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Electrocardiographic diagnosis of left ventricular hypertrophy: depolarization changes
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Journal of Electrocardiology 42 (2009) 228 – 232 www.jecgonline.com
Electrocardiographic diagnosis of left ventricular hypertrophy: depolarization changes Ljuba Bacharova, MD, PhD, MBA, a,⁎ E. Harvey Estes, MD b a
Abstract
Department of Biophotonics, International Laser Center, Bratislava, Slovak Republic b Duke University Medical Center, Durham, NC, USA Received 3 February 2009
Electrocardiographic signs of left ventricular hypertrophy (LVH) are on one hand accepted as independent cardiovascular risk factors and indicators of target organ damage in hypertensive patients, but, on the other hand they are strongly criticized for their low sensitivity. In this paper, a historic perspective on the ECG dignosis of LVH is presented, showing the development of current views on the role of ECG in LVH detection. Based on the fact that ECG provides information on the electrical properties of myocardium and on new knowledge about electrical remodeling in LVH, a shift of paradigm in our consideration of the diagnosis of left ventricular hypertrophy is proposed, based on changes in the electrical properties of hypertrophied myocardium. This new paradigm could explain the broad spectrum of QRS patterns seen in LVH, including increased QRS voltage, prolonged duration of QRS complex, left axis deviation, prolonged intrinsicoid deflection, LBBB and LAFB patterns, as well as pseudo-normal ECG findings. © 2009 Elsevier Inc. All rights reserved.
Interest in the electrocardiographic diagnosis of left ventricular hypertrophy (LVH) has changed since the electrocardiogram (ECG) first appeared as a clinical diagnostic tool at the beginning of the last century. Electrocardiographic indicators of LVH are now documented to be independent cardiovascular risk factors and have been accepted as indicators of target organ damage in hypertensive patients.1,2 At the same time, the use of the ECG to predict LVH suffers from low sensitivity and is severely criticized. Paradoxically, the availability and low cost of the ECG are more frequently stressed as strengths of the method than the sensitivity of the information provided by ECG in the diagnosis of LVH. This article will provide historical insight into the role of ECG in LVH diagnosis with a focus on the QRS complex and explore lessons that might be learned from this history. The ECG diagnosis of LVH has undergone an interesting development and can be divided into several distinct but overlapping periods (Fig. 1): 1. Period of introduction into clinical diagnosis: In this period, the ECG was one of the few available objective noninvasive methods providing information about the heart. This period was characterized by rapid development of this new method, exciting discoveries, and a sharp increase in interest. Normal and abnormal ECG findings were established and ⁎ Corresponding author. Tel.: +421 2 654 21 575; fax: +421 2 654 23 244. E-mail address: [email protected] 0022-0736/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2009.03.005
linked to normal as well as pathological conditions. The first description of increased QRS voltage in LVH was published at the beginning of the last century by Einthoven, who documented an increased R wave in a patient with mitral regurgitation.3 Other diagnostic methods at that time had limited ability to provide information or details about the anatomical, structural, and functional characteristics of the hypertrophied heart. 2. Period of stabilization: During this period, the ECG had become a well-established clinical diagnostic method, and the major abnormal ECG patterns had been described and categorized. The solid angle theory was proposed as a theoretical background for understanding the observed increase in QRS voltage.4 This included both spatial determinants (the extent of activation front and distance from the recording electrode) and non–spatial determinants (electrical conduction properties of myocardium, the conductivity of the medium, and the charge density per unit area of the polarized surface), all of which could influence the resultant QRS voltage. There was limited knowledge about the changes of electrical properties of hypertrophied myocardium.5 It should be stressed that in spite of the lack of evidence on electrical remodeling in LVH, electrophysiological aspects were considered in the interpretation of QRS changes in LVH. The effect of conduction delays in the left ventricle on the QRS changes was discussed as possibly more important than the effect of ventricular mass.6 The term “parietal block” was applied to a local disturbance in conduction, as opposed to bundle branch or fascicular blocks.
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232
229
Fig. 1. Periods of interest in ECG-LVH diagnosis: (1) Introductory period: introduction of ECG into clinical diagnosis, sharp increase in interest. (2) Period of stabilized interest: ECG becomes a well-established clinical diagnostic method, major ECG patterns are described and categorized. (3) Period of gradual decline: interest in ECG-LVH diagnosis directed at improving estimation of LVM, echocardiography recognized as gold standard for estimating LVM. (4) Period of persistent low-level interest: ECG evidence of LVH recognized as valid predictor of cardiovascular risk and clinical severity, and resolution of ECG-LVH with favorable effect of treatment. (5) Potential period of shift in paradigm: focus on the evaluation of the electrophysiological state of the hypertrophied myocardium and its added value for clinical diagnosis, prognosis, evaluation of therapy, and further research in electrical/mechanical relationships.
An altered relationship between the depolarization and repolarization of one ventricle with respect to the other ventricle (altered phase relationships between large areas) was also considered.7 However, it was still believed that 2 basic anatomical types of LVH—“hypertrophy” and dilatation, as seen in systolic and diastolic overload—could be distinguished by the means of the ECG. 3. Period of gradual decline in interest in ECG-LVH diagnosis: During this period, echocardiography, a new and
powerful noninvasive imaging method appeared, providing information on the dimensions of heart, its anatomical structure, and its hemodynamic function. The imperfect ECG discrimination between hypertrophy and dilatation, and the ECG estimation of left ventricular mass (LVM) were promptly replaced by echocardiography. An interesting shift could be observed in regard to the ECG diagnosis of LVH that persists until the present time: LVM has become accepted as the only clinical measure of LVH, and echocardiography
Fig. 2. Alternative theories of the ECG changes related to LVH. The classical vertical path principally considers changes in spatial determinants of QRS voltage in terms of solid angle theory, the extent of activation front, and the distance of the recording electrode from the activation front. In the horizontal path—changes in electrical properties of hypertrophied myocardium are considered, under 2 possible situations: (1) the charge density per unit of the double layer is decreased, which can result in a decrease in QRS amplitude; (2) there is a delay in impulse propagation, which can result in a variety of intraventricular conduction defects, with increased QRS voltage and/or prolonged QRS duration.
230
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232
has become a “gold standard” for evaluating the diagnostic performance of various competing ECG criteria. The effort of researchers has been focused on achieving the best agreement between ECG estimated LVM and LVM defined by echocardiography. Because this agreement was never achieved, the interest in ECG-LVH7 has gradually declined. This shift in clinical interest in the ECG in LVH assessment can be anecdotally illustrated by comparing comments on ECG diagnosis of LVH in 2 editions of Hurst's well known text, The Heart, from 1966 and 2004. In the 1966 edition,7 considerably more space is devoted to ventricular hypertrophies, and possible electrophysiological mechanisms of ECG changes in LVH are discussed. Four figures are included, including vectorcardiographic loops, illustrating ECG-LVH patterns. In the 2004 edition,8 noECGs and no theoretical considerations are presented, and the reader is quickly directed to the chapter on echocardiography. During this phase, changes in the P wave and the repolarization phase of the ECG were used as a component of the ECG “pattern” of LVH,7 but these were more often considered as secondary to ischemia or conduction defects and lost favor as an essential element of ECG-LVH. Paradoxically, although interest in the QRS changes of ECG-LVH has diminished, an enormous body of knowledge about electrical remodeling in LVH has emerged from research on arrhythmias (for review, see Bacharova9). 4. Period of persistent low level interest: Currently, the main interest in clinical LVH diagnosis has shifted to echocardiography. However, a level of interest in ECG persists based on sound evidence in the following 2 areas: • Cardiovascular risk assessment: ECG signs of LVH have been shown to be cardiovascular risk factors, independent of LVM or blood pressure.10-15 • The effect of antihypertensive treatment: Clinical studies have shown an association between ECGLVH signs and the severity of patients' disease and between prognosis and the favorable effect of treatment on the ECG signs of LVH.16-21
This evidence maintains clinical interest in ECG-LVH, whereas its role in predicting LVH diagnosis is still open to question. What lessons can be learned from this evolution in the clinical role of the ECG over the past century? First, it must be clearly stated that the ECG can never be a surrogate for the echocardiogram in LVM detection. This is not because of the lack of thought or the lack of comparative studies. It is simply not a logical premise because the ECG provides information about the electrical properties of myocardium and not the dimensions or weight of the heart. It follows that we should return to a consideration of the electrophysiological meaning of LVH in the interpretation of ECG. The electrophysiological aspects of QRS changes, assumed years ago, when the knowledge about the changes of electrical properties of hypertrophied myocardium was limited can now be linked with and studied in relation to the current knowledge about electrical remodeling, such as those gained in arrhythmia studies. Fig. 2 presents a flowchart of the shift in paradigm in ECG diagnosis of LVH. Theoretically, there are 2 possibilities with respect to the electrical properties of hypertrophied myocardium: (1) they are not changed or (2) they are changed. 1. Classical thinking stresses the spatial determinants of the QRS voltage in terms of the spatial angle theory: the extent of the activation front and the distance of the recording electrode. However, 2 basic “nonspatial” assumptions underlie this thinking: (i) the wave of activation is a uniform electromotive double layer, and (ii) the wave front moves through the myocardium (beyond the Purkinje network insertion) at a uniform rate.22 Similarly, Mashima23 presented the model of “ideal” hypertrophy causing enlargement of QRS amplitude. The assumptions contained within the ideal hypertrophy model are (i) the hypertrophy is diffuse and symmetrical, (ii) the sequence of electrical activation is unaltered, and (iii) the strength of the double layer and the velocity of the activation wave are the same as normal.
Fig. 3. Alternative approaches in the further research using ECG in LVH diagnosis: competitive approach aiming to the best estimation of LVM. Complementary approach considering ECG as complementary information on electrical properties of hypertrophied myocardium, aiming for an understanding of the variety of QRS pattern and elucidation of their association with pathophysiological processes and clinical outcomes.
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232
2. Current evidence shows however that the electrical properties of hypertrophied myocardium are strikingly 9,24-29 If so, then there are 2 possibilities: (i) changed. the charge density per unit of the double layer is decreased. This situation will result in a relative voltage deficit—a disproportion between the increased LVM and QRS voltage, which is lower than expected, or 9 even in a decrease in QRS amplitude ; (ii) there is a delay in impulse propagation. This situation will result in a variety of intraventricular conduction defects patterns, presenting as increased QRS voltage and prolonged QRS duration. The resulting individual ECG pattern can range over a broad spectrum, from pseudonormal QRS with decreased voltage to pseudofascicular/bundle branch blocks with increased voltage and prolonged duration. Investigation of the possible changes in electrical properties of hypertrophied myocardium in LVH and their combinations could help us to understand and explain the variability of ECG patterns seen in patients with LVH and their association with more severe clinical outcomes. As an example, the electrical events recorded in the ECG initiate the contraction of the myocardium. Could the conduction delays seen in LVH lead to a less efficient and less effective contractile effort by the ventricle? We know that dyssynergies are common in hypertrophied hearts. Can we correlate the presence of certain conduction-related ECG findings, such as left anterior descending coronary artery and increased QRS duration with a less dynamic ejection, and provide a link to poor prognosis and early mortality? Summarizing the lesson learned from history, electrocardiography must return from the dead-end path of attempting to understand the anatomy of LVH to one of attempting to understand the electrophysiology of LVH. We must combine the electrophysiological interpretations from the 1950s and 1960s with the current knowledge of electrical properties and redirect our research accordingly. Fig. 3 illustrates 2 possible approaches in ECGLVH diagnosis: • Competitive approach is the “classical” approach using the echocardiogram as a gold standard. This is a dead-end direction. • Complementary approach considering the ECG as a complementary source of information on the electrical properties of hypertrophied myocardium leading to a variety of patterns and then to elucidate the association of various patterns to clinical outcomes. This approach will be in accordance with the primary role of ECG: “The general objective of electrocardiography is definition of the electrophysiological state of the heart in medically useful terms.”30 Acknowledgment This article was supported in part through grant VEGA: 1/0530/09, Slovak Republic.
231
References 1. The 6th report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med 1997;157:2413. 2. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206. 3. Einthoven W. Le telecardiogramme. Arch Int Physiol 1906-1907;4:132. 4. Scher AM. Electrocardiographic theory and recording. In: Schlant RC, Hurst JW, editors. Advances in electrocardiography, vol. 2. New York: Grune & Stratton; 1976. p. 3. 5. Uhley HN. Study of the transmembrane action potential, electrogram, electrocardiogram and vectorcardiogram of rats with left ventricular hypertrophy. Am J Cardiol 1961;7:211. 6. Cabrera E, Estes EH, Hellerstein HK. In: Hurst JW, Wenger NK, editors. Electrocardiographic interpretation. New York: The Blakiston Division McGraw-Hill Book Co; 1963. p. 49. 7. Estes EH. Chapter 6: electrocardiography and vectorcardiography. In: Hurst JW, Logue RB, editors. The heart. New York: The Blakiston Division McGraw-Hill Book Company; 1966. p. 130. 8. Fuster V, Alexander RW, O'Rourke RA. Hurst's the heart. New York: Mc-Graw-Hill Medical Publishing Division; 2004. 9. Bacharova L. Electrical and structural remodeling in left ventricular hypertrophy—a substrate for a decrease in QRS voltage? ANE 2007;12: 260. 10. Kannel WB, Gordon T, Castelli WP, Margolis JR. Electrocardiographic left ventricular hypertrophy and risk of coronary heart disease: the Framingham Study. Ann Intern Med 1970;72:813. 11. Rautaharju PM, LaCroix AZ, Savage DD, et al. Electrocardiographic estimate of left ventricular mass versus radiographic cardiac size and the risk of cardiovascular disease mortality in the epidemiological followup study of the first National Health and Nutrition Examination Survey. Am J Cardiol 1988;62:59. 12. Verdecchia P, Porcellati C, Reboldi G, et al. Left ventricular hypertrophy as an independent predictor of acute cerebrovascular events in essential hypertension. Circulation 2001;104:2039. 13. Gonzales-Juanatey JR, Cea-Calvo L, Bertomeu V, Aznar J. Electrocardiographic criteria for left ventricular hypertrophy and cardiovascular risk in hypertensives. VIID study. Rev Esp Cardiol 2007;60:148. 14. De Bacquer D, De Backer G, Kornitzer M, et al. Prognostic value of ECG findings for total, cardiovascular disease, and coronary heart disease death in men and women. Heart 1998;80:570. 15. Zimetbaum PJ, Buxton AE, Batsford W, et al. Electrocardiographic predictors of arrhythmic death and total mortality in the multicenter unsustained tachycardia trial. Circulation 2004;110:766. 16. Okin PM, Wachtell K, Devereux RB, et al. Regression of electrocardiographic left ventricular hypertrophy and decreased incidence of new-onset atrial fibrillation in patients with hypertension. JAMA 2006; 296:1242. 17. Mathew J, Sleight P, Lonn E, et al. Reduction of cardiovascular risk by regression of electrocardiographic markers of left ventricular hypertrophy by the angiotensin-converting enzyme inhibitor ramipril. Circulation 2001;104:1615. 18. Schneider MP, Klingbeil AU, Delles C, et al. Effect of irbersartan versus atenolol on left ventricular mass and voltage. Results of the CardioVascular Irbesartan Project. Hypertension 2004;44:61. 19. Wachtell K, Okin PM, Olsen MH, et al. Regression of electrocardiographic left ventricular hypertrophy during antihypertensive therapy and reduction in sudden cardiac death: the LIFE Study. Circulation 2007; 116:700. 20. Okin PM, Devereux RB, Jern S, Kjeldsen SE, Julius S, Dahlöf B. Baseline characteristics in relation to electrocardiographic left ventricular hypertrophy in hypertensive patients: the Losartan Intervention For Endpoint Reduction (LIFE) in Hypertension Study. The Life Study Investigators. Hypertension 2000;36:766. 21. Okin PM, Devereux RB, Gerdts E, et al. LIFE Study Investigators. Impact of diabetes mellitus on regression of electrocardiographic left ventricular hypertrophy and the prediction of outcome during antihypertensive therapy: the Losartan Intervention For Endpoint
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22.
23. 24. 25.
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232 (LIFE) Reduction in Hypertension Study. Circulation 2006;113: 1588. Horan LG. Manifest orientation: the theoretical link between the anatomy of the heart and the clinical electrocardiogram. J Am Coll Cardiol 1987;9:1049. Mashima S. Theoretical considerations on the electrocardiogram of ventricular hypertrophy. J Electrocardiol 1976;9:133. Kleber AG, Rudy J. Basic mechanisms of cardiac impulse propagation and associated arrhythmias. Physiol Rev 2004;84:431. Spach MS, Heidlage JF, Dolber PC, Barr RC. Electrophysiological effects of remodeling cardiac gap junctions and cell size. Experimental and model studies of normal cardiac growth. Circ Res 2000;86:302.
26. Spach MS, Barr RC. Effects of cardiac microstructure on propagating electrical waveforms. Circ Res 2000;86:e23. 27. Tomaselli FG, Marban E. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovasc Res 1999;42:270. 28. Nattel S, Li D. Ionic remodeling in the heart. Pathophysiological significance and new therapeutic opportunities for atrial fibrillation. Circ Res 2000;87:440. 29. Akazawa H, Komuro I. Roles of cardiac transcription factors in cardiac hypertrophy. Circ Res 2003;92:1079. 30. Abildskov JA, Green LS. The recognition of arrhythmia vulnerability by body surface electrocardiographic mapping. Circulation 1987;75 (Suppl III):III-79.
Double ventricular response via dual atrioventricular nodal pathways resulting in sustained supraventricular nonreentrant tachycardia
Fig. 1
Fig. 2
Supraventricular tachycardia caused by 1:2 atrioventricular conduction (atrial rate at a cycle length of about 680 milliseconds) was observed on the esophageal electrogram (Fig. 1), and double His bundle and ventricular responses was caused by simultaneous fast and slow AV nodal pathway conduction with each atrial wave (Fig. 2). The patient underwent successful slow pathway ablation with complete disappearance of symptoms and electrocardiographic manifestations of 1:2 AV conduction. Atrial fibrillation can be erroneously diagnosed in such patients when Wenckebach periodicity is present during fast and slow AV nodal pathway conduction (J Cardiovasc Electrophysiol. 2006;17:312.). Every sinus beat with concomitant junctional premature beat resulting in a bigeminal rhythm should be considered on the differential diagnosis of such a surface ECG, but consistent HV intervals and the satisfying results of slow pathway ablation make it untenable. ESO indicates esophagus electrogram; HRA, high right atrial electrogram; His, His bundle electrogram; CSp, proximal electrogram of coronary sinus; CSm, middle electrogram of coronary sinus; CSd, distal electrogram of coronary sinus. Zhan Zhong-qun, MS, Wang Chong-quan, MD, and Dang Shu-yi, MD Shiyan, Hubei Province, China doi:10.1016/j.jelectrocard.2008.07.015
Journal of Electrocardiology 42 (2009) 228 – 232 www.jecgonline.com
Electrocardiographic diagnosis of left ventricular hypertrophy: depolarization changes Ljuba Bacharova, MD, PhD, MBA, a,⁎ E. Harvey Estes, MD b a
Abstract
Department of Biophotonics, International Laser Center, Bratislava, Slovak Republic b Duke University Medical Center, Durham, NC, USA Received 3 February 2009
Electrocardiographic signs of left ventricular hypertrophy (LVH) are on one hand accepted as independent cardiovascular risk factors and indicators of target organ damage in hypertensive patients, but, on the other hand they are strongly criticized for their low sensitivity. In this paper, a historic perspective on the ECG dignosis of LVH is presented, showing the development of current views on the role of ECG in LVH detection. Based on the fact that ECG provides information on the electrical properties of myocardium and on new knowledge about electrical remodeling in LVH, a shift of paradigm in our consideration of the diagnosis of left ventricular hypertrophy is proposed, based on changes in the electrical properties of hypertrophied myocardium. This new paradigm could explain the broad spectrum of QRS patterns seen in LVH, including increased QRS voltage, prolonged duration of QRS complex, left axis deviation, prolonged intrinsicoid deflection, LBBB and LAFB patterns, as well as pseudo-normal ECG findings. © 2009 Elsevier Inc. All rights reserved.
Interest in the electrocardiographic diagnosis of left ventricular hypertrophy (LVH) has changed since the electrocardiogram (ECG) first appeared as a clinical diagnostic tool at the beginning of the last century. Electrocardiographic indicators of LVH are now documented to be independent cardiovascular risk factors and have been accepted as indicators of target organ damage in hypertensive patients.1,2 At the same time, the use of the ECG to predict LVH suffers from low sensitivity and is severely criticized. Paradoxically, the availability and low cost of the ECG are more frequently stressed as strengths of the method than the sensitivity of the information provided by ECG in the diagnosis of LVH. This article will provide historical insight into the role of ECG in LVH diagnosis with a focus on the QRS complex and explore lessons that might be learned from this history. The ECG diagnosis of LVH has undergone an interesting development and can be divided into several distinct but overlapping periods (Fig. 1): 1. Period of introduction into clinical diagnosis: In this period, the ECG was one of the few available objective noninvasive methods providing information about the heart. This period was characterized by rapid development of this new method, exciting discoveries, and a sharp increase in interest. Normal and abnormal ECG findings were established and ⁎ Corresponding author. Tel.: +421 2 654 21 575; fax: +421 2 654 23 244. E-mail address: [email protected] 0022-0736/$ – see front matter © 2009 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2009.03.005
linked to normal as well as pathological conditions. The first description of increased QRS voltage in LVH was published at the beginning of the last century by Einthoven, who documented an increased R wave in a patient with mitral regurgitation.3 Other diagnostic methods at that time had limited ability to provide information or details about the anatomical, structural, and functional characteristics of the hypertrophied heart. 2. Period of stabilization: During this period, the ECG had become a well-established clinical diagnostic method, and the major abnormal ECG patterns had been described and categorized. The solid angle theory was proposed as a theoretical background for understanding the observed increase in QRS voltage.4 This included both spatial determinants (the extent of activation front and distance from the recording electrode) and non–spatial determinants (electrical conduction properties of myocardium, the conductivity of the medium, and the charge density per unit area of the polarized surface), all of which could influence the resultant QRS voltage. There was limited knowledge about the changes of electrical properties of hypertrophied myocardium.5 It should be stressed that in spite of the lack of evidence on electrical remodeling in LVH, electrophysiological aspects were considered in the interpretation of QRS changes in LVH. The effect of conduction delays in the left ventricle on the QRS changes was discussed as possibly more important than the effect of ventricular mass.6 The term “parietal block” was applied to a local disturbance in conduction, as opposed to bundle branch or fascicular blocks.
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232
229
Fig. 1. Periods of interest in ECG-LVH diagnosis: (1) Introductory period: introduction of ECG into clinical diagnosis, sharp increase in interest. (2) Period of stabilized interest: ECG becomes a well-established clinical diagnostic method, major ECG patterns are described and categorized. (3) Period of gradual decline: interest in ECG-LVH diagnosis directed at improving estimation of LVM, echocardiography recognized as gold standard for estimating LVM. (4) Period of persistent low-level interest: ECG evidence of LVH recognized as valid predictor of cardiovascular risk and clinical severity, and resolution of ECG-LVH with favorable effect of treatment. (5) Potential period of shift in paradigm: focus on the evaluation of the electrophysiological state of the hypertrophied myocardium and its added value for clinical diagnosis, prognosis, evaluation of therapy, and further research in electrical/mechanical relationships.
An altered relationship between the depolarization and repolarization of one ventricle with respect to the other ventricle (altered phase relationships between large areas) was also considered.7 However, it was still believed that 2 basic anatomical types of LVH—“hypertrophy” and dilatation, as seen in systolic and diastolic overload—could be distinguished by the means of the ECG. 3. Period of gradual decline in interest in ECG-LVH diagnosis: During this period, echocardiography, a new and
powerful noninvasive imaging method appeared, providing information on the dimensions of heart, its anatomical structure, and its hemodynamic function. The imperfect ECG discrimination between hypertrophy and dilatation, and the ECG estimation of left ventricular mass (LVM) were promptly replaced by echocardiography. An interesting shift could be observed in regard to the ECG diagnosis of LVH that persists until the present time: LVM has become accepted as the only clinical measure of LVH, and echocardiography
Fig. 2. Alternative theories of the ECG changes related to LVH. The classical vertical path principally considers changes in spatial determinants of QRS voltage in terms of solid angle theory, the extent of activation front, and the distance of the recording electrode from the activation front. In the horizontal path—changes in electrical properties of hypertrophied myocardium are considered, under 2 possible situations: (1) the charge density per unit of the double layer is decreased, which can result in a decrease in QRS amplitude; (2) there is a delay in impulse propagation, which can result in a variety of intraventricular conduction defects, with increased QRS voltage and/or prolonged QRS duration.
230
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232
has become a “gold standard” for evaluating the diagnostic performance of various competing ECG criteria. The effort of researchers has been focused on achieving the best agreement between ECG estimated LVM and LVM defined by echocardiography. Because this agreement was never achieved, the interest in ECG-LVH7 has gradually declined. This shift in clinical interest in the ECG in LVH assessment can be anecdotally illustrated by comparing comments on ECG diagnosis of LVH in 2 editions of Hurst's well known text, The Heart, from 1966 and 2004. In the 1966 edition,7 considerably more space is devoted to ventricular hypertrophies, and possible electrophysiological mechanisms of ECG changes in LVH are discussed. Four figures are included, including vectorcardiographic loops, illustrating ECG-LVH patterns. In the 2004 edition,8 noECGs and no theoretical considerations are presented, and the reader is quickly directed to the chapter on echocardiography. During this phase, changes in the P wave and the repolarization phase of the ECG were used as a component of the ECG “pattern” of LVH,7 but these were more often considered as secondary to ischemia or conduction defects and lost favor as an essential element of ECG-LVH. Paradoxically, although interest in the QRS changes of ECG-LVH has diminished, an enormous body of knowledge about electrical remodeling in LVH has emerged from research on arrhythmias (for review, see Bacharova9). 4. Period of persistent low level interest: Currently, the main interest in clinical LVH diagnosis has shifted to echocardiography. However, a level of interest in ECG persists based on sound evidence in the following 2 areas: • Cardiovascular risk assessment: ECG signs of LVH have been shown to be cardiovascular risk factors, independent of LVM or blood pressure.10-15 • The effect of antihypertensive treatment: Clinical studies have shown an association between ECGLVH signs and the severity of patients' disease and between prognosis and the favorable effect of treatment on the ECG signs of LVH.16-21
This evidence maintains clinical interest in ECG-LVH, whereas its role in predicting LVH diagnosis is still open to question. What lessons can be learned from this evolution in the clinical role of the ECG over the past century? First, it must be clearly stated that the ECG can never be a surrogate for the echocardiogram in LVM detection. This is not because of the lack of thought or the lack of comparative studies. It is simply not a logical premise because the ECG provides information about the electrical properties of myocardium and not the dimensions or weight of the heart. It follows that we should return to a consideration of the electrophysiological meaning of LVH in the interpretation of ECG. The electrophysiological aspects of QRS changes, assumed years ago, when the knowledge about the changes of electrical properties of hypertrophied myocardium was limited can now be linked with and studied in relation to the current knowledge about electrical remodeling, such as those gained in arrhythmia studies. Fig. 2 presents a flowchart of the shift in paradigm in ECG diagnosis of LVH. Theoretically, there are 2 possibilities with respect to the electrical properties of hypertrophied myocardium: (1) they are not changed or (2) they are changed. 1. Classical thinking stresses the spatial determinants of the QRS voltage in terms of the spatial angle theory: the extent of the activation front and the distance of the recording electrode. However, 2 basic “nonspatial” assumptions underlie this thinking: (i) the wave of activation is a uniform electromotive double layer, and (ii) the wave front moves through the myocardium (beyond the Purkinje network insertion) at a uniform rate.22 Similarly, Mashima23 presented the model of “ideal” hypertrophy causing enlargement of QRS amplitude. The assumptions contained within the ideal hypertrophy model are (i) the hypertrophy is diffuse and symmetrical, (ii) the sequence of electrical activation is unaltered, and (iii) the strength of the double layer and the velocity of the activation wave are the same as normal.
Fig. 3. Alternative approaches in the further research using ECG in LVH diagnosis: competitive approach aiming to the best estimation of LVM. Complementary approach considering ECG as complementary information on electrical properties of hypertrophied myocardium, aiming for an understanding of the variety of QRS pattern and elucidation of their association with pathophysiological processes and clinical outcomes.
L. Bacharova, E.H. Estes / Journal of Electrocardiology 42 (2009) 228–232
2. Current evidence shows however that the electrical properties of hypertrophied myocardium are strikingly 9,24-29 If so, then there are 2 possibilities: (i) changed. the charge density per unit of the double layer is decreased. This situation will result in a relative voltage deficit—a disproportion between the increased LVM and QRS voltage, which is lower than expected, or 9 even in a decrease in QRS amplitude ; (ii) there is a delay in impulse propagation. This situation will result in a variety of intraventricular conduction defects patterns, presenting as increased QRS voltage and prolonged QRS duration. The resulting individual ECG pattern can range over a broad spectrum, from pseudonormal QRS with decreased voltage to pseudofascicular/bundle branch blocks with increased voltage and prolonged duration. Investigation of the possible changes in electrical properties of hypertrophied myocardium in LVH and their combinations could help us to understand and explain the variability of ECG patterns seen in patients with LVH and their association with more severe clinical outcomes. As an example, the electrical events recorded in the ECG initiate the contraction of the myocardium. Could the conduction delays seen in LVH lead to a less efficient and less effective contractile effort by the ventricle? We know that dyssynergies are common in hypertrophied hearts. Can we correlate the presence of certain conduction-related ECG findings, such as left anterior descending coronary artery and increased QRS duration with a less dynamic ejection, and provide a link to poor prognosis and early mortality? Summarizing the lesson learned from history, electrocardiography must return from the dead-end path of attempting to understand the anatomy of LVH to one of attempting to understand the electrophysiology of LVH. We must combine the electrophysiological interpretations from the 1950s and 1960s with the current knowledge of electrical properties and redirect our research accordingly. Fig. 3 illustrates 2 possible approaches in ECGLVH diagnosis: • Competitive approach is the “classical” approach using the echocardiogram as a gold standard. This is a dead-end direction. • Complementary approach considering the ECG as a complementary source of information on the electrical properties of hypertrophied myocardium leading to a variety of patterns and then to elucidate the association of various patterns to clinical outcomes. This approach will be in accordance with the primary role of ECG: “The general objective of electrocardiography is definition of the electrophysiological state of the heart in medically useful terms.”30 Acknowledgment This article was supported in part through grant VEGA: 1/0530/09, Slovak Republic.
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Double ventricular response via dual atrioventricular nodal pathways resulting in sustained supraventricular nonreentrant tachycardia
Fig. 1
Fig. 2
Supraventricular tachycardia caused by 1:2 atrioventricular conduction (atrial rate at a cycle length of about 680 milliseconds) was observed on the esophageal electrogram (Fig. 1), and double His bundle and ventricular responses was caused by simultaneous fast and slow AV nodal pathway conduction with each atrial wave (Fig. 2). The patient underwent successful slow pathway ablation with complete disappearance of symptoms and electrocardiographic manifestations of 1:2 AV conduction. Atrial fibrillation can be erroneously diagnosed in such patients when Wenckebach periodicity is present during fast and slow AV nodal pathway conduction (J Cardiovasc Electrophysiol. 2006;17:312.). Every sinus beat with concomitant junctional premature beat resulting in a bigeminal rhythm should be considered on the differential diagnosis of such a surface ECG, but consistent HV intervals and the satisfying results of slow pathway ablation make it untenable. ESO indicates esophagus electrogram; HRA, high right atrial electrogram; His, His bundle electrogram; CSp, proximal electrogram of coronary sinus; CSm, middle electrogram of coronary sinus; CSd, distal electrogram of coronary sinus. Zhan Zhong-qun, MS, Wang Chong-quan, MD, and Dang Shu-yi, MD Shiyan, Hubei Province, China doi:10.1016/j.jelectrocard.2008.07.015