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Attenuation of the QRS voltage (QRSV) in patients with decompensated heart failure (HF) has been known for a long time, but its mechanism has been elusive. In a canine model of HF, QRSV was seen in intracardiac and epicardial electrograms (ECGs), but no surface ECGs were recorded in that study to evaluate the ECG expression of an equivalent standard ECG. 'Quasi-intracardial' ECGs in patients with peripheral oedema (PERED) of non-cardiac aetiology and no HF did not show changes while the simultaneously recorded standard surface ECGs showed QRSV. Therefore, a synthesis of the above two observations is implemented to propose the hypothesis that QRSV in patients with decompensated HF is because of a combination of heart-based influences, and the impact of the PERED, with different proportions of these two influences in different patients depending on the extent of changes in the heart (pressure, volume, ischaemia changes) and the passive body volume conductor (PERED).

Mechanism of attenuation of the QRS voltage in heart failure: a hypothesis