Recent work showed that AN leads to a decrement of the potentials of QRS complexes. Although the mechanism has been thought to be extracardiac in origin, and due to a decrease of the electrical impedance of the volume conductor from water overload, more proof on this will be welcome. It is hypothesized that the pacemaker “spikes” (PS) are independent of heart depolarization, and thus their change at the body surface with AN would be reflective of extracardiac influences. This study was designed to explore the impact of anasarca (AN) on the amplitude of PSs, and to further delineate the mechanism of ECG attenuation with AN.Methods
The sum of PS measurements in millimeters in the 6 limb leads (ΣPS6), and 12 ECG leads (ΣPS12), and the sum of QRS complexes in the 6 limb leads (ΣQRS6), and 12 ECG leads (ΣQRS12) were computed in six patients fitted with a pacemaker (3 with AN and 3 “controls”), and these variables were correlated with weight change.Results
Correlation of percentage change in weight and ΣPS12 was excellent (r =−0.88, P = 0.02), but not for ΣPS6 (r =−0.73, P = 0.1). Also, the percentage weight correlated well with ΣQRS6 (r =−0.82, P = 0.046), but not ΣQRS12 (r =−0.61, P = 0.2). Correlation of percentage change in ΣQRS6 and ΣPS6 was excellent (r = 0.91, P = 0.01), but not the percentage change in ΣQRS12 and ΣPS12 (r = 0.72, P = 0.11).Conclusions
PSs undergo amplitude attenuation in patients developing AN, similar to the one noted in the QRS complexes. Since these changes are independent of the cardiac activation, and are similar in extent to those impacting the QRS complexes, the attenuation of the voltage of the entire ECG curve in AN appears to be extracardiac in origin.