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Europace Advance Access originally published online on June 3, 2009
Europace 2009 11(8):995-1000; doi:10.1093/europace/eup127
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

REVIEWS

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

John E. Madias1,2,*

1 The Mount Sinai School of Medicine of the New York University, New York, NY, USA; 2 Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, USA

Attenuation of the QRS voltage ({downarrow}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, {downarrow}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 {downarrow}QRSV. Therefore, a synthesis of the above two observations is implemented to propose the hypothesis that {downarrow}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).

Key Words: Heart failure, Peripheral oedema, Surface electrocardiography, Standard electrocardiography, Intracardiac electrograms, Mechanism of ECG changes due to heart failure

* Corresponding author. Tel: +1 718 334 5005, Fax: +1 718 334 5990, Email: madiasj{at}nychhc.org

Manuscript submitted 6 April 2009. Accepted after revision 24 April 2009.


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