In patients with spontaneous subarachnoid hemorrhage, decreased autonomic cardiovascular modulation was significantly associated with the development of delayed cerebral ischemia and poor clinical outcome.
Observational (n=53)
Is dysfunction of autonomic cardiovascular modulation associated with delayed cerebral ischemia in patients with spontaneous subarachnoid hemorrhage?
Assessment of heart rate variability may predict an augmented risk of delayed cerebral ischemia and poor clinical outcome in patients with spontaneous subarachnoid hemorrhage.
Background: This study aims to assess associations between occurrence of delayed cerebral ischemia (DCI) in spontaneous subarachnoid hemorrhage (SAH) and possible dysfunction of autonomic cardiovascular modulation compared to transcranial Doppler ultrasound (TCD). Methods: In this prospective observational study, 53 patients with spontaneous SAH were enrolled, and 17 patients met DCI criteria, i.e., new cerebral infarction > 72 h after SAH onset on follow-up CT scans. Autonomic modulation as well as TCD-frequencies were monitored within 24 h after SAH onset and then daily until day 10. From 5 min time-series of R–R-interval (RRI) and blood-pressure (BP) recordings, parameters of sympathetic, parasympathetic and total autonomic cardiovascular modulation were calculated, including time- and frequency-domain parameters. Data were compared between patients with and without DCI. Further subgroup analyses were performed according to functional outcome after 3 to 6 months (i.e., favorable outcome, modified Rankin Scale (mRS) ≤ 3 vs. unfavorable outcome, mRS > 3) regardless of DCI. Results: RRI and BP values as well as TCD frequencies did not differ between patients with and without DCI. Compared to No DCI patients, the cohort of DCI patients had significantly lower values of sympathetic modulation (RRI-LF powers, SBP-LF powers) on days 5 and 9 after SAH, significantly lower values of total autonomic modulation (RRI-SD, RRI-CV, RRI-total powers) and insignificantly lower values of parasympathetic modulation (RMSSDs, RRI-HF powers) on day 5 after SAH. Parameters of sympathetic, parasympathetic, and total autonomic modulation did not differ significantly between patients with favorable and unfavorable outcomes, but showed slightly lower values in the unfavorable outcome group. Yet, additionally calculated value of normalized RRI-LF and normalized RRI-HF powers, as well as LF/HF ratios were significantly different in the unfavorable outcome cohort. Conclusions: Not only within the acute phase, but also during the first days after disease onset, spontaneous SAH induces a decrease in sympathetic, parasympathetic and total autonomic cardiovascular modulation. In contrast to standard diagnostic evaluation for detecting clinically relevant vasospasms—i.e., TCD—autonomic dysfunction was associated with development of DCI and poor clinical outcome. Thus, assessment of heart rate variability may predict augmented risk of cardiovascular complications and may represent a promising adjunctive marker within multimodal neuromonitoring in SAH patients.
Borutta et al. (Tue,) conducted a observational in spontaneous subarachnoid hemorrhage (n=53). Delayed cerebral ischemia (DCI) vs. No DCI was evaluated on Autonomic cardiovascular modulation parameters (sympathetic, parasympathetic, and total). In patients with spontaneous subarachnoid hemorrhage, decreased autonomic cardiovascular modulation was significantly associated with the development of delayed cerebral ischemia and poor clinical outcome.