ISE/ISHNE expert consensus statement on the ECG diagnosis of left ventricular hypertrophy: The change of the paradigm.

The ECG diagnosis of LVH is predominantly based on the QRS voltage criteria. The classical paradigm postulates that the increased left ventricular mass generates a stronger electrical field, increasing the leftward and posterior QRS forces, reflected in the augmented QRS amplitude. However, the low sensitivity of voltage criteria has been repeatedly documented. We discuss possible reasons for this shortcoming and proposal of a new paradigm. The theoretical background for voltage measured at the body surface is defined by the solid angle theorem, which relates the measured voltage to spatial and non-spatial determinants. The spatial determinants are represented by the extent of the activation front and the distance of the recording electrodes. The non-spatial determinants comprise electrical characteristics of the myocardium, which are comparatively neglected in the interpretation of the QRS patterns. Various clinical conditions are associated with LVH. These conditions produce considerable diversity of electrical properties alterations thereby modifying the resultant QRS patterns. The spectrum of QRS patterns observed in LVH patients is quite broad, including also left axis deviation, left anterior fascicular block, incomplete and complete left bundle branch blocks, Q waves, and fragmented QRS. Importantly, the QRS complex can be within normal limits. The new paradigm stresses the electrophysiological background in interpreting QRS changes, i.e., the effect of the non-spatial determinants. This postulates that the role of ECG is not to estimate LV size in LVH, but to understand and decode the underlying electrical processes, which are crucial in relation to cardiovascular risk assessment.

New electrocardiographic aspects of the P wave: Its value in clinical cardiology.

In this article, we will comment on new aspects of P-wave morphology that help us to better diagnose atrial blocks and atrial enlargement, and their clinical implications. These include: (1) Atypical ECG patterns of advanced interatrial block; (2) The ECG diagnosis of left atrial enlargement versus interatrial block; (3) Atrial fibrillation and advanced interatrial block: The two sides of the same coin; and (4) P-wave parameters: Clinical implications.

ISE/ISHNE Expert Consensus Statement on ECG Diagnosis of Left Ventricular Hypertrophy: The Change of the Paradigm. The joint paper of the International Society of Electrocardiology and the International Society for Holter Monitoring and Noninvasive Electrocardiology.

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.

Left Ventricular Hypertrophy and Ventricular Tachyarrhythmia: The Role of Biomarkers.

Left ventricular hypertrophy (LVH) refers to a complex rebuilding of the left ventricle that can gradually lead to serious complications-heart failure and life-threatening ventricular arrhythmias. LVH is defined as an increase in the size of the left ventricle (i.e., anatomically), therefore the basic diagnosis detecting the increase in the LV size is the domain of imaging methods such as echocardiography and cardiac magnetic resonance. However, to evaluate the functional status indicating the gradual deterioration of the left ventricular myocardium, additional methods are available approaching the complex process of hypertrophic remodeling. The novel molecular and genetic biomarkers provide insights on the underlying processes, representing a potential basis for targeted therapy. This review summarizes the spectrum of the main biomarkers employed in the LVH valuation.

ECG in left ventricular hypertrophy: A change in paradigm from assessing left ventricular mass to its electrophysiological properties.

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.

A counterpoint paper: Comments on the electrocardiographic part of the 2018 Fourth Universal Definition of Myocardial Infarction endorsed by the International Society of Electrocardiology and the International Society for Holter and Noninvasive Electrocardiology.

The Fourth Universal Definition of Myocardial Infarction (FUDMI) focuses on the distinction between nonischemic 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 (a) detecting acute ischemia, (b) triage, and (c) 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.

A counterpoint paper: Comments on the electrocardiographic part of the 2018 Fourth Universal Definition of Myocardial Infarction.

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.

Molecular Mechanisms, Diagnostic Aspects and Therapeutic Opportunities of Micro Ribonucleic Acids in Atrial Fibrillation.

Micro ribonucleic acids (miRNAs) are short non-coding RNA molecules responsible for regulation of gene expression. They are involved in many pathophysiological processes of a wide spectrum of diseases. Recent studies showed their involvement in atrial fibrillation. They seem to become potential screening biomarkers for atrial fibrillation and even treatment targets for this arrhythmia. The aim of this review article was to summarize the latest knowledge about miRNA and their molecular relation to the pathophysiology, diagnosis and treatment of atrial fibrillation.

Differences in the Selvester QRS score after primary PCI strategy and conservative treatment for STEMI patients with negative T waves.

BACKGROUND: According to current guidelines, the main indications for PCI in patients with STEMI are ST-segment deviations and defined time from the onset of symptoms. Negative T wave at admission can be a sign of prolonged ischemia or spontaneous reperfusion. In both situations, the urgent intervention is questionable. We evaluated the infarct size and in-hospital mortality in STEMI patients with negative T wave in cases of primary PCI strategy compared with conservative treatment. METHODS: A retrospective analysis of 116 STEMI patients with negative T wave at the presenting ECG was performed. Sixty-eight patients (59%) underwent primary PCI strategy (PCI group), and 48 (41%) were treated conservatively (non-PCI group). The infarct size estimated by using the Selvester score, and in-hospital mortality were evaluated. RESULTS: The difference between Selvester score values at admission and at discharge in the non-PCI group was statistically significant (1.48; 95% CI 0.694-2.27), while no significant difference was observed in the PCI group (-0.07; 95% CI -0.546-0.686). The in-hospital mortality was higher in the non-PCI group; however, the numbers were relatively small: PCI 2 (2.9%) and non-PCI 5 (10.4%). CONCLUSION: In this study, we showed a reduction in the infarct size estimated by Selvester score in STEMI patients with negative T wave who were treated conservatively, while there was no significant change in the infarct size after primary PCI strategy. The higher mortality in patients treated conservatively could be attributed to higher age and comorbidities in the non-PCI group. It seems that conservative treatment strategy might be an option in STEMI patients with negative T wave.

Missing Link between Molecular Aspects of Ventricular Arrhythmias and QRS Complex Morphology in Left Ventricular Hypertrophy.

The aim of this opinion paper is to point out the knowledge gap between evidence on the molecular level and clinical diagnostic possibilities in left ventricular hypertrophy (LVH) regarding the prediction of ventricular arrhythmias and monitoring the effect of therapy. LVH is defined as an increase in left ventricular size and is associated with increased occurrence of ventricular arrhythmia. Hypertrophic rebuilding of myocardium comprises interrelated processes on molecular, subcellular, cellular, tissue, and organ levels affecting electrogenesis, creating a substrate for triggering and maintaining arrhythmias. The knowledge of these processes serves as a basis for developing targeted therapy to prevent and treat arrhythmias. In the clinical practice, the method for recording electrical phenomena of the heart is electrocardiography. The recognized clinical electrocardiogram (ECG) predictors of ventricular arrhythmias are related to alterations in electrical impulse propagation, such as QRS complex duration, QT interval, early repolarization, late potentials, and fragmented QRS, and they are not specific for LVH. However, the simulation studies have shown that the QRS complex patterns documented in patients with LVH are also conditioned remarkably by the alterations in impulse propagation. These QRS complex patterns in LVH could be potentially recognized for predicting ventricular arrhythmia and for monitoring the effect of therapy.

A different effect of obesity on ECG in premenopausal and postmenopausal women.

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 ±â€¯0.4 mV, 1.17 ±â€¯0.35 mV, 1.4 ±â€¯0.46 mV, and 1.35 ±â€¯0.39 mV, resp.). (EA: 56.4 ±â€¯18.0°, 38.22 ±â€¯18.38°, 45.82 ±â€¯18.63°, and 36.75 ±â€¯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.

Left Ventricular Hypertrophy by the Surface ECG.

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".

Galen Wagner, M.D., Ph.D. (1939-2016) as international mentor of young investigators in electrocardiology.

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.

The 4th Report of the Working Group on ECG diagnosis of Left Ventricular Hypertrophy.

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.

The identification of the QRS complex offset in the presence of ST segment deviation.

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.

Modeling and visualization of the activation wavefront propagation to improve understanding the QRS complex changes indicating left ventricular hypertrophy.

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.

QRS complex waveform indicators of ventricular activation slowing: Simulation studies.

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.

The effect of conduction velocity slowing in left ventricular midwall on the QRS complex morphology: A simulation study.

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).