Session SA2.2

Arterial Blood Pressure Variability before and after Chronic Pacing Induced Heart Failure in Conscious Dogs

F Aletti*, XI Chen, JA Sala-Mercado, RL Hammond,
DS O'Leary, G Baselli, R Mukkamala

Politecnico di Milano
Milano, Italy

Few previous studies have examined the effects of heart failure on beat-to-beat arterial blood pressure (ABP) variability with the same subjects serving as the control. We mathematically analyzed short-term beat-to-beat ABP variability in conscious dogs before and after chronic ventricular pacing, a well-established model of moderate heart failure. We previously performed experiments in four adult mongrel dogs (20-25 kg). We installed chronic instrumentation in the dogs including a fluid-filled catheter in the abdominal aorta for beat-to-beat ABP, an ultrasonic flow probe around the ascending aorta for beat-to-beat cardiac output (CO), and stainless steel electrodes on the right ventricular free wall for chronic pacing. After recovery from the major surgeries, we recorded the hemodynamic measurements from the dogs while fully awake and at rest for approximately five minutes. We then instituted ventricular pacing at 240 bpm for ~30 days. After discontinuing the pacing, we likewise recorded the hemodynamic measurements. We applied autoregressive power spectral analysis to the beat-to-beat ABP fluctuations (sampled to 2 Hz and normalized by its mean value) measured before and after the chronic pacing induced heart failure. We then computed the overall ABP power or variance, the low frequency (LF, < 0.1 Hz) ABP power, and the high frequency (HF, 0.1 – 0.5 Hz) ABP power. We utilized the paired t-test to determine if there were any significant differences in the ABP powers before and after chronic pacing induced heart failure. Our results showed that ABP variability significantly decreased following chronic pacing induced heart failure overall (0.00425±0.00072 (unitless) versus 0.00185±0.00021, p = 0.047), in the LF band (0.00188±0.00035 versus 0.00070±0.00011, p = 0.046), and in the HF band (0.00035±0.00006 versus 0.00016±0.00004, p = 0.020). We also applied linear system identification techniques to quantify the contributions of beat-to-beat CO variability in the genesis of beat-to-beat ABP variability. However, we found no significant differences in these CO contributions to ABP variability following chronic pacing induced heart failure. In conclusion, our results suggest that changes in autonomic reflexes and hemodynamics induced by heart failure significantly dampen the mechanisms responsible for generating ABP variability.

(Abstract Control Number: 192)