Cardiac baroreflex sensitivity and beat-to-beat blood pressure variability within 3 months of traumatic brain injury

Background: Patients with traumatic brain injury (TBI) have an elevated long-term risk for development of hypertension and cardiovascular disease (CVD). The arterial baroreflex is a major mechanism governing blood pressure (BP) regulation on a beat-to-beat basis. In patients with moderate to severe traumatic brain injury (TBI), cardiac baroreflex sensitivity (cBRS) is impaired within the first 48 hours after TBI and predicts early mortality. The extent to which cBRS remains impaired beyond the acute phase of TBI is less clear. In addition, the impact of this reduced cBRS on BP dynamics has not been studied. This is important because impaired baroreflex function may enhance beat-to-beat BP variability (BPV), which confers cardiovascular risk beyond elevations in mean BP alone. Herein, we studied patients with TBI outside of acute care (i.e., the intensive care unit) but within 3 months of injury and tested the hypothesis that patients with TBI would exhibit reduced cBRS, which would be associated with greater beat-to-beat BPV. Methods: Beat-to-beat BP (Finometer), heart rate (lead II EKG), and respiration (capnography) were measured during at least 5 minutes of quiet supine rest in 13 patients with moderate to severe TBI (2F/11M; 36 ± 10 years, Glasgow Coma Scale at scene 8 ± 5; 45 ± 20 days post injury) while admitted for inpatient rehabilitation and 13 healthy controls (4F/9M; 35 ± 9 years). The cBRS was assessed via the sequence technique by identifying sequences of three or more consecutive cardiac cycles where systolic BP and R-R interval change in the same direction. The slope of these changes (i.e., gain) was calculated for each sequence and the average of all slopes was computed to assess overall cBRS gain, as well as separately for up sequences (up gain; both variables increasing) and down sequences (down gain; both variables decreasing). Beat-to-beat BPV was quantified as the standard deviation (SD) and range for systolic BP, diastolic BP, and mean BP. Results: The TBI group exhibited lower cBRS overall gain (TBI: 7.3±4.5 vs. CON: 17.4±9.5 ms/mmHg, P=0.003), as well as up (TBI: 7.1±4.6 vs. CON: 16.7±9.8 ms/mmHg, P=0.005) and down (TBI: 7.7±4.7 vs. CON: 17.8±9.3 ms/mmHg, P=0.003) gains compared with controls. Systolic (P=0.165) and mean (P=0.079) BP SD were not different between groups. However, diastolic BP SD was significantly lower in patients with TBI compared to controls (TBI: 3.1±0.8 vs. CON: 3.9±1.0 mmHg, P=0.032). The ranges for systolic, diastolic, and mean BP were not different between groups (all P >0.1). The overall cBRS gain was not associated with any BPV measures in individuals with TBI. Conclusion: These findings suggest that cBRS is impaired within 3 months of TBI, but this does not translate to augmented beat-to-beat BPV. The extent to which the sustained impairment in cBRS predisposes these patients to future BP dysregulation and hypertension/CVD later in life remains to be defined. Funding sources: NINDS 5R01NS13324502 This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.