Abstract Details

Title Do Commonly Obtained Laboratory Data Differ between Lacunar and Non-Lacunar Strokes in the Acute Setting?

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P03 - (-)

Poster/Presentation
Number 185

Objective

Background BACKGROUND: Previous reports emphasize clinical, neuropathological and imaging differences between lacunar and non-lacunar stroke. Lacunar stroke is caused by an intrinsic abnormality in small cerebral arterioles; in contrast, non-lacunar stroke is commonly a result of atherothromboembolic phenomena originating from large arteries or the heart. We investigated differences between these two subtypes of ischemic stroke in terms of laboratory data commonly obtained on admission.

Design/Methods DESIGN/METHODS: We retrospectively reviewed all ischemic stroke admissions to our center for 2 years. Inclusion criteria were: 1) DWI/ADC changes on MRI, 2) stroke onset ?14 days. We excluded patients with: 1) intracranial hemorrhage; 2) previous hospitalization within 90 days; 3) current admission for another disease when the stroke occurred; 4) no MRI evidence of infarction. Patients were classified into lacunar and non-lacunar stroke as defined by the TOAST criteria. Patients' initial [admission?] WBC, granulocyte percentage, hemoglobin, hematocrit, RBC, platelet count, mean platelet volume, erythrocyte sedimentation rate, high sensitivity C-reactive protein (hs-CRP) were recorded. Duplicates and labs drawn >24 hours after admission were excluded. Between-group differences were assessed using independent t-tests (?=0.05).

Results RESULTS: 207 patients were included in the analysis, 45 with lacunar stroke and 162 with non-lacunar stroke. Significantly higher mean hs-CRP levels were noted in patients with non-lacunar stroke than in those with lacunar stroke (15.06 mg/L versus 6.77 mg/L, p<0.031). There were no statistically significant differences between the other laboratory data analyzed.

Conclusions CONCLUSIONS: hs-CRP, a clinically available and commonly obtained laboratory measure, is elevated in non-lacunar stroke patients as compared to lacunar stroke patients. This finding supports the existence of different pathways leading to these two main types of cerebral infarction, possibly related to distinct contributions from systemic inflammation.

Authors/Disclosures
Anthony J. Vaughn, MD, FAAN (Mercy Health Center) PRESENTER	No disclosure on file
	No disclosure on file
Calin I. Prodan, MD (Univ of Oklahoma - Neurology Dept)	The institution of Dr. Prodan has received research support from US Department of Veterans Affairs (Merit award CX000340).
Massimo Filippi, MD, FAAN (Ospedale San Raffaele, Neuroimaging Research Unit)	Dr. Filippi has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Alexion, Almirall, Biogen, Merck, Novartis, Roche, Sanofi. Dr. Filippi has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Alexion, Biogen, Bristol-Myers Squibb, Merck, Novartis, Roche, Sanofi, Sanofi-Aventis, Sanofi-Genzyme, Takeda. Dr. Filippi has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Bayer, Biogen, Celgene, Chiesi Italia SpA, Eli Lilly, Genzyme, Janssen, Merck-Serono, Neopharmed Gentili, Novartis, Novo Nordisk, Roche, Sanofi, Takeda, and TEVA. Dr. Filippi has received personal compensation in the range of $10,000-$49,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Springer Nature. The institution of Dr. Filippi has received research support from Biogen Idec, Merck-Serono, Novartis, Roche, the Italian Ministry of Health, the Italian Ministry of University and Research, and Fondazione Italiana Sclerosi Multipla.

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