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The ECG diagnosis of LVH is predominantly based on the QRS voltage criteria, i.e. the increased QRS complex amplitude in defined leads. The classical ECG diagnostic paradigm postulates that the increased left ventricular mass generates a stronger electrical field, increasing the leftward and posterior QRS forces. These increased forces are reflected in the augmented QRS amplitude in the corresponding leads. However, the clinical observations document increased QRS amplitude only in the minority of patients with LVH. The low sensitivity of voltage criteria has been repeatedly documented. We discuss possible reasons for this shortcoming and proposal of a new paradigm. [Display omitted] [ABSTRACT FROM AUTHOR]

Left ventricular hypertrophy (LVH) detected electrocardiographically is documented as an independent cardiovascular risk factor. However, the reasoning for using electrocardiography (ECG) for LVH detection is frequently referring to its low cost and availability, which should compensate for the main problem of the ECG criteria for LVH detection (ECG-LVH) - the high number of ECG false negative results and the resulting low sensitivity. This opinion paper is focused on the scientific evidence for advocating the usefulness of ECG in LVH assessment. The classical paradigm assumes that the increased left ventricular mass generates a stronger electrical field that has to be reflected in the increased QRS amplitude. However, the solid angle theorem postulates that the recorded ECG voltage depends not only on the extent of the activation front that is increased in LVH, but also on the electrical characteristics of myocardium. There is an accumulated evidence from animal and clinical studies documenting significant alterations of structural and functional properties of hypertrophied myocardium, both of cardiomyocytes as well as of interstitium. These alterations are associated with significant changes of active and passive electrical properties of myocardium modifying the resultant QRS amplitudes. The new paradigm should consider the altered electrical properties of hypertrophied myocardium in interpreting the whole spectrum of QRS patterns seen in LVH patients: the increased QRS voltage, the QRS voltage within normal limits, occurrence of left axis deviation and left bundle branch block. Thus further research is necessary for utilizing the unique diagnostic information provided by ECG: to link the agreements as well as the disagreements between ECG and imaging methods findings to pathophysiological processes and patho-anatomical backgrounds, to the risk assessment and the clinical status of patients with LVH. [ABSTRACT FROM AUTHOR]

The Fourth Universal Definition of Myocardial Infarction (FUDMI) [published simultaneously in 2018 in numerous journals including Circulation, Journal of the American College of Cardiology and European Heart Journal] focuses mainly on the distinction between non-ischemic myocardial injury and myocardial infarction (MI), along with the role of cardiovascular magnetic resonance, in order to define the etiology of myocardial injury. As a consequence, there is less emphasis on updating the parts of the definition concerning the electrocardiographic (ECG) changes related to MI. Evidence of myocardial ischemia is a prerequisite for the diagnosis of MI and the ECG is the main available tool for i) detecting acute ischemia, ii) triage and iii) risk stratification upon presentation. This review focuses on multiple aspects of ECG interpretation that we firmly believe should be considered for incorporation in any future update to the Universal Definition of MI. Our counterpoint view is that: a) the use of the ECG following coronary artery bypass surgery should be better explored and defined; b) the emphasis in the FUDMI on convex versus concave ST-elevation, which is questionable, should be balanced by the fact that many patients with true ST-elevation MI (STEMI) present with a concave form of ST elevation; c) reciprocal ST-depression in STEMI caused by right coronary artery or left circumflex artery occlusion, should be set against the fact that not all anterior STEMIs present with reciprocal ST-depression which can also be seen in cardiomyopathy and left ventricular hypertrophy; d) the "posterior" leads V7-V9 should be placed on a horizontal line from V4, rather than follow the 5th intercostal space; e) ST-depression in V1-V3 is not a manifestation of ischemia of the basal inferior segment, placed horizontally; f) Interpreting ST-T changes in patients with conduction abnormalities and pacemakers should be further defined. [ABSTRACT FROM AUTHOR]

Both obesity and menopause are significant cardiovascular risk factors. In postmenopausal women the protective effect of estrogens is reduced and menopause is frequently associated with occurrence of other significant cardiovascular factors including obesity. This study was focused on evaluating the effect of obesity on the QRS complex in pre- and postmenopausal women. We present results of analysis of 199 electrocardiograms of pre- and postmenopausal women analyzed in relation to the body mass index within normal limits (BMI 20 to 24.9 kg/m2) and obesity (BMI > 30 kg/m2), respectively. Obesity in premenopausal women and menopause significantly affected both the electrical axis (EA) and maximum QRS spatial vector magnitude (QRSmax). The highest QRSmax and electrical axis values were observed in premenopausal lean women, and they were significantly higher as than in the premenopausal obese women, postmenopausal lean and obese women (QRSmax: 1.66 ± 0.4 mV, 1.17 ± 0.35 mV, 1.4 ± 0.46 mV, and 1.35 ± 0.39 mV, resp.). (EA: 56.4 ± 18.0°, 38.22 ± 18.38°, 45.82 ± 18.63°, and 36.75 ± 17.51°). The differences between obese premenopausal women, lean and obese postmenopausal women were not statistically significant. These differences were reflected in 12-lead ECG amplitude. The presence of additional cardiovascular risk factors did not affect the ECG parameters. Obesity significantly affected QRS complex in premenopausal women. This effect was comparable with the effect of menopause. Because all QRS complex changes were within normal limits, these results suggest that ECG evaluation in women should go beyond traditional diagnostic categories and consider the relationship between ECG changes and two cardiovascular risk factors - obesity and menopause. [ABSTRACT FROM AUTHOR]

This paper describes a substantial part of the international mentoring network of students and young investigators in electrocardiology that developed around Dr. Galen Wagner (1939-2016), including many experiences of his mentees and co-mentors. The paper is meant to stimulate thinking about international mentoring as a means to achieve important learning experiences and personal development of young investigators, to intensify international scientific cooperation, and to stimulate scientific production. [ABSTRACT FROM AUTHOR]

The 4th Report provides a brief review of publications focused on the electrocardiographic diagnosis of left ventricular hypertrophy published during the period of 2010 to 2016 by the members of the Working Group on ECG diagnosis of Left Ventricular Hypertrophy. The Working Group recommended that ECG research and clinical attention be redirected from the estimation of LVM to the identification of electrical remodeling, to better understanding the sequence of events connecting electrical remodeling to outcomes. The need for a re-definition of terms and for a new paradigm is also stressed. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Activation wavefront propagation was computed and visualized in a geometrical heart model for pathological cases of reduced velocity of propagation, left ventricular hypertrophy and their combination. Selected parameters of a multiple dipole equivalent heart generator were computed and compared for three heart geometries and several degrees and extents of reduction of propagation velocity. First, the influence of geometrical changes modeling the left ventricular hypertrophy at reference propagation velocity was compared with reduction of the propagation velocity in the reference heart geometry. Reduced propagation velocity yielded similar or greater changes of the magnitude of the (electrical) heart vector representing the activation wavefront than the geometrical changes. Observations of the wavefront propagation with reduced velocity revealed longer presence of a large extent of the wavefront during depolarization which resulted in increased magnitude of the heart vector. The duration of depolarization was significantly prolonged only when the propagation velocity was decreased to 25% of its normal value. Changes of the direction of the maximal heart vector were dependent on the position of the region where the propagation velocity was reduced. Then the combination of the left ventricular hypertrophy and reduced propagation velocity was studied. Such combination enhanced the enlargement of the electrical heart vector and significantly prolonged the duration of depolarization. The influence of reduced activation velocity on the observed parameters was greater than the effect of the enlargement of the left ventricular mass. The presented study showed that intramyocardial conduction disturbances might cause increase of the actual surface area of propagation wavefront leading to changes of the amplitudes of ECG signals comparable with the changes resulting from the left ventricular hypertrophy. Intramyocardial conduction disturbances, as well as the modeled 50% increase of the thickness of the left ventricular wall, did not cause prolongation of the QRS complex out of normal range. Considerable prolongation of the QRS complex duration was observed only for transmural slowing of the propagation velocity to 25% of its reference value in large ventricular areas or for combination of such slowing with the left ventricular hypertrophy. [ABSTRACT FROM AUTHOR]

Unlabelled: Midwall fibrosis is a frequent finding in different types of left ventricular hypertrophy. Fibrosis presents a local conduction block that can create a substrate for ventricular arrhythmias and lead to the continuous generation of reentry. Having also impact on the sequence of ventricular activation it can modify the shape of QRS complex. In this study we simulated the effects of slowed conduction velocity in the midwall in the left ventricle and in its anteroseptal region on the QRS morphology using a computer model.Material and Methods: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids; the left ventricular wall is represented by five layers. The impulse propagation velocity was decreased by 50% in one and two midwall layers, respectively, in the whole left ventricle and in LV anterior region. The effects of slowed conduction velocity on the QRS complex of the 12-lead electrocardiogram are presented as 12-lead electrocardiograms and corresponding values of ECG criteria for left ventricular hypertrophy (ECG-LVH criteria): Gubner criterion, Sokolow-Lyon index (SLI) and Cornell voltage.Results: All simulated situations led to increased R wave amplitude in the lead I and of S wave in the lead III, showing a leftward shift of the electrical axis and increased values of ECG-LVH criteria based on limb leads alone or in combination with precordial leads (Gubner criterion, Cornell voltage). The slowed conduction velocity in the whole LV influenced the QRS complex voltage in precordial leads, having an impact on the SLI and Cornell voltage. The changes were pronounced if two layers were involved.Conclusion: Using computer modeling we showed that the midwall slowing in conduction velocity modified the QRS complex morphology. The QRS complex changes were consistent with ECG-LVH criteria, i.e. QRS patterns usually interpreted as the effect of left ventricular hypertrophy (the increased left ventricular mass). [ABSTRACT FROM AUTHOR]

Background and purpose Culprit coronary artery assessment in the triage ECG of patients with suspected acute coronary syndrome (ACS) is relevant a priori knowledge preceding percutaneous coronary intervention (PCI). We compared a model-based automated method (Olson method) with an expert-rule based method for the culprit artery assessment. Methods In each of the 53 patients who were admitted with the working diagnosis of suspected ACS, scheduled for emergent angiography with a view on revascularization as initial treatment and subsequently found to have an angiographically documented completely occluded culprit artery, culprit artery location was assessed in the preceding ECG by both the model-based Olson method and the expert-rule based method that considered either visual or computer-measured J-point amplitudes. ECG culprit artery estimations were compared with the angiographic culprit lesion locations. Proportions of correct classifications were compared by a Z test at the 5% significance level. Results The Olson method performed slightly, but not significantly, better, when the expert-rule based method used visual assessment of J-point amplitudes (88.7% versus 81.1% correct; P = 0.28). However, the Olson method performed significantly better when the expert-rule based method used computer-measured J-point amplitudes (88.7% versus 71.7% correct; P < 0.05). Conclusion The automated model-based Olson method performed at least at the level of expert cardiologists using a manual rule-based method. [ABSTRACT FROM AUTHOR]

Background Obstructive sleep apnea (OSA) has been reported to be associated with an increased risk of ventricular arrhythmias and conduction disturbances. The aim of this study was to analyze the QRS complex morphology potentially indicative of intraventricular conduction impairment in patients with mild to severe OSA. Material and methods One hundred ninety-three consecutive patients, who underwent complete overnight polysomnography, were divided into four groups based on the OSA severity: (1) no OSA, (2) mild OSA, (3) moderate OSA and (4) severe OSA (apnea-hypopnea index < 5, 5–15, 15–30, > 30/h, respectively). Resting 12-lead ECG was recorded, the QRS parameters included QRS amplitude in individual leads, QRS spatial vector magnitude (QRSmax), electrical axis (EA), ECG criteria for left ventricular hypertrophy (ECG-LVH) and right ventricular hypertrophy (ECG-RVH), and occurrence of fragmented QRS (fQRS). Results Severity of OSA was significantly associated with a gradual significant shift of the electrical axis to the left (45.5 ± 22.5°; 34.8 ± 17.1°; 32.9 ± 18.2°; 29.8 ± 10.0°; respectively), while the QRSmax values were low in all patient groups, with a significant difference between no OSA and severe OSA groups. The multivariate analysis showed that QRSmax was independently associated with age and the interaction between gender and OSA severity (p = 0.001, and p = 0.004, respectively; adjusted R 2 = 0.178). The electrical axis was found to be independently associated with age and OSA severity (p = 0.037, and p = 0.026, respectively; R 2 = 0.109). Changes of electrical axis and of QRSmax were reflected in corresponding changes in the amplitude of 12-lead ECG and in low occurrence of ECG-LVH and ECG-RVH criteria. The OSA groups had higher occurrence of fQRS. Conclusion OSA patients displayed a combination of changes in QRS complex morphology, the leftward shift of EA, low QRS voltage and fQRS, suggestive of depolarization sequence deterioration that might be indicative of considerable electrical remodeling. [ABSTRACT FROM AUTHOR]

Left ventricular hypertrophy (LVH) is defined as an increase in left ventricular mass (LVM) associated with structural changes of myocardium. The increase in LVM and associated changes are associated with changes in depolarization and repolarization, manifested as a variety of altered QRS and T patterns. Increased QRS voltage has been considered to be a specific ECG finding in LVH, and ECG criteria based on this increased QRS voltage are generally recommended. These ECG changes are also predictive of adverse cardiovascular outcomes. However, it must also be noted that the majority of patients with increased LVM do not have increased QRS voltage. While this is often considered a limitation of ECG in LVH diagnosis, the authors of this minireview consider it more likely that the electrical effects, represented in the altered ECG, and the increased LVM are independent effects, associated by virtue of their common relationship with an underlying pathologic state. This revised view challenges cardiologists and electrocardiologists to explore the interrelationships between electrical, biochemical, and mechanical alterations of myocardial remodeling seen with heart disease, to advance our understanding of this process and its effects, including the evolution of the ECG changes known as "LVH". [ABSTRACT FROM AUTHOR]

The classical paradigm of electrocardiographic diagnosis of left ventricular hypertrophy (LVH) is based on empirical finding of increased QRS voltage in cases of LVH and a continuous effort is devoted to finding ECG criteria that agree best with LVH classification according to an ECG-independent standard such as echocardiographic LVH (echo-LVH) based on increased left ventricular mass (LVM). Since there are more disagreements than agreements, this review is focused on discrepancies, i.e. false negative and false positive ECG findings. It summarizes the results of simulation studies on the effect of slowed conduction velocity and reduced intercellular coupling on the QRS pattern. The results from these simulation studies suggest that reduced myocardial conduction velocity which is either diffuse or regional, or reduced intracellular coupling, may account at least in part for the changes in the QRS patterns observed in patients with LVH. [ABSTRACT FROM AUTHOR]

Background Acute myocardial infarction creates regions of altered electrical properties of myocardium resulting in typical QRS patterns (pathological Q waves) and ST segment deviations observed in leads related to the MI location. The aim of this study was to present a graphical method for imaging the changes in the sequence of depolarization and the ST segment deviations in myocardial infarction using the Dipolar ElectroCARdioTOpography (DECARTO) method. Material and Methods Simulated ECG data corresponding to intramural, electrically inactive areas encircled by transmural areas with slowed impulse propagation velocity in anteroseptal and inferior locations were used for imaging the altered sequence of depolarization and the ST vector. The ECGs were transformed to areas projected on the image surface so as to image the process of ventricular depolarization based on the orientation and magnitude of the instantaneous QRS vectors, and the estimated "myocardium at risk" based on the ST segment deviation. Results The images are presented as Mercator projections with the texture of anatomical segments of the heart and the corresponding coronary artery distribution. The changes in depolarization sequence were visible as dislocations of activated areas circumventing the affected areas, while the "myocardium at risk" estimated from the ST segment deviation pointed to the affected area. Conclusion The presented method of imaging ECG allows visualizing changes in sequence of depolarization as well as the ST segment deviations in myocardial infarction and they can be visually compared with non-ECG imaging methods. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Reduction or interruption of the blood supply to myocardium due to occlusion of coronary artery and consequent ischemia leads to changes of electrogenesis: changes in morphology and duration of action potentials and slowing of conduction velocity in the affected area. In this study we simulated the effects of localized changes in depolarization sequence on the QRS and ST segment patterns, using computer modeling. Methods: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows changing the velocity of impulse propagation in the myocardium. An intramural electrically inactive area encircled by a transmural area with slowed impulse propagation velocity was introduced in anteroseptal and inferior locations. The effects on the QRS complex and the ST segment of the 12-lead electrocardiogram are presented. Results: The intramural electrically inactive area caused QRS changes typical for corresponding locations of a myocardial infarction observed in patients, which were further considerably modified by slowed impulse propagation velocity in the surrounding area. Additionally, areas of slowed impulse propagation velocity led to ST segment deviations in the “reciprocal” leads, shifting the ST segment towards the affected areas. Conclusion: Using computer modeling we showed that the localized alteration of impulse propagation not only modified the QRS complex, but produced also changes in the ST segment consistent with changes which are usually interpreted as the effect of “injury current”. [Copyright &y& Elsevier]

Abstract: An increased QRS voltage is considered to be specific for the electrocardiogram (ECG) diagnosis of left ventricular hypertrophy (LVH). However, the QRS-complex patterns in patients with LVH cover a broader spectrum: increased QRS voltage, prolonged QRS duration, left axis deviation, and left anterior fascicular block– and left bundle branch block–like patterns, as well as pseudo-normal QRS patterns. The classical interpretation of the QRS patterns in LVH relates these changes to increased left ventricular mass (LVM) per se, while tending to neglect the modified active and passive electrical properties of the myocardium. However, it has been well documented that both active and passive electrical properties in LVH are altered. Using computer simulations, we have shown that an increased LVM is not the only determinant of QRS complex changes in LVH, as these changes could also be produced without changing the left ventricular mass, implying that these QRS patterns can be present in patients before their LVM exceeds the arbitrary upper normal limits. Our results link the experimental evidence on electrical remodeling with clinical interpretation of ECG changes in patients with LVH and stress the necessity of a complex interpretation of the QRS patterns considering both spatial and nonspatial determinants in terms of the spatial angle theory. We assume that hypertrophic electrical remodeling in combination with changes in left ventricular size and shape explains the variety of ECG patterns as well as the discrepancies between ECG and left ventricular mass. [Copyright &y& Elsevier]

Abstract: Although electrocardiography has been used to estimate left ventricular hypertrophy and to obtain useful prognostic information in different clinical settings, its correlation with left ventricular mass is poor and, therefore, its sensitivity and specificity for the diagnosis of left ventricylar hypertrophy are low. Experimental work has demonstrated that the increase in voltage and duration of the QRS complex of the electrocardiogram are not only related to left ventricular mass but also to changes in the electrophysiological properties of the myocardium. Therefore, a new strategy is needed to use electrocardiography not to estimate left ventricular mass but aimed to add useful prognostic information. [Copyright &y& Elsevier]

Abstract: Objective: This study was undertaken to evaluate the nature and onset of changes in the QRS complex in the offspring of patients with diabetes mellitus (DM) and metabolic syndrome (MetS). Methods and Methods: A total of 529 subjects, divided into 5 groups, were included in the study: (i) group DM (n = 92), patients with DM; (ii) group MetS (n = 125), patients with MetS; (iii) group O-DM (n = 109), offspring of patients with DM; (iv) group O-MetS (n = 122), offspring of patients with MetS; and (v) group HO (n = 81), offspring of healthy subjects. QRS parameters analyzed included amplitude, maximum QRS spatial vector magnitude, electrical axis (EA), and 3 electrocardiogram (ECG) criteria for left ventricular hypertrophy based on amplitude criteria: Sokolow-Lyon index, Cornell voltage, and Gubner criterion. Results: Patients with DM and MetS showed a significant leftward shift of the EA when compared with the control group. A modest but significant leftward shift of EA was also observed in both offspring groups. These EA and maximum QRS spatial vector magnitude changes were reflected in the individual leads of the 12-lead ECG. The prevalence of a positive diagnosis by accepted electrocardiographic criteria (ECG left ventricular hypertrophy) was low. Conclusion: Patients with DM and MetS displayed significant changes in QRS complex that suggest depolarization sequence deterioration. Similar changes were observed also in the offspring of patients with DM and MetS, which suggests early subclinical cardiovascular damage. These findings have implications for prevention, early diagnosis, and treatment in the offspring of patients with DM and MetS. [Copyright &y& Elsevier]

Abstract: By definition, the electrocardiographic (ECG) patterns of left bundle-branch block (LBBB) represent distinctive changes in duration and shape of the QRS complex caused by intraventricular conduction delay in the left ventricle (LV) due to structural abnormalities in the His-Purkinje conduction system and/or ventricular myocardium. However, impaired conduction in the working myocardium is not taken into consideration in the practical ECG diagnosis. Because the degree of LV myocardium impairment could be of importance for clinical evaluation of patients, we studied the effects of blocked and of delayed onsets of activation in the LV to simulate complete and incomplete LBBBs and slowed conduction in the LV myocardium by applying an analytical computer model. We demonstrated that typical LBBB patterns were caused both by block or delay in the onset of the LV activation, as well as by impaired conduction in the myocardium itself while maintaining the location and onset of the LV activation. The most important difference was the absence of initial anteriorly oriented electrical forces in cases of the simulated complete LBBB and of incomplete LBBB if the onset of LV activation was delayed (≥6 milliseconds). Under the conditions defined in this model that did not consider myocardial infarction, the presence of initial anteriorly oriented electrical forces was indicative of preserved conduction in the left bundle and of impaired conduction in LV working myocardium. Conclusion: The elucidation of the participation of working myocardium impairment in the intraventricular conduction delay in the LV could be of vital significance for the clinical management of patients with LBBB patterns, for example, indicated for resynchronization therapy. [Copyright &y& Elsevier]

Abstract: Background: The electrocardiographic (ECG) diagnosis of left ventricular hypertrophy (LVH) is based on the assumption that QRS voltage increases with left ventricular mass. However, most of patients with echocardiographically detected LVH do not have increased QRS voltage. Reduced intercellular coupling has been observed in LVH patients and animal models. The purpose of this study was to show that this uncoupling can explain relatively low QRS voltage in LVH patients. Methods: Electrocardiograms and vectorcardiograms (VCG) were simulated with a realistic large-scale computer model of the human heart and torso that reliably represented the effects of reduced coupling on both propagation and ECG voltage. Results: 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. Conclusions: Low QRS voltage does not necessarily contradict a diagnosis of LVH but may be an indication for electrical uncoupling. The diagnostic value of this “relative voltage deficit” needs to be demonstrated in clinical studies. [Copyright &y& Elsevier]

Abstract: The contributions of reduced conduction velocity (CV) and prolonged action potential duration (APD) to QT interval prolongation and T wave and T vector loop morphology in left ventricular hypertrophy (LVH) were studied using an analytical computer model. Three types of anatomic LVH were simulated: concentric and eccentric hypertrophy, and left ventricular dilatation. In each LVH type, depolarization changes were simulated by CV slowing and primary repolarization changes by APD prolongation. Both CV slowing and APD prolongation prolonged the QT interval; however, the secondary and primary repolarization changes differed in additional electrocardiogram (ECG) characteristics creating specific vectorcardiographic/ECG patterns. The secondary repolarization changes were characterized by prolonged QT interval, accompanied by pronounced QRS changes, including increased maximum spatial QRS vector magnitude, prolonged QRS duration, QRS morphology consistent with intraventricular conduction delay, lower values of the T/QRS duration ratio, increased maximum spatial T vector magnitude, narrow and prolonged discordant T vector loops, and discordant tall T waves creating a pattern of ST strain in the precordial ECG leads. QT prolongation in primary repolarization changes was accompanied with inconsiderable changes of QRS amplitude and duration, higher values of the T/QRS duration ratio, widened rounded T loops, and notched or bifid T waves in left precordial leads of the 12-lead ECG. These simulation data are consistent with the accumulated evidence suggesting that LVH induces changes in CV and APD. Our results emphasize the need for simultaneous consideration of morphologic QRS and T wave patterns together with QT prolongation in clinical evaluation of LVH. [Copyright &y& Elsevier]

Abstract: The increased QRS voltage is considered to be a specific electrocardiogram (ECG) sign of left ventricular hypertrophy (LVH), and it is expected that the QRS voltage reflects the increase in left ventricular mass (LVM). However, the increased QRS voltage is only one of QRS patterns observed in patients with LVH. According to the solid angle theory, the resultant QRS voltage is influenced not only by spatial (anatomic) but also by nonspatial (electrophysiologic) determinants. In this study, we used a computer model to evaluate the effect of changes in anatomy and conduction velocity of the left ventricle on QRS complex characteristics. Material and Methods: The model defines the geometry of cardiac ventricles analytically as parts of ellipsoids and allows to change dimensions of the ventricles, as well as the conduction velocity in the individual layers of myocardium. Three types of anatomic changes were simulated: concentric hypertrophy, eccentric hypertrophy, and dilatation. The conduction velocity was slowed in the inner layer of the left ventricle representing the Purkinje fiber mesh and in the layers representing the working myocardium. The outcomes of the model are presented as the time course of the spatial QRS vector magnitude, the vectorcardiographic QRS loops (VCGs) in horizontal, left sagittal, and frontal planes, as well as derived 12-lead ECGs. The following indicators of the 12-lead ECG were evaluated: the left axis deviation, the intrinsicoid deflection in V6, Cornell voltage, Cornell voltage-duration product, and Sokolow-Lyon index. Results: The increase in LVM did not affect the QRS voltage proportionally, and the LVM and type of hypertrophy were not the only determinants of the QRS patterns. The conduction velocity slowing resulted in a spectrum of QRS patterns including increased QRS voltage and duration, left axis deviation, prolonged intrinsicoid deflection, VCG patterns of left bundle branch block, as well as pseudo-normal VCG/ECG patterns. The anatomic changes and conduction velocity slowing affected differently Sokolow-Lyon index and Cornell criteria. Conclusion: We showed that the LVM is not the only determinant of the QRS complex changes in LVH, but it is rather a combination of anatomic and electric remodeling that creates the whole spectrum of the QRS complex changes seen in LVH patients. The slowed conduction velocity in the model heart produced QRS patterns consistent with changes described in LVH, even if the LVM was not changed. [Copyright &y& Elsevier]

Identification of the QRS-complex duration in acute myocardial infarction (MI) is of great importance, having diagnostic, therapeutic and prognostic consequences. In acute MI with ST-segment deviation, the terminal part of QRS complex is distorted, without a clear demarcation between QRS and ST segment, making the identification of the QRS-complex offset problematic. Almer et al. [2016] propose a method that shifts the offset of the QRS complex deep into the ST segment. This method is in agreement with computer simulations showing the overlapping of depolarization and repolarization, as a possible additional factor resulting in the ST-segment deviation. [ABSTRACT FROM AUTHOR]

Abstract: The problem of discrepancies between left ventricular mass (LVM) and electrocardiography (ECG) findings in diagnosis of left ventricular hypertrophy (LVH) is approached from the perspective of the diagnostic ability of ECG. Contrary to current clinical understanding of LVH as an increase in LVM, the LVH is defined as the organ manifestation of the hypertrophic growth of cardiomyocytes accompanied by changes in interstitium. This complex understanding of the hypertrophic rebuilding of LV myocardium in LVH is the crucial requirement to understand the role of ECG in LVH diagnosis. The basic statements of the article are based on the fact that ECG provides information on the electrical field generated by the heart; therefore, [•] ECG cannot be a surrogate method for the LVM estimation by its nature. The hypothesis that the ECG estimates LVM requires modification for the additional effects of myocardial tissue changes and conduction on the ECG. [•] The added value of ECG in LVH diagnosis is given by its ability to register the electrical field of the heart and thus to estimate the electrical status of the myocardium. [Copyright &y& Elsevier]

Abstract: 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. [Copyright &y& Elsevier]

Abstract: A graphic method was developed for presentation of the location and extent of the myocardium at risk in patients with acute myocardial infarction (AMI). This method is based on a mathematical processing of ST-segment deviations of standard 12-lead electrocardiogram following the concept of Titomir and Ruttkay-Nedecky in their dipolar electrocardiotopographic method. The center of the location of the area at risk is given by the spatial orientation of the resultant spatial ST vector, and the extent of the area at risk is derived from the Aldrich score. The areas at risk are projected on a spherical image surface, on which a texture of the anatomical quadrants of the ventricular surface and its coronary artery supply are projected. The method was tested in 10 patients with AMI with single-vessel disease, including 6 patients with an occlusion in the proximal left anterior descending coronary artery (LAD), 3 patients with an occlusion in the right coronary artery, and one patient with occlusion in the left circumflex coronary artery. The estimated areas at risk were compared with myocardial perfusion single photon emission computed tomography. Eight (80%) patients of 10 were correctly localized according to the Aldrich decision rules for the location of AMI. The areas at risk in patients with LAD occlusion correctly localized by the Aldrich score were situated in the anteroseptal and anterosuperior quadrants. In the inferior AMI group, the area at risk was localized in the posterolateral and inferior quadrants. The visual comparison with myocardial perfusion single photon emission computed tomography (SPECT) showed best agreement in patients with LAD involvement. The initial testing showed that this method allows a graphic presentation of estimated area at risk using clinically defined diagnostic rules. The area at risk can be displayed in images that are familiar for clinicians and can be compared with or superimposed on results of other imaging methods used in cardiology. [Copyright &y& Elsevier]

Abstract: Background and Purpose: On the basis of our previous results of animal and human studies, we assume that the discrepancies between increased left ventricular mass (LVM) and electrocardiographic (ECG) findings not exceeding the upper normal limits in left ventricular hypertrophy (LVH) are conditioned by the electrical remodeling of hypertrophied myocardium. We assumed that these discrepancies observed in the early stage of LVH in spontaneously hypertensive rats (SHR) are associated with a decreased expression of connexin 43. Methods: Standard 12-lead ECG was recorded in 20-week-old male SHR and age-matched and sex-matched normotensive Wistar rats (Institute of Experimental Pharmacology SAV, Dobra Voda, Slovakia). The approximated maximum QRS spatial vector magnitude (QRSmax) was calculated from leads V2, aVF, and V5. Left ventricular mass was weighed, and the specific potential (SP) of myocardium was calculated as the QRSmax-to-LVM ratio. Left ventricular protein levels of connexin 43 were analyzed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting. Results: The LVM values were significantly higher in SHR than in normotensive controls (0.96 ± 0.03 g and 0.680 ± 0.07 g, respectively; P < .001). The QRSmax values in SHR did not follow the increase either in systolic blood pressure or in LVM. The SP values in SHR were significantly lower than those in control rats (0.92 ± 0.11 mV/g and 1.358 ± 0.06 mV/g, respectively; P < .01). A 37% decrease in connexin 43 level was observed in SHR. Conclusions: The QRS voltage did not follow the increase in the LVM in 20-week-old SHR, and the values of connexin 43 were lower in SHR than in normotensive controls. We believe that the discrepant findings between ECG voltage and LVM can be caused by the electrical remodeling in the early stages of LVH. [Copyright &y& Elsevier]

Abstract: The aim of this study was to evaluate the understanding of the term central terminal (CT) and to consider the consequences of this level of understanding. A total of 150 questionnaires was distributed during the 30th International Congress of Electrocardiology 2003, Helsinki, Finland; 42 (28%) of the anonymous questionnaires returned were considered adequate for the purpose of this study. The questionnaire addressed the following areas of interest: (1) the location of the CT; (2) the location of the negative poles of unipolar leads; (3) the naming of the electrocardiogram lead groups; (4) the relationship between the leads and cardiac electrical views; and (5) impact on accuracy of clinical diagnosis. The findings revealed diversity in understanding the basic term, a shift in understanding the term CT to abstract/theoretical understanding, and gaps in understanding the concept of CT and the more recent theories of the cardiac electric field. [Copyright &y& Elsevier]

• The terms "fascicular and/ or bundle branch blocks" imply conduction alteration in the His-Purkinje system. • These QRS patterns are in majority cases associated with altered structure of ventricular working myocardium. • The altered structure of working myocardium can cause alterations in electrical impulse propagation itself. [ABSTRACT FROM AUTHOR]

Abstract: The Working Group on Electrocardiographic Diagnosis of Left Ventricular Hypertrophy, appointed by the Editor of the Journal of Electrocardiology, presents the alternative conceptual model for the ECG diagnosis of left ventricular hypertrophy (LVH). It is stressed that ECG is a record of electrical events, not of mechanical events and/ or anatomical characteristics. Considering the electrical characteristics of pathologically changed myocardium should lead to better understanding and improved clinical usefulness of the ECH in the clinical diagnosis of LVH. [Copyright &y& Elsevier]