The Old Habits Need to be Abandoned and the Term “Overload” Replaced by “High Amplitude Criteria”

Left ventricular overload?

Brazilian electrocardiograms (ECG) reports have long labeled voltage-positive tracings as “left ventricular overload,” a legacy of historical teaching that linked hemodynamic loads to characteristic repolarization patterns. The problem is not the physiology but the nomenclature: overload is a hemodynamic claim, whereas the ECG measures electrical phenomena. Contemporary evidence reframes voltage positivity as an electrical phenotype with variable correlation to left ventricular mass (LVM) and geometry. In this article, we argue that Brazil should retire “overload,” adopt “high-amplitude criteria” as the report label, and explicitly teach the underlying concept of left ventricular electrical remodeling (LVER), so that our language matches what the ECG actually measures.

Phrasing “left ventricular overload” feels pragmatic — if surface ECG is “insensitive” to anatomic hypertrophy, perhaps what it detects is something else, namely “overload.” The evidence base argues otherwise. Electrocardiography records electric fields at the body surface; it does not directly measure mass, geometry, or loading conditions. This distinction is the core of the modern paradigm articulated by Ljuba Bacharova et al.: QRS voltage and morphology reflect an interplay of spatial determinants (source geometry, torso conductivity, electrode distance) and non-spatial determinants (conduction velocity, intercellular coupling, fibrosis, ionic remodeling), such that the same LVM can yield different voltages — and high voltage can arise with normal mass — depending on the myocardium’s electrical properties. The Working Group’s “4^th Report” in the Journal of Electrocardiology integrates mechanistic simulation studies with population data and draws three conclusions that are decisive for our terminology. First, increased LVM and geometric type (concentric, eccentric, dilation) are not the main or only determinants of QRS patterns; combinations of anatomy and slowed activation propagation produce the observed spectrum from “pseudo-normal” tracings through high voltage and prolonged intrinsicoid deflection to left bundle branch block. Second, diffuse conduction slowing or midwall conduction abnormalities — without any increase in mass — can generate QRS changes that meet conventional electrocardiographic-left ventricular hypertrophy (LVH) criteria in a normal-sized ventricle. Third, in community cohorts the electrical and anatomic phenotypes frequently diverge, and each carries independent prognostic information.

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