Left ventricular hypertrophy on the ECG has always been an area of clinical frustration. Despite decades of use, the electrocardiographic criteria often have a sensitivity below 50% for detecting a true increase in left ventricular mass.
Traditionally, we attribute this limitation to a “weakness” of the method. But perhaps the question is poorly framed. The ECG does not measure mass. It records differences in electrical potential at the body surface. And that depends on more than the myocardium.
A recent study using cardiac magnetic resonance (CMR) added an important piece to this puzzle: the distance between the left ventricle and the chest wall can influence QRS voltage as much as, or even more than, ventricular mass itself.
The physics behind QRS voltage
Since Wilson's classic work, we have known that the magnitude of the electrical potential recorded at the surface depends, among other factors, on the distance between the electrical source and the electrode. Put simply:
- The greater the mass → the greater the dipole moment
- The greater the distance (r) → the lower the recorded voltage (inverse-square relationship with distance)
In other words, the ECG measures an electrical field that passes through tissues with different conduction properties.
This means that two patients with the same ventricular mass may show completely different voltages if the distance between the left ventricle and the chest wall differs.
What CMR revealed
In the study published in the Journal of Electrocardiology in 2025, Lundström and colleagues evaluated 49 healthy individuals (including athletes) with a normal median BMI, using CMR as the anatomical reference standard.
Three main variables were analyzed:
- Left ventricular mass (LVM)
- Chest wall–left ventricle distance (CWLV)
- Thoracic subcutaneous adipose tissue area (SAT)
The distance measured in the apical two-chamber view (CWLV2CH) showed excellent reproducibility (ICC = 0.995).
The central finding was straightforward:
- CWLV was the strongest predictor of Sokolow-Lyon voltage
- The association remained significant even after adjustment for LVM
- The CWLV + LVM model explained 53% of the variability in voltage (adjusted R² = 0.53)
In other words, the distance to the heart was an independent determinant of QRS amplitude.
The role of subcutaneous fat
Even in a non-obese population, the thoracic subcutaneous fat area was negatively correlated with QRS amplitudes.
This point is particularly interesting.
We tend to associate low voltage with advanced obesity. However, the study shows that even physiological variations in the amount of adipose tissue are enough to attenuate voltage.
From an electrical standpoint, fat acts as:
- A distance factor (increases r)
- A possible modulator of conductivity
Although the conductive effect was not statistically dominant, the geometric component appears relevant even in individuals with a normal BMI.
Differences between men and women
One of the most thought-provoking findings was seen in women.
For the classic ECG criteria for left ventricular hypertrophy, especially the Sokolow-Lyon index, ventricular mass showed no significant correlation with voltage.
On the other hand, the distance to the heart and subcutaneous fat showed a consistent negative association.
This helps explain why voltage criteria perform worse in women. Part of the limitation may be anatomical rather than electrophysiological.
Practical clinical implications
Some scenarios become easier to understand in light of these data:
- A patient with clinically suspected LVH and a "normal" ECG
- Athletes with large ventricular mass but voltage below the cutoff
- Women with persistently negative criteria despite documented remodeling
The ECG is not necessarily “wrong”. It is recording an electrical field modulated by distance and interposed tissue.
This does not invalidate the classic criteria, but it calls for caution in interpretation. The absence of a voltage criterion does not rule out left ventricular hypertrophy, especially when anatomical factors favor signal attenuation.
Conclusion
Left ventricular hypertrophy on the ECG does not depend on myocardial mass alone.
It also depends on:
- The distance between the ventricle and the chest wall
- The amount of subcutaneous adipose tissue
- Individual chest geometry
The ECG measures an electrical vector propagating through tissues. When we interpret voltage criteria, we are dealing with an anatomical variable embedded in the signal.
Perhaps the problem was never the sensitivity of the ECG.
Perhaps the problem is believing that it measures only muscle.
References
- Pewsner D, Jüni P, Egger M, Battaglia M, Sundstrom J, Bachmann LM. Accuracy of electrocardiography in diagnosis of left ventricular hypertrophy in arterial hypertension: systematic review . BMJ. 2007;335(7622):711.
- Lundström M, Carlhäll CJ, Bussman A, Brundin M, Palm A, Froelicher VF, et al. The effect of anatomical factors on ECG amplitudes – a cardiac magnetic resonance study . J Electrocardiol. 2025;93:154150.
- Wilson FN. The distribution of the potential differences produced by the heart beat within the body and at its surface . Am Heart J. 1930;5(5):599–616.
- Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads . Am Heart J. 1949;37(2):161–86.
