Ljuba Bacharova

Effect of changes in left ventricular anatomy and conduction velocity on the QRS voltage and morphology in left ventricular hypertrophy: a model study

UNLABELLED 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.

Electrocardiographic patterns of left bundle-branch block caused by intraventricular conduction impairment in working myocardium: a model study.

UNLABELLED 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.

Electrical and Structural Remodeling in Left Ventricular Hypertrophy—A Substrate for a Decrease in QRS Voltage?

Electrical remodeling in advanced stages of cardiovascular diseases creates a substrate for triggering and maintenance of arrhythmias. The electrical remodeling is a continuous process initiated already in the early stages of cardiological pathology. The aim of this opinion article was to discuss the changes in electrical properties of myocardium in left ventricular hypertrophy (LVH), with special focus on its early stage, as well as their possible reflection in the QRS amplitude of the electrocardiogram. It critically appraises the classical hypothesis related to the QRS voltage changes in LVH. The hypothesis of the relative voltage deficit is discussed in the context of supporting evidence from clinical studies, animal experiments, and simulation studies. The underlying determinants of electrical impulse propagation which may explain discrepancies between “normal” ECG findings and increased left ventricular size/mass in LVH are reviewed.

Electrocardiography-left ventricular mass discrepancies in left ventricular hypertrophy: electrocardiography imperfection or beyond perfection?

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, (1) 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. (2) 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.

The Dipolar ElectroCARdioTOpographic (DECARTO)-like method for graphic presentation of location and extent of area at risk estimated from ST-segment deviations in patients with acute myocardial infarction

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.

Similarities and differences between electrocardiogram signs of left bundle-branch block and left-ventricular uncoupling

AIMS A left bundle-branch block (LBBB) electrocardiogram (ECG) type may be caused by either a block in the left branch of the ventricular conduction system or by uncoupling in the working myocardium. We used a realistic large-scale computer model to evaluate the effects of uncoupling with and without left-sided block and in combination with biventricular pacing. METHODS AND RESULTS Action potential propagation was simulated using a reaction-diffusion model of the human ventricles. Electrocardiograms and cardiac electrograms were computed from the simulated action potentials by solving the bidomain equations. In all situations, diffuse uncoupling reduced QRS amplitude, prolonged QRS duration, and rotated the QRS axis leftward. Uncoupling by 50% increased QRS duration from 90 to 120 ms with a normal conduction system and from 140 to 190 ms when the left bundle branch was blocked. Biventricular pacing did not change QRS duration but reduced total ventricular activation time. CONCLUSION Uncoupling in the working myocardium can mimic left-sided block in the ventricular conduction system and can explain an LBBB ECG pattern with relatively low amplitude. Biventricular pacing improves ventricular activation in true LBBB with or without uncoupling but not in case of 50% uncoupling alone.

Discrepancy between increased left ventricular mass and “normal” QRS voltage is associated with decreased connexin 43 expression in early stage of left ventricular hypertrophy in spontaneously hypertensive rats

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 V(2), aVF, and V(5). 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.

Relation between QRS amplitude and left ventricular mass in the initial stage of exercise-induced left ventricular hypertrophy in rats.

The aim of the study was to analyze the relationship between QRS amplitude and left ventricular mass (LVM) in early stages of two different experimental models of left ventricular hypertrophy (LVH) in rats: in exercise-induced hypertrophy and pathological hypertrophy due to genetically conditioned pressure overload. Three groups of experimental animals were studied: healthy control Wistar-Kyoto rats (WKYs), spontaneously hypertensive rats (SHRs), and WKY rats exposed to training by intermittent swimming (SWIM). Orthogonal electrocardiograms were recorded in each group at the age of 12 and 20 weeks, and the maximum spatial QRS vector (QRSmax) was calculated. Then the animals were sacrificed and LVM was measured. The specific potential of myocardium (SP) was calculated as a ratio of QRSmax to LVM. The QRSmax values did not follow the changes in LVM. At the end of the follow-up period, the highest values of QRSmax were recorded in the control WKY rats (0.80 ± 0.05 mV). The QRSmax values in both groups with experimental LVH were significantly lower as compared with control animals (SHR 0.44 ± 0.02 mV, p < 0.001; SWIM 0.53 ± 0.04 mV, p < 0.001). Similarly, the SP values were significantly lower in both groups with experimental LVH as compared with control animals (SHR 0.42 ± 0.02 mV/g, p < 0.001; SWIM 0.55 ± 0.05 mV/g, p < 0.001). A decrease in QRSmax and SP was observed in both models of experimental LVH. We attributed these findings to the changes in electrogenetic properties of myocardium in the early stage of developing LVH. In other words, it is changes of nonspatial determinants that influence the resultant QRS voltage in terms of the solid angle theory.

The Role of ECG in the Diagnosis of Left Ventricular Hypertrophy

The traditional approach to the ECG diagnosis of left ventricular hypertrophy (LVH) is focused on the best estimation of left ventricular mass (LVM) i.e. finding ECG criteria that agree with LVM as detected by imaging. However, it has been consistently reported that the magnitude of agreement is rather low as reflected in the low sensitivity of ECG criteria. As a result, the majority of cases with true anatomical LVH could be misclassified by using ECG criteria of LVH. Despite this limitation, it has been reported that the ECG criteria for LVH provide independent information on the cardiovascular risk even after adjusting for LVM. Understanding possible reasons for the frequent discrepancy between common ECG LVH criteria and LVH by echo or MRI would help understanding the genesis of ECG changes that occur as a consequence of increased LV mass.

Alterations in the QRS complex in the offspring of patients with metabolic syndrome and diabetes mellitus: early evidence of cardiovascular pathology

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.