title: Monitoring of heart failure: comparison of left atrial pressure with intrathoracic impedance and natriuretic peptide measurements in an experimental model of ovine heart failure.
abstract: Monitoring of HF (heart failure) with intracardiac pressure, intrathoracic impedance and/or natriuretic peptide levels has been advocated. We aimed to investigate possible differences in the response patterns of each of these monitoring modalities during HF decompensation that may have an impact on the potential for early therapeutic intervention. Six sheep were implanted with a LAP (left atrial pressure) sensor and a CRT-D (cardiac resynchronization therapy defibrillator) capable of monitoring impedance along six lead configuration vectors. An estimate of ALAP (LAP from admittance) was determined by linear regression. HF was induced by rapid ventricular pacing at 180 and 220 bpm (beats/min) for a week each, followed by a third week with daily pacing suspensions for increasing durations (1-5 h). Incremental pacing induced progressively severe HF reflected in increases in LAP (5.9 ± 0.4 to 24.5 ± 1.6 mmHg) and plasma atrial (20 ± 3 to 197 ± 36 pmol/l) and B-type natriuretic peptide (3.7 ± 0.7 to 32.7 ± 5.4 pmol/l) (all P<0.001) levels. All impedance vectors decreased in proportion to HF severity (all P<0.001), with the LVring (left ventricular)-case vector correlating best with LAP (r2=0.63, P<0.001). Natriuretic peptides closely paralleled rapid acute changes in LAP during alterations in pacing (P<0.001), whereas impedance changes were delayed relative to LAP. ALAP exhibited good agreement with LAP. In summary, impedance measured with an LV lead correlates significantly with changes in LAP, but exhibits a delayed response to acute alterations. Natriuretic peptides respond rapidly to acute LAP changes. Direct LAP, impedance and natriuretic peptide measurements all show promise as early indicators of worsening HF. ALAP provides an estimate of LAP that may be clinically useful.
authors.affiliation: Christchurch Cardioendocrine Research Group, University of Otago, Christchurch, New Zealand. miriam.rademaker@otago.ac.nz
authors.forename: Miriam T
authors.initials: MT
authors.lastname: Rademaker
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Charles
authors.forename: Iain C
authors.initials: IC
authors.lastname: Melton
authors.forename: A Mark
authors.initials: AM
authors.lastname: Richards
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Frampton
authors.forename: Jeff
authors.initials: J
authors.lastname: Siou
authors.forename: Fujian
authors.initials: F
authors.lastname: Qu
authors.forename: Neal L
authors.initials: NL
authors.lastname: Eigler
authors.forename: Dan
authors.initials: D
authors.lastname: Gutfinger
authors.forename: Richard W
authors.initials: RW
authors.lastname: Troughton
mesh_terms: D000818:Animals; D016279:Atrial Function, Left / Q000502:physiology*; D015415:Biomarkers / Q000097:blood; D002304:Cardiac Pacing, Artificial; D002307:Cardiography, Impedance; D004195:Disease Models, Animal; D005240:Feasibility Studies; D006325:Heart Atria / Q000503:physiopathology; D006333:Heart Failure / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D045265:Natriuretic Peptides / Q000097:blood*; D034561:Sheep, Domestic
chemical_list: D015415:Biomarkers; D045265:Natriuretic Peptides