Key result
Posterior circulation ischemic stroke, even without brainstem involvement, was associated with significantly reduced cardiovagal modulation and compromised baroreflex compared to healthy controls.
Why the study?
It remains unclear whether posterior circulation ischemic stroke without brainstem involvement compromises cardiovascular autonomic modulation.
Does posterior circulation ischemic stroke without brainstem involvement compromise cardiovascular autonomic modulation compared to healthy controls?
Observational (n=91)
Does posterior circulation ischemic stroke without brainstem involvement compromise cardiovascular autonomic modulation compared to healthy controls?
Posterior circulation ischemic stroke triggers cardiovascular autonomic dysfunction, characterized by reduced cardiovagal modulation and increased sympathetic modulation, even without brainstem involvement.
Answers are grounded in this paper and cite their sources.
May warrant CAM monitoring in PCIS regardless of brainstem involvement; hypothesis-generating for autonomic interventions in posterior stroke.
BACKGROUND AND PURPOSE: Ischemic stroke may induce cardiovascular autonomic dysfunction, but most previous studies have included patients with anterior circulation ischemic stroke or brainstem stroke. It remains unclear whether posterior circulation ischemic stroke (PCIS) without brainstem involvement also compromises cardiovascular autonomic modulation (CAM). Therefore, we aimed to assess CAM in PCIS patients with and without brainstem involvement. METHODS: In four subgroups of 61 PCIS patients (14 occipital lobe, 16 thalamic, 12 cerebellar, and 19 brainstem strokes) and 30 healthy controls, we recorded RR intervals (RRIs), systolic (SBP) and diastolic blood pressure (DBP), and respiration at supine rest during the first week after stroke onset. We calculated parameters reflecting total CAM (RRI-standard deviation [RRI-SD], RRI-total powers), predominantly sympathetic CAM (RRI-low-frequency [LF] powers and SBP-LF powers] and parasympathetic CAM (root mean square of successive RRI differences [RMSSD], RRI-high-frequency [HF] powers), sympathetic-parasympathetic balance (RRI-LF/HF ratios), and baroreflex sensitivity (BRS). Values were compared among the four PCIS groups and controls using one-way ANOVA Kruskal-Wallis tests, with post-hoc analyses. Significance was assumed for p < 0.05. RESULTS: In each PCIS subgroup, values for RRI, RRI-SD, RMSSD, RRI-HF powers, and BRS were significantly lower, while SBP-LF powers were higher than in the controls. Only in patients with occipital lobe stroke were RRI-LF/HF ratios significantly higher than in controls. Otherwise, autonomic variables did not differ among the four PCIS subgroups. CONCLUSIONS: During the first week after stroke onset, our PCIS patients with occipital lobe, thalamic, cerebellar, or brainstem strokes all had reduced cardiovagal modulation, compromised baroreflex, and increased peripheral sympathetic modulation. The RRI-LF/HF ratios suggest that sympathetic predominance is slightly more prominent after occipital lobe stroke. PCIS may trigger cardiovascular autonomic dysfunction even without brainstem involvement.
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Wang et al. (2022) conducted an observational in Posterior circulation ischemic stroke (n=91). Posterior circulation ischemic stroke vs. Healthy controls was evaluated on Cardiovascular autonomic modulation parameters (RRI, RRI-SD, RMSSD, RRI-HF powers, BRS, SBP-LF powers). Posterior circulation ischemic stroke, even without brainstem involvement, was associated with significantly reduced cardiovagal modulation and compromised baroreflex compared to healthy controls.
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