenced by spatial determinants, such as the extent of the activation front and the distance of the recording electrode from this wave front, as well as by non-spatial characteristics—the electrophysiological properties of myocardium. Both animal and human studies have documented that there are nonspatial (electrophysiologic) changes in hypertrophied myocardial cells which might contribute to the ECG changes seen in this state, causing changes in the wave form and the speed of conduction of the process through the myocardium [4]. However, our ability to detect and measure these electrical alterations in patients is limited. We can partially
2
L. Bacharova et al. / Journal of Electrocardiology xx (2016) xxx–xxx
overcome this limitation by using computer simulation/ modeling, which allows the study of situations under explicitly defined conditions that are otherwise difficult to investigate. This paper describes results of a set of computer modeling experiments [5–9] addressing anatomical changes of the left ventricle, as well as the effect of diffuse and localized slowing of ventricular activation, on the QRS morphology and duration, and discusses visual QRS patterns.
Diffuse transmural activation propagation slowing in the whole left ventricle The first simulation studies [5,6] demonstrated the effect of different anatomical patterns of cardiac enlargement: concentric hypertrophy, eccentric hypertrophy, and dilatation without increased mass. We showed that myocardial mass and type of hypertrophy were neither the only nor the principal determinants of the QRS patterns. It was the combination of anatomic changes and the transmural slowing of ventricular activation (slowing in all ventricular wall layers of the model heart) which resulted in maximal changes. As is presented in Figs. 1 and 2, various combinations resulted in a spectrum of QRS patterns similar to those seen in patients with LVH, from pseudo-normal ECG findings, thorough increased QRS voltage and duration, prolonged intrinsicoid deflection, left axis deviation, to a QRS pattern of left bundle branch block [5,6]. Diffuse transmural slowing of conduction velocity in the simulated normal-sized left ventricle also produced a remarkable alteration in the QRS complex, mimicking the ECG abnormalities with LVH, but without a change in left ventricular size (Fig. 3A).
Regional activation propagation slowing The QRS changes consistent with classical ECG-LVH criteria were also observed with a localized transmural or intramural slowing in conduction velocity in the simulated “non-hypertrophied” (normal-sized) hearts (Fig. 3B, C)
[7,8]. (“Intramural slowing” was defined as slowing in the mid wall layers of the model left ventricle as oppose to the “transmural slowing.”) In classical ECG interpretation of left ventricular hypertrophy, the effect of localized impairment of myocardium is not considered (it is considered in unique entities such as myocardial infarction). However, local ischemic changes (regional slowing) can occur in LVH due to the disproportionate increase in myocardial mass and its blood supply, as well as concomitant ischemic heart disease. The simulation studies [7,8] showed that the local slowing in ventricular activation either transmural or mid wall, can mimic ECG-LVH QRS changes, producing left axis deviation. These changes mimic ECG changes in the limb leads such as a leftward shift of the electrical axis, an increase in RaVL amplitude, the pattern of a fascicular block, increased QRS voltage in precordial leads, all of which could result in a diagnosis of LVH with commonly used ECG criteria.
The effect of reduced intercellular coupling Using a different model – a realistic large-scale computer model of the human heart and torso [9] – the effect of reduced intercellular coupling was studied, an alteration that has been documented in LVH patients and animal models. It was shown that 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.
Lessons learned These simulation findings contribute to our understanding and interpretation of increased QRS voltage in patients with an actual increase in left ventricular mass by raising the possibility that this can result from mechanisms unrelated to the extent of the wave front or proximity to the recording electrodes. It can also result from slowed ventricular activation, both generalized and localized, and with and without an increase in left ventricular mass.
Fig. 1. Simulated 12-lead electrocardiograms: The effect of the anatomical type of left ventricular hypertrophy on the QRS complex. A: concentric hypertrophy, B: eccentric hypertrophy, C: dilatation. Blue: reference ECG, red: pathological ECG.
L. Bacharova et al. / Journal of Electrocardiology xx (2016) xxx–xxx
3
Fig. 2. Simulated 12-leaed electrocardiograms: The effect of transmural slowing in ventricular activation on the QRS complex in different anatomical types of left ventricular hypertrophy. A: concentric hypertrophy, B: eccentric hypertrophy, C: dilatation. Blue: reference ECG, red: pathological ECG.
They can also help us understand the so-called false positive examples in which various ECG criteria are positive, yet the LV mass is not increased. They can also explain the more frequent problem of a false negative ECG in patients who have a definite increase in heart weight, yet the ECG does not meet the usual criteria for this diagnosis. Our overall observations suggest that there is no direct correlation between QRS amplitude or QRS morphology and left ventricular mass. The complexity of this relationship underscores the conclusions of The Working Group in its earlier reports [10,11]. Seeking a more specific and sensitive ECG method of detecting increased left ventricular mass is not likely to succeed, nor is it necessary given the superior ability of direct methods for this task (echocardiography and cardiac magnetic resonance imaging). Our research efforts would be more productively deployed in exploring the cellular origin of ECG changes, and in their usefulness in predicting adverse clinical outcomes. The QRS voltage is influenced by complex and multifactorial cardiac and extracardiac processes, both structural and electrophysiological, that can have opposite effects on the QRS voltage and morphology. Additionally,
diffuse or regional impulse propagation slowing in ventricular myocardium can result from different cardiac pathologies, such as left ventricular hypertrophy, ischemia or fibrosis.
Limitations The general limitation of any modeling study is the required simplification of complicated processes. The limitations of the model used in these studies [12] include, also, an analytically defined ventricular shape, defined areas of impaired conduction velocity, and a defined 50% slowing in ventricular activation. Slowing by 50% theoretically corresponds to an advanced clinical stage of pathology, probably also including critical gap junctional uncoupling, ischemia, and the replacement of myocardial cells with fibrotic tissue. The presented simulation studies are focused on QRS complex morphology. However, the electrical remodeling of the heart in LVH is a more complex process affecting depolarization and repolarization of ventricles as well as of
Fig. 3. Simulated 12-leaed electrocardiograms: The effect of ventricular activation slowing in the normal-sized model heart. A: transmural slowing of ventricular activation in the whole left ventricle, B: transmural slowing of ventricular activation in the anteroseptal region of the left ventricle, C: ventricular activation slowing in the midwall of the left ventricle. Blue: reference ECG, red: pathological ECG.
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L. Bacharova et al. / Journal of Electrocardiology xx (2016) xxx–xxx
atria, as illustrated by the six components of the Romhilt-Estes LVH score [13]. The presented results are a part of the effort of The Working Group on ECG Diagnosis of Left Ventricular Hypertrophy [10,11,14]. The Working Group is now preparing a new report. In addition to the simulation studies reported today, it will include new research on the predictive ability of ECG abnormalities once ascribed to LVH [15–17]. Each of the six ECG abnormalities comprising the Romhilt– Estes score is independently predictive of cardiovascular disease, and each is different from the other five in their pattern of prediction of specific cardiovascular outcomes, and their overlap with other risk factors [16,17]. The report will also include new research linking MRI evidence of mid-wall ventricular alterations in hypertrophy and the presence of electrical abnormalities [18]. Conclusions Both the simulation studies and the other studies which are encompassed in The Working Group reports demonstrate that the electrical alterations seen with heart disease are much more complex and more interrelated with the fundamental physiological processes that lead to human disease than previously suspected. Some ECG abnormalities may be able to predict a specific pathophysiological state. We look forward to a more varied and interdisciplinary research agenda, clarifying the complex chain of electrical events seen in the ECG, and linking them to the genetic, chemical, and mechanical components of heart disease. The ECG may be predictive of specific types of myocardial disease, specific pathological processes, and other information that could be used to control or reverse abnormal physiology. This is the ultimate “added value” which could evolve from a fresh look at the venerable ECG. Acknowledgment This paper was partly supported by Grant VEGA 2/0071/ 16 from the VEGA Grant Agency, Slovak Republic. References [1] Kannel WB. Left ventricular hypertrophy as a risk factor: the Framingham experience. J Hypertens Suppl 1991;9:S3–8. [2] Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, Böhm M, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2013;31:1281–357.
[3] Sundström J, Lind L, Arnlöv J, Zethelius B, Andrén B, Lithell HO. Echocardiographic and electrocardiographic diagnoses of left ventricular hypertrophy predict mortality independently of each other in a population of elderly men. Circulation 2001;103:2346–51. [4] Hill JA. Hypertrophic reprogramming of the left ventricle: translation to the ECG. J Electrocardiol 2012;45:624–9. [5] Bacharova L, Szathmary V, Kovalcik M, Mateasik A. Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study. J Electrocardiol 2010;43:200–8. [6] Bacharova L, Szathmary V, Mateasik A. ECG patterns of left bundle branch block caused by intraventricular conduction impairment in working myocardium: a model study. J Electrocardiol 2011;44:768–78. [7] Bacharova L, Szathmary V, Mateasik A. QRS complex and ST segment manifestations of ventricular ischemia: the effect of regional slowing of ventricular activation. J Electrocardiol 2013;46:497–504. [8] Bacharova L, Szathmary V, Svehlikova J, Mateasik A, Gyhagen J, Tysler M. The effect of conduction velocity slowing in left ventricular midwall on the QRS complex morphology: a simulation study. J Electrocardiol 2016;49:164–70. [9] Bacharova L, Mateasik A, Krause R, Prinzen F, Auricchio A, Potse M. The effect of reduced intercellular coupling on electrocardiographic signs of left ventricular hypertrophy. J Electrocardiol 2011;44:571–6. [10] Bacharova L, Estes EH, Bang L, Rowlandson I, Schillaci G, Verdecchia P, et al. The first statement of the Working Group on ECG Diagnosis of Left Ventricular Hypertrophy. J Electrocardiol 2010;43:197–9. [11] Bacharova L, Estes EH, Bang LE, Hill JA, Macfarlane PW, Rowlandson I, et al. Second statement of the Working Group on Electrocardiographic Diagnosis of Left Ventricular Hypertrophy. J Electrocardiol 2011;44:568–70. [12] Szathmáry V, Osvald R. An interactive computer model of propagated activation with analytically defined geometry of ventricles. Comput Biomed Res 1994;27:27–38. [13] Romhilt DW, Estes Jr EH. A point-score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J 1968;75:752–8. [14] Bacharova L, Schocken D, Estes H, Strauss D. The role of ECG in the diagnosis of left ventricular hypertrophy (in the 21st century). Curr Cardiol Rev 2014;10:257–61. [15] Bacharova L, Chen H, Estes EH, Mateasik A, Bluemke D, Lima J, et al. Determinants of discrepancies in detection and comparison of the prognostic significance of left ventricular hypertrophy by electrocardiogram and cardiac magnetic resonance imaging. Cardiol 2015;115:515–22. [16] Estes EH, Zhang Z-M, Li Y, Tereshchenko LG, Soliman EZ. The Romhilt-Estes left ventricular hypertrophy score and its components predict all-cause mortality in the general population. Am Heart J 2015;170:104–9. [17] Estes EH, Zhang Z-M, Li Y, Tereshchenko LG, Soliman EZ. Individual components of the Romhilt–Estes left ventricular hypertrophy score differ in their prediction of cardiovascular events: the Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J 2015;170:1220–6. [18] Bacharova L, Ugander M. Left ventricular hypertrophy: the relationship between the electrocardiogram and cardiovascular magnetic resonance imaging. Ann Noninvasive Electrocardiol 2014;9:524–33.