title: Intracardiac impedance monitors hemodynamic deterioration in a chronic heart failure pig model.
abstract: BACKGROUND
  A large number of heart failure (HF) patients benefit from cardiac resynchronization therapy. Measurements of intrathoracic impedance (ITZ) by implantable devices correlate with intrathoracic fluid content and are used for monitoring lung edema formation in HF patients. However, intrathoracic fluid is only an indirect parameter of cardiac function. We hypothesized that changes in intracardiac impedance correlate with left ventricular (LV) volume changes. Therefore, measurements of intracardiac impedance between a right ventricular lead and a LV lead may be used to monitor long-term changes of LV function.
  
  
  RESULTS
  HF was successfully induced in nine mini-pigs by continuous high-rate pacing. Hemodynamic parameters as well as intracardiac impedance and ITZ were measured before HF induction and after 20 +/- 5 days of high-rate pacing. After the pacing period, we found a significant deterioration of hemodynamics, reflected by a reduction of ejection fraction from 71+/-11% to 48+/-7% and an increase of LV end diastolic pressure (EDP) from 12 +/- 4 mmHg to 26 +/- 8 mmHg. Worsening of cardiac function correlated with a significant >30% decrease of end diastolic intracardiac impedance, in accordance with a >20% increase of end diastolic volume (EDV). ITZ decreased by more than 8%. We observed a significant inverse correlation between end diastolic intracardiac impedance and EDP (r =-0.81, P < 0.001).
  
  
  CONCLUSIONS
  In this animal model, changes of intracardiac impedance revealed hemodynamic deterioration as reflected by EDV and EDP pressure. Thus, intracardiac impedance is a promising new application to monitor heart failure status within implantable devices.
authors.affiliation: Department of Cardiology, University of Tübingen, Germany.
authors.forename: Carsten
authors.initials: C
authors.lastname: Stahl
authors.forename: Wolfram
authors.initials: W
authors.lastname: Beierlein
authors.forename: Tobias
authors.initials: T
authors.lastname: Walker
authors.forename: Andreas
authors.initials: A
authors.lastname: Straub
authors.forename: Zolt
authors.initials: Z
authors.lastname: Nagy
authors.forename: Karolin
authors.initials: K
authors.lastname: Knubben
authors.forename: Tim O
authors.initials: TO
authors.lastname: Greiner
authors.forename: Michael
authors.initials: M
authors.lastname: Lippert
authors.forename: Gerald
authors.initials: G
authors.lastname: Czygan
authors.forename: Stefan
authors.initials: S
authors.lastname: Paule
authors.forename: Oliver
authors.initials: O
authors.lastname: Schweika
authors.forename: Volker
authors.initials: V
authors.lastname: Kühlkamp
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002303:Cardiac Output, Low / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology*; D002307:Cardiography, Impedance / Q000379:methods*; D003326:Coronary Circulation; D004195:Disease Models, Animal; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D013318:Stroke Volume; D013552:Swine; D013556:Swine, Miniature; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology*