Printer Friendly

The structural and electrical remodeling of myocardium in LVH and its impact on the QRS voltage.


Electrocardiographically detected left ventricular hypertrophy (LVH) and echocardiographically detected left ventricular hypertrophy are independent predictors of cardiovascular risk, both are defined as cardiac target organ damage in hypertensive patients. However, in clinical practice the preference is given to echocardiography and the discrepant electrocardiographic (ECG) findings are underestimated or even neglected in clinical decision-making. The aim of this opinion paper was to present a view on the relation between the increased left ventricular mass and discrepant ECG findings in hypertensive patients. The concept of the "relative voltage deficit" in hypertension and in LVH assessment is presented. The current knowledge on the structural and electrical remodeling in LVH is discussed in the context of changes of active and passive electrical properties of myocardium, underlying the changes in QRS amplitude in LVH. (Anadolu Kardiyol Derg 2007: 7 Suppl 1; 37-42)

Key words: left ventricular hypertrophy, electrocardiography, specific potential of myocardium, electrical remodeling


Left ventricular hypertrophy (LVH) detected either electrocardiographically or echocardiographically, has been shown to be a strong predictor of cardiac morbidity and mortality in patients with essential hypertension and in the general population (1-3). Therefore the detection of LVH has an explicit impact on the prognosis of the patient. In hypertensive patients, both electrocardiographically and echocardiographically detected LVH is defined as cardiac target organ damage according to JNC VI/VII and its presence has an impact on the decision concerning the therapy (4, 5). It was shown that echocardiographically detected LVH and electrocardiographically detected LVH are independent risk factors, bearing independent information on risk (6, 7). However, in the electrocardiographic (ECG) diagnostics, the effort of clinical electrocardiologists is focused on finding ECG criteria, which would best estimate the left ventricular mass.

This opinion paper is focused on the voltage criteria in the ECG diagnostics of LVH. An alternative view on the relation between electrocardiographic and echocardiographic findings in hypertension is presented, based on the current knowledge on the structural and electrical remodeling in LVH.

Traditional clinical concept of electrocardiographic diagnostics of left ventricular hypertrophy

The traditional electrocardiographic diagnostics of LVH is based on the so-called voltage criteria--the increased QRS voltage in defined leads. It is hypothesized that excitation of the larger and thicker muscle mass results in larger and longer living activation boundaries, which in turn, result in the more than usual preponderance of the leftward and posteriorly oriented electrical forces. The diagnostic performance of the ECG criteria is evaluated with respect to the gold standard--which is currently the echocardiographically estimated left ventricular mass (LVM). Figure 1 shows the traditional understanding of the relation between echocardiographic (EchoCG) and electrocardiographic findings in the evaluation of the diagnostic performance of ECG in LVH assessment in clinical practice. Only ECG results, where an agreement between ECG and EchoCG findings is achieved, are considered to be "true". In the case of LVH only "true positive" findings are accepted, since negative results does not presume/ imply any pathology. The ECG findings assigned as "false" negative or positive are not considered/recognized as informative for LVH diagnostics.


Number of voltage criteria has been recommended over the years since Einthoven (8) described the increased R wave amplitude in a patient with mitral regurgitation. In spite of a variety of recommended criteria, they have common characteristics:

1. The best ECG criteria are those estimating best the LV mass. Currently, echocardiography is used as a "gold standard" for testing the diagnostic performance of ECG criteria.

2. Discrepancies between ECG and EchoCG findings with respect to echocardiography are considered "false", it means implicitly "wrong", and they are not considered for diagnostic decision-making;

3. ECG criteria suffer from low sensitivity, since the number of "false" negative ECG results is high.

This traditional concept of ECG diagnostics of LVH has a significantly weak point. In general, if two methods are bearing independent information, taking one of these methods as a "gold standard" and adjusting the results of the other method to the "gold standard" results, suppresses the unique information of the other method. In our case, if ECG and EchoCG are bearing independent information, then taking EchoCG as a "gold standard" suppresses the unique information of ECG. Therefore, when talking about independent information of ECG, then the discrepancies between the methods are probably the bearers of the independent information. And since the number of the "false" negative results is very high, (they are dominant findings in hypertension and LVH), here might exist some additional diagnostic potential of electrocardiography in LVH diagnostics.

Cardiovascular risk assessment--electrocardiographic signs of LVH as signs of cardiac organ damage in hypertension

As it is mentioned above, epidemiological studies on cardiovascular risk assessment have brought evidence that electrocardiographic and echocardiographic signs of LVH are independent predictors of cardiovascular risk (6, 7). These findings are incorporated also in clinical guidelines for hypertension and both electrocardiographically and echocardiographically diagnosed LVH is defined as cardiac target organ damage.

Acceptation of both ECG signs of LVH and EchoCG signs of LVH represents an essential shift in the attitude toward the ECG-LVH diagnostics, although the attention paid to either of these methods is unbalanced and skewed in favor of echocardiography.

As illustrated in Figure 2, patients with ECG signs of LVH include both true positive and false positive ECG findings, and patients with EchoCG signs of LVH include true positive and false negative ECG findings. Since the common subgroup of patients is that with the "true positive" findings, it is expected that they will bear the same information. It seems logical that the "independent" information on the cardiovascular risk should be based on the discrepancies between these two methods, namely on the information provided by the "false positive" and the "false negative" ECG results. It needs to be stressed that the most frequent finding in hypertensive patients is in the category of "false negative" ECG results.


The concept of the relative voltage deficit and the specific potential of myocardium

In our previous papers (9, 10) we have presented an alternative approach to the ECG diagnostics of LVH, which is based on the following premises and statements:

1. Discrepancies between ECG and EchoCG results are informative;

2. The electrical properties of myocardium are altered by the process of structural and electrical remodeling in LVH;

3. A unit of pathologically changed myocardium in LVH is a less efficient generator of cardioelectric field as compared to a unit of healthy myocardium. It follows that if a hypertensive patient and a healthy subject should have comparable LVM, then the QRS voltage in hypertensive patient will be lower. The voltage which is lower than expected with respect to the mass in hypertrophied hearts (i.e. the false negative results) is assigned as the "relative voltage deficit";

4. The relative voltage deficit starts already in the early stage of LVH development and varies with the progress of LVH. It is reduced in the stage of compensated LVH and enhanced again in the stage of developing heart failure;

5. The ratio of QRS to LVM called "specific potential of myocardium" has been introduced as a parameter for the quantification of the relative voltage deficit.

Figure 3 shows our understanding of the relation between the LVM and electrical properties of myocardium. Instead of using words "true" and "false" which imply correctness and incorrectness, we prefer the following description of the relation between mass and function in terms of its electrical characteristics, giving different meanings to the subset of results:

* True negative results=left ventricular (LV) mass and function within normal limits;

* False positive=left ventricle with normal size and hyperfunction;

* True positive=increased mass and adequately increased function;

* False negative=increased mass with relative voltage deficit.


As it was mentioned above, the latter category represents the majority of findings in hypertensive patients.

We have shown in both experimental and clinical studies that hypertrophied left ventricle is not as a strong generator of cardiac electric field as a healthy one, and that the LVM is not the major determinant of the QRS voltage.

In experimental studies, we have focused on the early stage of LVH development, when the general deterioration of myocardium occurring in developing heart failure is not yet present. We have found the relative voltage deficit in several models of experimental LVH: due to pressure overload, volume overload, and so-called physiological LVH in swimming rats (11-13). We have shown also that drugs further modify the relationship between the LVM and QRS voltage (14, 15), and that QRS does not parallel the changes in LVM.

In clinical studies, we observed lower specific potential (SP) values in hypertensive patients as compared to healthy subjects contrasting with higher values of the maximum QRS vector magnitude (QRSmax) in hypertensive patients (16). A gradual decrease in QRS voltage was also observed in girls during the first 21 months of intensive training of competitive sport (17). In a population study, lower values of both QRSmax and SP were recorded in hypertensive subjects with newly diagnosed hypertension as compared to healthy subjects (18). The more, the lower values of SP were observed also in hypertensive patients without either ECG or EchoCG signs of LVH, e.g. in patients without target organ damage according to JNC VI/VII classification. This finding is of utmost importance. It is in agreement with our findings in experimental studies and could contribute to the early diagnostics of subclinical target organ damage, which is stressed by the European guidelines for the management of arterial hypertension (19, 20).

Summarizing, we assume that the relative voltage deficit, manifested as lower values of SP, or even lower values of QRS in hypertensive patients as compared to healthy subjects, reflects the hypertrophic structural and electrical rebuilding of myocardium and can be unmasked already in early stages of LVH when the results of both ECG and EchoCG are still within the arbitrary given "normal" limits.

The rationale for this statement is based on our extensive knowledge regarding the structural and electrical remodeling in LVH as a potential substrate for arrhythmias.

Structural and electrical remodeling in LVH impact on QRS voltage

Left ventricular hypertrophy is characterized by gradual structural and electrical remodeling, leading finally to an electrical instability of myocardium, triggering, and maintaining arrhythmias, and to heart failure. These processes are closely interrelated and initiated already in the early stage of LVH process. The main characteristics of myocardium affected by the structural and electrical remodeling leading to changes in the electrical impulse generation and propagation are schematically presented in Figures 4 and 5. The structural and electrical remodeling cannot be strictly separated especially at the microscopic levels (e.g. related to gap junctions or ion channels), this division was used for the sake of simplification.


In clinical understanding, the term "structural remodeling" refers usually to changes in the LVH shape in terms of eccentric and concentric hypertrophy. However, the changed shape of the left ventricle is conditioned by underlying changes at tissue, cellular and subcellular levels and these changes have been reported already in early stages of hypertension and LVH, both in animal models and in humans (21, 22). At the cellular level, the increase in the size of individual cardiomyocytes is the basic characteristics in LVH. It has been shown that changes in diameter, length, branching, and number of connected cardiomyocytes to an individual cardiomyocyte consequently affect the electrical properties of myocardium (23-25).

Electrical remodeling

Electrical remodeling is a term comprising complex changes in active and passive electrical properties of myocardium and evidence on the electrical remodeling in LVH has been accumulated in relation to arrhythmias. The pertinent literature on the electrical remodeling and arrhythmias deals mostly with the role of repolarization changes, however, electrical and structural remodeling affects also depolarization and could be therefore reflected in changes of QRS voltage.

Resting membrane potential and action potential

With respect to active electrical properties of myocardium, the main changes in LVH are observed during the repolarization phase of action potential (AP), especially the prolongation of AP duration. The findings on the depolarization phase of AP are not that explicit, and they are not consistent. However, significant changes in resting membrane potential, upstroke velocity or amplitude of the action potential, as well as conduction velocity in hypertrophied myocardium were reported (26-28). The reasons for differences in results can include differences in the experimental model of left ventricular hypertrophy, species and preparation employed, variations in the severity of hypertrophy, methodological aspects, etc., but there is a solid base of evidence on the changes of the active electrical characteristics of hypertrophied myocardium. Moreover, it has been shown that changes in passive electrical properties may themselves induce changes in action potential characteristics (29, 30).

Gap junction remodeling and effect of Cx43 reduction

According to current knowledge, gap junctions are considered to be crucial for the propagation of the cardiac impulse. In advanced stages of cardiac pathology, connexin expression and intracellular coupling are diminished and gap junction channels become redistributed. These changes have been strongly implicated in the pathogenesis of lethal ventricular arrhythmias. In the case of LVH, studies on humans, experimental animal models and cultured cardiomyocytes report alterations in the distribution and expression of connexin43 (Cx43) already in early stages of developing hypertrophy, creating a solid basis for changes in electrical impulse propagation (31-33).

The effect of Cx43 reduction

Studies on genetically engineered models of connexin43 knockout mice or of conditionally knockout mice expressing progressively decreasing levels of Cx43 and model studies showed, that reduction in gap junction content (about 40%) have only moderate or no effect on ventricular conduction velocity, but up to 95% decrease of Cx43 protein reduces conduction velocity and increases dispersion of conduction (34-36).

The reduction in total Cx43 levels itself may have only moderate effect on the conduction velocity. However, in conjunction with other hypertrophy-induced changes of active and passive electrical properties of myocardium, it can contribute to alterations in conduction of electrical impulses, e.g. a decrease in gap junction conductance by lowering Ph, and [Ca.sup.2+] ions concentration changes in cytoplasmic resistivity and cellular geometry. The more, in a pathological heart, Cx43 expression is heterogeneous, i.e. some regions have a virtually normal density of Cx43 expression, while others lack Cx43 almost completely. In conjunction with other disease-related changes this gives rise to discontinuities in conduction. It should be also mentioned that measures of total connexin levels do not provide information on the quantity of functional (open) channels; hence, a reduction of connexin43 may not, per se, be detrimental (37-40).

Ion channel remodeling

Changes in AP shape and duration result from alteration in the functional expression of depolarizing and repolarizing currents. Depolarization is influenced by depolarizing currents: the fast sodium current /Na, L-type calcium current /Ca(L) and [Na.sup.+]-[Ca.sup.2+] exchanger /Na/Ca. The ion channel remodeling and mechanisms involved in this process are reviewed in details (41-43), and it is documented that the ion channel involvement in hypertrophic remodeling is present already in the early stages of LVH.

The factors involved in the structural, gap junction and ion channel remodeling are mutually interrelated and it is suggested that the passive myocardial structure has a major effect on the role of membrane currents in the propagation of the action potential. The non-membrane change (i.e., decreased intercellular coupling) can cause the membrane to switch to a different process (calcium instead of sodium current). It follows, that the functional role of excitation currents (ie /Na and /Ca(L) can be determined to a significant extent by passive structural factors external to the membrane and not only by intrinsic membrane factors. These processes are further modified by a broad spectrum of changes observed in LVH, such as ion concentration (e.g. [Na.sup.+], [Ca.sup.2+]), gene expression, metabolic changes, energy metabolism, and many others (29, 43, 44).

Microscopic heterogeneity

Microscopic heterogeneity in the size of hypertrophied cardiomyocytes (21), connexin expression and gap junction location (42), action potential characteristics and membrane currents (45) are probably additional factors resulting in alteration of the normal ordered pattern of the microconduction pathway, creating microscopic cellular heterogeneity, even when the activation front is not deformed.

Impact of obesity on the ECG sign of LVH

Our approach brings also an alternative view on the controversial ECG findings in obese patients. Obesity is frequently associated with hypertension and hypertrophy, and is traditionally considered to be an indirect cause of LVH, through the hemodynamic mechanisms including increased heart rate and stroke volume. The prevailing traditional concept in electrocardiographic diagnostics of LVH postulates that obesity has an attenuating effect on ECG amplitudes due to the increased amount of adipose tissue in the chest wall affecting the resistance of the current flow and the distance between the precordial electrode and the heart. Therefore, adjusting formulas are recommended for ECG-LVH diagnostics (46, 47).

However, the impact of obesity on QRS voltage is not explicit. There is evidence showing that low voltage is not a significant feature in the ECG of obese (48). Frank et al. (49) found increasing QRS voltage with increasing obesity. Rautaharju et al. (50) showed that breast tissue appears to have a practically negligible effect on ECG amplitudes in women. Also a decrease in QRS voltage is reported in obese subjects after weight loss (48, 51). Conflicting evidence can be found even in the same study, reporting high frequency of both low voltage and various markers of left ventricular hypertrophy in the same group of obese subjects (52).

We assume that the direct effect of adiposity on the heart is the important adiposity-related factor affecting the QRS voltage, modifying its electrical properties as the generator of cardiac electrical field. The direct effect of adiposity on the heart includes the increase in epicardial fat, the infiltration of adipocytes from the epicardial adipose tissue to areas between the myocardial fibers (53, 54), metabolic and endocrine disorders (55, 56), and the direct cardiotoxicity (57).

It was shown, that the body mass index is not the main determinant of epicardial fat thickness, or intramyocardial adiposity (58), therefore the adjustment of the QRS voltage on the body mass index is not the solution. In electrocardiographic terms, the direct effect of adiposity on the heart--epicardial and intramyocardial adiposity--results in the reduction of the proportion of electrically active myocardial tissue and modification of its electrical properties. Our understanding of the changed electrical properties of myocardium in obesity is in accordance with current views on novel mechanism for heart disease in obesity whereby excessive lipid accumulation within the myocardium directly causes left ventricular remodeling and LVH hypertrophy (59).


It is shown in this review that the traditional concept of "ideal" hypertrophy defined in 1976 by Mashima (60), can be reformulated on the basis of the recent knowledge on the electrical remodeling of myocardium in LVH. Mashima's term "ideal hypertrophy" refers to hypertrophy causing the enlargement of the QRS amplitude under these conditions: (i) the hypertrophy is diffuse and symmetrical, (ii) the sequence of electrical activation is unaltered, (iii) the strength of the double layer and the velocity of the activation wave are the same as normal. Mashima assumed that discrepancies between the LVH size and QRS voltage in actual cases indicate deviations from the "ideal" state, such as individual variations in the body build and surrounding tissue can obscure the genuine effect of hypertrophy. With respect to the strength of double layer, its alteration by myocardial edema and "other pathological processes" was mentioned.

Recent knowledge on the electrical remodeling shows that myocardial remodeling in LVH is multifactorial and complex. This process involves changes in the structure and function of myocardium, including myocyte hypertrophy and apoptosis, changes in electrical and contractile phenotype, and alterations in the quantity and composition of the extracellular matrix. These complex changes are interrelated and the relative contribution of individual components to the QRS amplitude induced by LVH changes over the time depending on the stage and severity of LVH, co-morbidities and treatment. Therefore the sources for deviations from "ideal" hypertrophy can be summarized as follows: (i) the hypertrophy is a heterogeneous process, although at the organ level it appears as symmetrical, (ii) the structural changes and changes in active and passive properties of myocardium can alter conduction velocity; (3) the structural changes and changes in active and passive properties of myocardium can alter the strength of the double layer. Our approach to the false negative ECG results is based on the complex understanding of the changes of electrical properties of myocardium in LVH. The concept of the relative voltage deficit in LVH, and the specific potential of myocardium:

* Distinguishes the anatomical and electrical information in LVH diagnostics and utilizes both,

* Considers the so-called false negative results as true results, showing the deviation from "ideal" hypertrophy caused by interrelated structural and electrical remodeling,

* Considers non-linear changes of structural and electrical characteristics and their interplay in different stages of LVH development.

This approach stresses the need to relate the anatomical size and the function of the heart as a source of cardio-electric field. The unique information and the added value of ECG in LVH diagnostics is in providing the information on the electrical properties of the heart and their alteration due to hypertrophic process, and not in the imperfect estimation of the left ventricular mass. The specific potential of myocardium allows also to quantify the early changes in LVH remodeling of myocardium in hypertensive patients without traditional ECG and EchoCG signs of LVH--the subclinical target organ damage.


Supported by the grant VEGA 1/3406/06 from The Science Grant Agency, Slovak Republic.


(1.) 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: 813-22.

(2.) Rautaharju PM, LaCroix AZ, Savage DD, Haynes SG, Madans JH, Wolf HK, et al. Electrocardiographic estimate of left ventricular mass versus radiographic cardiac size and the risk of cardiovascular disease mortality in the epidemiological follow-up study of the first National Health and Nutrition Examination Survey. Am J Cardiol 1988; 62: 59-66.

(3.) Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Left ventricular mass and incidence of coronary heart disease in an elderly cohort: The Framingham Study. Ann Int Med 1989; 110: 101-7.

(4.) The 6th report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Arch Intern Med 1997; 157: 2413-46.

(5.) Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42: 1206-52.

(6.) Kannel WB. Left ventricular hypertrophy as a risk factor: the Framingham experience. J Hypertens Suppl 1991; 9: S3-8.

(7.) Sundstrom J, Lind L, Arnlov J, Zethelius B, Andren 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.

(8.) Einthoven W. Telecardiogramme. Arch Int Physiol 1906-1907; 4: 132-63.

(9.) Bacharova L. Effect of left ventricular hypertrophy on the cardiac electrical field: The concept of the specific potential of myocardium. Exp Clin Cardiol 1998; 3: 128-33.

(10.) Bacharova L, Kyselovic J. Electrocardiographic diagnosis of left ventricular hypertrophy: Is the method obsolete or should the hypothesis be reconsidered? Medical Hypotheses 2001; 57: 487-90.

(11.) Bacharova L, Kyselovic J, Klimas J. The initial stage of left ventricular hypertrophy in spontaneously hypertensive rats is manifested by a decrease in the QRS amplitude/left ventricular mass ratio. Clin Exp Hypertens 2004; 26: 557-67.

(12.) Bacharova L, Bernadic M, Fizelova A. Electrocardiographic manifestation of experimental left ventricular hypertrophy. In: Jagielski J, Gornicki M, editors. Electrocardiology 91. Singapore: World Scientific Publ Co; 1992. p. 29-32.

(13.) Bacharova L, Michalak K, Kyselovic J, Klimas J. The relation between QRS amplitude and left ventricular mass in the initial stage of exercise-induced left ventricular hypertrophy in rats. Clin Exp Hypertens 2005; 27: 533-41.

(14.) Bacharova L, Kyselovic J, Klimas J, Kucerova D. Changes in QRS amplitude to left ventricular mass relation in rats treated by antihypertensive drugs. In: Hiraoka M, Ogawa S, Kodama I, Inoue H, Kasanuki H, Katoh T, editors. Advances in Electrocardiology 2004. Singapore: World Scientific; 2005. p. 636-9.

(15.) Michalak K, Klimas J, Krenek P, Bacharova L, Kyselovic J. ECG signs of left ventricular hypertrophy in rats exposed to training combined with the effect of anabolic steroids (Abstract). J Mol Cell Cardiol 2002; 34: A87.

(16.) Bacharova L, Melotova J, Sedlakova K: The "specific potential" as a parameter of myocardial changes in left ventricular hypertrophy. In: Abel H, editor. Electrocardiology 1988. Amsterdam: Elsevier Science Publisher, Excerpta Medica; 1989. p. 195-8.

(17.) Bacharova L, Tibenska M, Kucerova D, Kyselovicova O, Medekova H, Kyselovic J. The effect of one year aerobic gymnastics training on the QRS amplitude in teenage female athletes. Proceedings of the International Congress on Electrocardiology; 2005; June 2-4; Gdansk, Poland. [CD-ROM]. Folia Cardiologica 2005; 12 Suppl D.

(18.) Bacharova L, Baum OV, Mamadov MN, Muromtseva GA, Popov LA, Rozanov VB, et al. Relation between QRS amplitude and LVM in mild hypertension. Abstract Book of the International Society of Computerized Electrocardiology, ISCE; 2006; April 22-27; Niagara-on-the-Lake, Canada; 2006.

(19.) European Society of Hypertension-European Society of Cardiology Guidelines Committee. 2003 European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens 2003; 21: 1011-53.

(20.) Mancia G, Grassi G; European Society of Hypertension; European Society of Cardiology. Joint National Committee VII and European Society of Hypertension/ European Society of Cardiology Guidelines for evaluating and treating hypertension: A two-way road? J Am Soc Nephrol 2005; 16 Suppl 1: S74-7.

(21.) Kawamura K, Kashii C, Imamura K. Ultrastructural changes in hypertrophied myocardium of spontaneously hypertensive rats. Jpn Circ J 1976; 40: 1119-45.

(22.) Sawada K, Kawamura K. Architecture of myocardial cells in human cardiac ventricles with concentric and eccentric hypertrophy as demonstrated by quantitative scanning electron microscopy. Heart Vessels 1991; 6: 129-42.

(23.) Joyner RW. Effects of the discrete pattern of electrical coupling on propagation through an electrical syncytium. Circ Res 1982; 50: 192-200.

(24.) 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: 302-11.

(25.) Kucera JP, Rudy Y. Mechanistic insight into very slow conduction in branching cardiac tissue. A model study. Circ Res 2001; 89: 799-806.

(26.) Gulch RW, Bauman NR, Jacob R. Analysis of myocardial action potential in left ventricular hypertrophy of Goldblatt rats. Basic Res Cardiol 1979; 74: 69-82.

(27.) Ryder KO, Bryant SM, Hart G. Membrane current changes in left ventricular myocytes isolated from guinea pig after abdominal aortic coarctation. Cardiovasc Res 1993; 27: 1278-87.

(28.) Nordin C, Siri F, Aronson RS. Electrophysiologic characteristics of single myocytes isolated from hypertrophied guinea-pig hearts. J Mol Cell Cardiol 1989; 21: 729-39.

(29.) Thomas SP, Kucera JP, Bircher-Lehmann L, Rudy Y, Saffitz JE, Kleber AG. Impulse propagation in synthetic strands of neonatal cardiac myocytes with genetically reduced levels of connexin 43. Circ Res 2003; 92: 1209-16.

(30.) Henriquez AP, Vogel R, Muller-Borer BJ, Henriquez CS, Weingart R, Cascio WE. Influence of dynamic gap junction resistance on impulse propagation in ventricular myocardium: a computer simulation study. Biophys J 2001; 81: 2112-21.

(31.) Peters NS, Green CR, Poole-Wilson PA, Severs NJ. Reduced content of connexin43 gap junctions in ventricular myocardium from hypertrophied and ischemic human hearts. Circulation 1993; 88: 864-75.

(32.) Okabe M, Kawamura K, Terasaki F, Hayashi T. Remodeling of cardiomyocytes and their branches in juvenile, adult, and senescent spontaneously hypertensive rats and Wistar Kyoto rats: comparative morphometric analyses by scanning electron microscopy. Heart Vessels 1999; 14: 15-28.

(33.) Formigli L, Ibba-Manneschi L, Perna AM, Pacini A, Polidori L, Nediani C, et al. Altered Cx43 expression during myocardial adaptation to acute and chronic volume overload. Histol Histopathol 2003; 18: 359-69.

(34.) Beauchamp P, Choby C, Desplantez T, de Peyer K, Green K, Yamada KA, et al. Electrical propagation in synthetic ventricular myocyte strands from germline connexin43 knockout mice. Circ Res 2004; 95: 170-8.

(35.) Jongsma HJ, Wilders R. Gap junctions in cardiovascular disease. Circ Res 2000; 86: 1193-7.

(36.) van Rijen HVM, Eckardt D, Degen J, Theis M, Ott T, Willecke K, et al. Slow conduction and enhanced anisotropy increase the propensity for ventricular tachyarrhythmias in adult mice with induced deletion of connexin43. Circulation 2004; 109: 1048-55.

(37.) Saffitz JE. Regulation of intracellular coupling in acute and chronic heart disease. Braz J Med Biol Res 2000; 33: 407-13.

(38.) Jalife J, Morley GE, Vaidya D. Connexins and impulse propagation in the mouse heart. J Cardiovasc Electrophysiol 1999; 10: 1649-63.

(39.) Rohr S. Role of gap junctions in the propagation of the cardiac action potential. Cardiovasc Res 2004; 62: 309-22.

(40.) Teunissen BEJ, Jongsma HJ, Bierhuizen MFA. Regulation of myocardial connexins during hypertrophic remodeling. Eur Heart J 2004; 25: 1979-89.

(41.) Tomaselli FG, Marban E. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovasc Res 1999; 42: 270-83

(42.) Hill JA. Electrical remodeling in cardiac hypertrophy. Trends Cardiovasc Med 2003; 13: 316-22.

(43.) Shaw RM, Rudy Y. Ionic mechanisms of propagation in cardiac tissue. Roles of sodium and L-type calcium currents during reduced excitability and decreased gap junction coupling. Circ Res 1997; 81: 727-41.

(44.) Kucera JP, Rohr S, Rudy Y. Localization of sodium channels in intercalated disks modulates cardiac conduction. Circ Res 2002; 91: 1176-82.

(45.) Main MC, Bryant SM, Hart G. Regional differences in action potential characteristics and membrane currents of guinea-pig left ventricular myocytes. Exp Physiol 1998; 83: 747-61.

(46.) Norman JE Jr, Levy D, Campbell G, Bailey JJ. Improved detection if echocardiographic left ventricular hypertrophy using a new electrocardiographic algorithm. J Am Coll Cardiol 1993; 21: 1680-6.

(47.) Rautaharju PM, Zhou SH, Park LP. Improved ECG models for left ventricular mass adjusted for body size, with specific algorithms for normal conduction, bundle branch blocks, and old myocardial infarction. J Electrocardiol 1996; 29 (Suppl): 261-9.

(48.) Eisenstein I, Edelstein J, Sarma R, Sanmarco M, Selvester RH. The electrocardiogram in obesity. J Electrocardiol 1982; 15: 115-8.

(49.) Frank S, Colliver JA, Frank A. The electrocardiogram in obesity: statistical analysis of 1,029 patients. J Am Coll Cardiol 1986; 7: 295-9.

(50.) Rautaharju PM, Park L, Rautaharju FS, Crow R. A standardized procedure for locating and documenting ECG chest positions. Consideration of the effect of breast tissue on ECG amplitudes in women. J Electrocardiol 1998; 31: 17-29.

(51.) Brohet CR, Tuna N. Quantitative analysis of the vectorcardiogram in obesity. J Electrocardiol 1975; 8: 1-11.

(52.) Fraley MA, Birchem JA, Senkottaiyan N, Alpert MA. Obesity and electrocardiogram. Obes Rev 2005; 6: 275-81.

(53.) Shirani J, Berezowski K, Roberts WC. Quantitative measurement of normal and excessive (cor adiposum) subepicardial adipose tissue, its clinical significance, and its effect on electrocardiographic QRS voltage. Am J Cardiol. 1995; 76: 414-8.

(54.) Corradi D, Maestri R, Callegari S Pastori P, Goldoni M, Luong TV, et al. The ventricular epicardial mass in normal, ischemic and hypertrophic hearts. Cardiovasc Pathol 2004; 13: 313-6.

(55.) Allard MF, Schonekess BO, Henning SL, English DR, Lopaschuk GD. Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts. Am J Physiol Heart Circ Physiol 1994; 267: H42-50.

(56.) Iacobellis G, Corradi D, Sharma AM. Epicardial adipose tissue: anatomical, biomolecular and clinical relation to the heart. Nat Cardiovasc Clin Pract Med 2005; 2: 536-43.

(57.) Zhou Y-T, Grayburn P, Karim A, Shimabukuro M, Higa M, Baetens D, et al. Lipotoxic heart disease in obese rats: Implications for human obesity. Proc Natl Acad Sci USA 2000; 97: 1784-9.

(58.) Iacobellis G, Assael F, Ribaudo MC, Zappaterreno A, Alessi G, Di Mario U, et al. Epicardial fat from echocardiography: A new method for visceral adipose tissue prediction. Obes Res 2003; 11: 304-10.

(59.) McGavock JM, Victor RG, Unger RH, Szczepaniak LS. Adiposity of the heart, revisited. Ann Intern Med 2006; 144: 517-24.

(60.) Mashima S. Theoretical considerations on the electrocardiogram of ventricular hypertrophy. J Electrocardiol 1976; 9: 133 - 8.

Ljuba Bacharova International Laser Center, Bratislava, Slovak Republic

Address for Correspondence: Ljuba Bacharova, Assoc. Prof., MD, PhD, MBA, International Laser Center, Ilkovicova 3, 812 19 Bratislava, Slovak Republic Phone: +421.2.654 21 575 Fax: +421.2.654 23 244 E-mail:
COPYRIGHT 2007 Galenos Yayincilik
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2007 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Bacharova, Ljuba
Publication:The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)
Article Type:Clinical report
Geographic Code:4EXSV
Date:Jul 1, 2007
Previous Article:Twenty-millisecond interventricular difference as assessed by body surface potential mapping identifies patients with clinical improvement after...
Next Article:Defibrillation threshold testing and neurologic outcome.

Related Articles
Understanding ST depression in the stress-test ECG.
The relation between QRS amplitude and left ventricular mass in patients with hypertension identified at screening.
Evaluation of the electrocardiographic criteria for left ventricular hypertrophy.
Understanding ST depression in the stress-test ECG.
New approaches to the diagnosis of left and right ventricular hypertrophy by means of dipolar electrocardiotopography.
The structural and electrical remodeling of myocardium in LVH and its impact on the QRS voltage.
Repolarization abnormalities and arrhythmogenesis in hypertrophic myocardium.
Beat-to-beat variability of repolarization: a new parameter to determine arrhythmic risk of an individual or identify proarrhythmic drugs.
Angiotensin I converting enzyme gene polymorphism and exercise trainability in elderly women: an electrocardiological approach.

Terms of use | Privacy policy | Copyright © 2020 Farlex, Inc. | Feedback | For webmasters