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Published on: December 28, 2014
Relationships of Hematocrit With Chronic Covert and Acute Symptomatic Lacunar Ischemic Lesions
David J Roh1, Ricardo Murguia-Fuentes1, Kursat Gurel1
1From the Departments of Neurology (D.J.R., K.G., S.R., P.P.B., K.K., A.J.S.-A., D.J.B., R.S.M., J. Gutierrez), Pathology and Cell Biology (A.C., E.A.H.), Biomedical Engineering (R.J., E.K.), Psychiatry (J. Guo), and Department of Radiology (V.S.), Vagelos College of Physicians and Surgeons, Columbia University, New York, NY; Department of Neurology (R.M.-F.), Louisiana State University Health Shreveport; Department of Neurology (F.K.), St. Louis University, MO; Department of Neurology (M.S.), Weill Cornell Medical Center, New York, NY; Department of Neurology (T.R.), University of Miami/Jackson Memorial Hospital, FL; National Institute of Neurological Disorders and Stroke (C.B.W.),, Bethesda, MD; and Department of Epidemiology (M.S.V.E.), Mailman School of Public Health, Columbia University, New York, NY.
Background And Objectives:
Red blood cell (RBC) concentrations are known to associate with ischemic stroke. It is unclear whether RBC concentrations associate specifically with small vessel disease lacunar infarcts. We investigated the hypothesis that RBC concentrations associate with both chronic covert and acute symptomatic brain MRI lacunar infarcts.
Methods:
A cross-sectional observational analysis was performed across 2 cohorts with available hematocrit (as the assessment of RBC concentration exposure) and MRI outcome data. The primary setting was a population-based cohort of stroke-free, older adult (>50 years) participants from the Northern Manhattan Study (NOMAS) enrolled between 2003 and 2009. A second replication sample consisted of patients admitted with acute stroke and enrolled into the Columbia Stroke Registry (CSR) between 2005 and 2020. Associations of hematocrit with (1) chronic, covert lacunar infarcts and (2) symptomatic (i.e., acute) lacunar strokes were separately assessed from the NOMAS and CSR cohorts, respectively, using general additive models after adjusting for relevant covariates.
Results:
Of 1,218 NOMAS participants analyzed, 6% had chronic, covert lacunar infarcts. The association between hematocrit and these covert lacunar infarcts was U-shaped (χ2 = 9.21 for nonlinear associations; p = 0.03), with people with hematocrit extremes being more likely to have covert lacunar infarcts. Of the 1,489 CSR patients analyzed, 23% had acute lacunar strokes. In this sample, only the relationships of increased hematocrit concentrations and lacunar strokes were replicated (adjusted coefficient β = 0.020; SE = 0.009; p = 0.03).
Discussion:
We identified relationships of hematocrit with MRI lacunar infarcts in both stroke-free and ischemic stroke cohorts, respectively. The relationship between increased hematocrit concentrations with lacunar infarcts was replicated in both cohorts. Further studies are required to clarify the mechanisms behind the relationships of hematocrit with ischemic cerebral small vessel disease.
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