Jeff Siou

Ambulatory monitoring of congestive heart failure by multiple bioelectric impedance vectors.

OBJECTIVES This study was designed to investigate the properties of multiple bioelectric impedance signals recorded during congestive heart failure (CHF) by utilizing various electrode configurations of an implanted cardiac resynchronization therapy system. BACKGROUND The monitoring of CHF has relied mainly on right-side heart sensors. METHODS Fifteen normal dogs underwent implantation of cardiac resynchronization therapy systems using standard leads. An additional left atrial (LA) pressure lead sensor was implanted in 5 dogs. Continuous rapid right ventricular (RV) pacing was applied over several weeks. Left ventricular (LV) catheterization and echocardiography were performed biweekly. Six steady-state impedance signals, utilizing intrathoracic and intracardiac vectors, were measured through ring (r), coil (c), and device Can electrodes. RESULTS Congestive heart failure developed in all animals after 2 to 4 weeks of pacing. Impedance diminished gradually during CHF induction, but at varying rates for different vectors. Impedance during CHF decreased significantly in all measured vectors: LV(r)-Can, -17%; LV(r)-RV(r), -15%; LV(r)-RA(r), -11%; RV(r)-Can, -12%; RV(c)-Can, -7%; and RA(r)-Can, -5%. The LV(r)-Can vector reflected both the fastest and largest change in impedance in comparison with vectors employing only right-side heart electrodes, and was highly reflective of changes in LV end-diastolic volume and LA pressure. CONCLUSIONS Impedance, acquired by different lead electrodes, has variable responses to CHF. Impedance vectors employing an LV lead are highly responsive to physiologic changes during CHF. Measuring multiple impedance signals could be useful for optimizing ambulatory monitoring in heart failure patients.

Usefulness of monitoring congestive heart failure by multiple impedance vectors

Introduction: We investigated trends in intrathoracic impedance measured between multiple implanted electrodes for monitoring pulmonary edema secondary to congestive heart failure (CHF) in an experimental model. Methods: Biventricular ICDs were implanted in 16 dogs and 5 sheep. Continuous RV pacing (230–250 bpm) was applied over several weeks. Meanwhile, impedance was measured every hour along 4 intrathoracic and 2 intracardiac vectors. Four cardiogenic impedance vectors were also monitored. Cardiac function was assessed biweekly by catheterization and echocardiography. Left atrial (LA) pressure was measured daily by an implanted LA pressure sensor. Results: All animals developed CHF after 2–4 weeks of pacing as evidenced by changes in function (EF, 52 vs. 34%; LV end-diastolic volume, 65 vs. 97 ml; LV end-diastolic pressure, 7 vs. 16 mmHg; LA volume, 17 vs. 33 ml; LA pressure, 7 vs. 26 mmHg), clinical symptoms, or autopsy. Steady state impedance decreased during CHF: LV-Can, 17±9%; LV-RV, 15±8%; LV-RA, 13±6%; RV-Can, 13±8%; RVcoil-Can, 8±6%; RA-Can, 6±6%. Change in LV-Can impedance was greater than that of RA-Can, RV-Can, and RVcoil-Can (P<0.05). LV-Can impedance correlated well with LA pressure (r2=0.73), while RV-Can and RVcoil-Can were weakly correlated (r2=0.43 and r2=0.52, respectively). Changes in LV-RV and LV-RA impedances were also larger than those of RVcoil-Can and RA-Can (P<0.05). Meanwhile, all impedances were associated with circadian variability at baseline (5±2%) which diminished during CHF (2±1%); P=0.02. Furthermore, significant variations were observed in cardiogenic impedances during progression into CHF as evidenced by reduced peak-to-peak amplitude and increased fractionation of the signals. Conclusions: All impedance vectors decreased during CHF. Impedance measurement employing left heart sensors correlated well with LA pressure, and may improve detection of CHF onset compared to sensing by RA or RV leads alone. This approach has important clinical implications for managing heart failure patients in the ambulatory setting.

Monitoring of heart failure: comparison of left atrial pressure with intrathoracic impedance and natriuretic peptide measurements in an experimental model of ovine heart failure

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.