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Carotid Baroreflex Responsiveness in Patients with Heart Failure with a Preserved Ejection Fraction
Author(s) -
Francisco Michael,
Alpenglow Jeremy,
Bunsawat Kanokwan,
Iacovelli Jarred,
Ma Christy,
Ryan John,
Quencer Keith,
Kaufman Claire,
Wray Walter
Publication year - 2022
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2022.36.s1.r3735
Subject(s) - medicine , baroreflex , heart failure with preserved ejection fraction , cardiology , blood pressure , heart failure , ejection fraction , carotid sinus , pulse pressure , mean arterial pressure , heart rate
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; p<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.