Identifying autonomic nervous system dysfunction in acute cerebrovascular attack by assessments of heart rate variability and catecholamine levels

Abstract

Objective:This study aimed to evaluate changes in the autonomic nervous system caused by cerebral lesions due to acute stroke. We assessed heart rate variability and catecholamine levels in lieu of stroke lesion localization.Materials and Methods:A total of 60 stroke patients and 31 healthy controls were enrolled in the study. Plasma epinephrine and norepinephrine levels were measured on the first, third, and seventh days following the stroke event. Heart rate variability was evaluated with time-domain and frequency-domain analyses via 24-hour Holter monitor recordings.Results:On the first and third day following the stroke, norepinephrine levels were significantly higher in all patient groups as compared to controls. Epinephrine levels on the first, third and seventh days after the stroke were significantly higher in patients with lesions in the right middle cerebral artery territory than controls. In frequency-domain analysis, patients with right middle cerebral artery territory lesions had greater low frequency and low frequency to high frequency ratio values than controls. Time-domain analysis revealed significant decreases in the standard deviation from the mean for 5-minute 288 R-R intervals in patients with lesions in the right middle cerebral artery and posterior cerebral artery territory when contrasted with controls. Patients with lesions in the right middle cerebral artery territory demonstrated the highest increase in the percentage of consecutive R-R intervals differing by more than 50 ms (pNN50) as compared to the control group.Conclusion:These findings indicate that autonomic dysfunction favoring an increase in sympathetic activity occurs in acute stroke patients.

Arterial blood pressure and heart rate response in patients with acute ischemic stroke - Correlation with the severity of cardiovascular autonomic dysfunction

“…Our study data indicate the presence of a significant difference between the values of SBP, DBP and MAP between stroke patients and the control group, similar to the results of other authors (16). Patients with ischemic stroke and insular cortex damage present more often an increase of BP (17) and HR values, compared to those without involvement of the IC and those with left IC involvement.…”

Changes of deceleration and acceleration capacity of heart rate in patients with acute hemispheric ischemic stroke

“… 3 , 16 However, the decrease in AC reflects a decrease in sympathetic activity, which is inconsistent with studies concluding that the sympathetic activity of stroke increased through the detection of catecholamine concentrations. 16 , 17 In the clinic, increased blood pressure, heart rate, and other characteristics of enhanced sympathetic activity are common in patients with cerebral infarction. In our study, we also found that R–R intervals of patients with infarction were shorter than those in controls, which might be a reflection of sympathetic hyperactivity.…”

The role of β2 adrenergic receptor on infection development after ischaemic stroke

“…Furthermore, the timepoint of 3 ​h post-stroke may be too acute for SNS dysregulation to be detected in the circulation. Indeed, a previous study showed plasma NA was elevated at 5 ​h following experimental stroke ( Smith et al., 1986 ), while others show an elevation after the first day in stroke patients ( Akıl et al., 2015 ; McCulloch et al., 2019 ). Additionally, the concentration of NA in the plasma is dependent on the rate of release and the rate of removal from the plasma whereby reduced removal of NA can increase detection of plasma NA without a change in SNS output ( Goldstein et al., 2003 ).…”

“…In light of new evidence showing a role for the SNS on immune regulation, we explored the effect of inhibiting β-adrenergic receptor on post-stroke outcomes. Indeed, plasma NA and other catecholamines are elevated in patients with stroke ( Akıl et al., 2015 ; McCulloch et al., 2017 ; Myers et al., 1981 ), thus the notion of NA-mediated post-stroke immune suppression is a possibility. In this study, we revealed stroke induced a systemic activation of the SNS as indicated by elevated levels of plasma catecholamines and UCP-1 activity.…”

“…After stroke, symptoms of impaired cardiac function, heart rate variability, baroreflex sensitivity, and blood pressure changes provide strong evidence of altered SNS activity ( Bassi et al., 2007 ; Xiong et al., 2018 ). Indeed, elevated catecholamines in the form of noradrenaline (NA) has been reported in the plasma of patients within the first 7 days following stroke onset, further suggestive of SNS hyperactivity ( Eşref et al., 2015 ; McCulloch et al., 2019 ; Myers et al., 1981 ; Naredi et al., 2000 , 2006 ). Of the adrenergic receptors, β 2 adrenergic receptor (β 2 AR) is most widely expressed on immune cells ( Scanzano and Cosentino, 2015 ), and findings from various preclinical studies suggest that activation of the β 2 AR on immune cells significantly impact immune functions.…”