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Published on: June 10, 2020
Systemic inflammation and cerebrovascular injury in acute stroke
Tuna Demirbas1, Neslin Sahin1, Fatih Turkmen1
1University of Health Sciences, Istanbul Gaziosmanpasa Training and Research Hospital, Department of Radiology - Istanbul, Türkiye.
Insights
The neutrophil-to-lymphocyte ratio is linked to both small vessel disease and arterial calcification in stroke patients, suggesting inflammation drives cerebrovascular injury. This ratio may help assess overall cerebrovascular disease burden.
Area of Science:
- Neurology
- Cardiovascular Research
- Inflammation Studies
Background:
- Systemic inflammation is implicated in cerebrovascular injury.
- Cerebral small vessel disease and intracranial arterial calcification are often assessed independently.
- Understanding their combined burden is crucial for acute ischemic stroke management.
Purpose of the Study:
- To investigate the association between systemic inflammatory indices and the combined burden of small vessel disease and intracranial arterial calcification.
- To determine if inflammatory markers can predict global cerebrovascular disease severity in acute ischemic stroke patients.
Main Methods:
- Retrospective study of 166 acute ischemic stroke patients.
- Assessment of small vessel disease (white matter hyperintensities, lacunes, microbleeds, enlarged perivascular spaces) via MRI.
- Evaluation of intracranial arterial calcification severity using CT.
- Calculation of inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR) and systemic inflammatory response index (SIRI).
- Multivariate regression analyses to identify independent predictors.
Main Results:
- Neutrophil-to-lymphocyte ratio (NLR) independently predicted total small vessel disease burden (β=0.39, p=0.026) and intracranial arterial calcification severity (β=0.181, p=0.030).
- SIRI was not a significant predictor after adjustment.
- NLR was also associated with cerebral microbleeds and hypertension.
- Platelet indices correlated with infarct size and enlarged perivascular spaces.
Conclusions:
- Neutrophil-to-lymphocyte ratio (NLR) is independently associated with both microvascular and macrovascular cerebrovascular injury.
- Findings support an inflammation-driven continuum in cerebrovascular disease.
- NLR may serve as a practical biomarker for assessing global cerebrovascular disease burden in acute ischemic stroke.
Objective:
Systemic inflammation contributes to cerebrovascular injury, yet cerebral small vessel disease and intracranial arterial calcification are typically evaluated separately. The aim of this study was to investigate the association between systemic inflammatory indices and the combined burden of small vessel disease and intracranial arterial calcification in acute ischemic stroke.
Methods:
This retrospective study included 166 patients with acute anterior circulation ischemic stroke. Total small vessel disease burden (white matter hyperintensities, lacunes, cerebral microbleeds, and enlarged perivascular spaces) was assessed on magnetic resonance imaging. Intracranial arterial calcification severity was evaluated on non-contrast computed tomography using a semiquantitative grading system. Inflammatory indices, including neutrophil-to-lymphocyte ratio and systemic inflammatory response index, were calculated from baseline blood samples. Multivariate regression analyses were performed to identify independent predictors.
Results:
A total of 166 patients (mean age 64.5±9.8 years) were included. In multivariate analysis, the neutrophil-to-lymphocyte ratio was an independent predictor of both total small vessel disease burden (β=0.39, p=0.026) and intracranial arterial calcification severity (β=0.181, p=0.030), whereas the systemic inflammatory response index was not significant after adjustment. Additionally, the neutrophil-to-lymphocyte ratio was independently associated with cerebral microbleeds and hypertension, and platelet-related indices were associated with infarct size and enlarged perivascular spaces.
Conclusion:
Neutrophil-to-lymphocyte ratio is independently associated with both microvascular and macrovascular cerebrovascular injury, supporting an inflammation-driven continuum. It may serve as a practical biomarker for assessing global cerebrovascular disease burden.
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