Session: 753 APS Arterial Baroreflex Function and Blood Pressure Regulation Poster Session
(753.4) Carotid Baroreflex Responsiveness in Patients with Heart Failure with a Preserved Ejection Fraction
Monday, April 4, 2022
10:15 AM – 12:15 PM
Location: Exhibit/Poster Hall A-B - Pennsylvania Convention Center
Poster Board Number: E429
Michael Francisco (University of Utah, George E. Wahlen Department of Veterans Affairs Medical Center), Jeremy Alpenglow (University of Utah), Kanokwan Bunsawat (University of Utah), Jarred Iacovelli (University of Utah), Christy Ma (University of Utah), John Ryan (University of Utah), Keith Quencer (University of Utah), Claire Kaufman (University of Utah), Walter Wray (University of Utah, George E. Wahlen Department of Veterans Affairs Medical Center)
Presenting Author University of Utah, George E. Wahlen Department of Veterans Affairs Medical Center
The carotid baroreflex (CBR) plays an important role in blood pressure regulation by modulating heart rate (HR) and vasomotor tone. In humans, CBR function can be investigated non-invasively using the variable pressure neck collar, which alters carotid sinus transmural pressure through application of positive and negative pressure within the neck chamber. Using this technique, derangements in CBR function have been identified in a variety of patient populations, but whether patients with heart failure with a preserved ejection fraction (HFpEF) suffer from disease-related changes in CBR responsiveness has yet to be determined. We evaluated beat-to-beat changes in HR and mean arterial pressure (MAP) in response to 5-sec pulses of neck pressure (NP, +40 Torr) and neck suction (NS, -80 Torr) to simulate carotid hypotension and hypertension, respectively in 5 patients with HFpEF (69±3 yrs and BMI: 38±4) and 4 healthy, older controls (68±2 yrs and BMI: 26±3). Resting HR was lower in patients with HFpEF compared to control subjects (77±7 vs. 68±6 bpm, respectively; plt;0.005), while MAP was similar between groups (88±2 vs. 88±5mmHg, HFpEF vs controls). Following NP, a disease-related decrement in CBR responsiveness was evident, with diminished changes in HR (2±1 vs 9±1 bpm, HFpEF vs controls, p=0.041) and MAP (4±2 vs 8±1 mmHg, p=0.095) in the HFpEF group. Similarly, changes in both HR (-6±1 vs -8±1 bpm, HFpEF vs controls, p=0.21) and MAP (-5±1 vs -8±1 mmHg, HFpEF vs controls, p=0.16) in response to carotid hypertension provoked by NS were reduced in patient with HFpEF. Though preliminary in nature, these initial findings appear to indicate a decline in carotid baroreflex-mediated cardiac and vasomotor control in patients with HFpEF that is likely to contribute significantly to autonomic nervous system dysregulation in this patient group.
