title: Decrease/disappearance of pacemaker stimulus "spikes" due to anasarca: further proof that the mechanism of attenuation of ECG voltage with anasarca is extracardiac in origin.
abstract: BACKGROUND
  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 (SigmaPS6), and 12 ECG leads (SigmaPS12), and the sum of QRS complexes in the 6 limb leads (SigmaQRS6), and 12 ECG leads (SigmaQRS12) 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 SigmaPS12 was excellent (r = -0.88, P = 0.02), but not for SigmaPS6 (r = -0.73, P = 0.1). Also, the percentage weight correlated well with SigmaQRS6 (r = -0.82, P = 0.046), but not SigmaQRS12 (r = -0.61, P = 0.2). Correlation of percentage change in SigmaQRS6 and SigmaPS6 was excellent (r = 0.91, P = 0.01), but not the percentage change in SigmaQRS12 and SigmaPS12 (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.
authors.affiliation: Mount Sinai School of Medicine of the New York University, and the Division of Cardiology, Elmhurst Hospital Center, New York and Elmhurst, New York. madiasj@nychhc.org
authors.forename: John E
authors.initials: JE
authors.lastname: Madias
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002318:Cardiovascular Diseases / Q000503:physiopathology* / Q000628:therapy; D004487:Edema / Q000503:physiopathology*; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010138:Pacemaker, Artificial; D015430:Weight Gain / Q000502:physiology