Electrical remodeling in left ventricular hypertrophy—is there a unifying hypothesis for the variety of electrocardiographic criteria for the diagnosis of left ventricular hypertrophy?

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.     

The initial stage of left ventricular hypertrophy in spontaneously hypertensive rats is manifested by a decrease in the QRS amplitude/left ventricular mass ratio

In this study we tested the hypothesis of the relative voltage deficit, i.e. the discrepancy between increased left ventricular mass (LVM) and QRS amplitudes, in an experimental model of spontaneously hypertensive rats (SHR) during the period of a moderate increase in blood pressure. To address this issue we recorded orthogonal electrocardiograms of male SHR at the age of 12 and 20 weeks. During this period the systolic blood pressure (sBP) increased from 165 +/- 3 mmHg to 195 +/- 1 mmHg (p < 0.001). Age and sex matched WKY rats were used as control groups. The sBP values in WKY normotensive control groups were within normal limits (122 +/- 8 mmHg and 130 +/- 4mmHg, respectively). The maximum QRS spatial vector magnitude (QRSmax) was calculated from X, Y, Z amplitudes of the orthogonal electrocardiograms. The animals were sacrificed and the left ventricular mass was weight. The specific potential of myocardium (SP) was calculated as a ratio of QRSmax to LVM. The LVM in SHR (0.86 +/- 0.05 g and 1.05 +/- 0.07 g, respectively) was significantly higher as compared to WKY (0.65 +/- 0.07 g and 0.70 +/- 0.02 g), and the increase of LVM closely correlated with the sBP increase. On the other hand, QRSmax in SHR did not follow either the increase of sBP, or LVM. The QRSmax values in SHR did not differ from those of WKY at the age of 12 weeks (0.59 +/- 0.14 mV compared to 0.46 +/- 0.05 mV), and they were even lower in SHR at the age of 20 weeks (0.74 +/- 0.08 mV compared to 0.44 +/- 0.05 mV, p < 0.001). The values of SP, quantifying the relative voltage deficit, were significantly lower in SHR as compared to the WKY control. The values decreased significantly in SHR with increasing age, sBP and LVM, i.e., with the progression of hypertrophic remodeling of the left ventricle. The results of this study support the hypothesis of the relative voltage deficit in LVH. These results are consistent with the finding of a high number of false negative ECG results in clinical ECG diagnostics of LVH, and could contribute to an understanding of the diagnostic importance of the false negative ECG results, their re-evaluation and utilization for clinical diagnosis and prognosis.     

Electrocardiographic diagnosis of left ventricular hypertrophy: is the method obsolete or should the hypothesis be reconsidered?

The current ECG diagnosis of LVH is based on QRS voltage criteria and aims to estimate left ventricular mass. Its underlying hypothesis includes unstated assumptions about the non-spatial determinants of QRS voltage;that the electrical properties of hypertrophied myocardium do not differ from those healthy myocardium, and that they are not changed in the course of developing LVH. Since these two assumptions are not true, the performance of the voltage criteria is limited and is reflected in the high number of so-called false negative ECG results, as well as their low sensitivity. The reconsidered hypothesis is based on a more complex understanding of LVH and on the analysis of information provided by electrocardiography. It considers false negative results for LVH diagnosis as a relative voltage deficit, and introduces a new parameter for its quantification: the specific potential (the relative QRS voltage).The relative voltage deficit is related to changes of active and passive electrical properties (electrophysiological remodelling) of the hypertrophied myocardium. This new hypothesis also takes into account changes of the relative QRS voltage in different stages of LVH. The potential of this concept is its usefulness as a parameter in the frame of diagnostics of LVH, of diffuse changes of myocardium, in cardiovascular risk assessment, and well as for evaluation of the effects of therapy.     

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.     

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,

• 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.