RESUMO
BACKGROUND AND PURPOSE: Brain arterial luminal diameters are reliably measured with automated imaging software. Nonautomated imaging software alternatives such as a Picture Archiving Communication System are more common bedside tools used for manual measurement. This study is aimed at validating manual measurements against automated methods. METHODS: We randomly selected 600 participants from the Northern Manhattan Study (NOMAS) and 260 participants from the Atahualpa Project studied with 1.5 Tesla MR angiography. Using the Radiant measuring tool, three independent readers (general practitioner, neurology resident, and vascular neurologist) measured manually the diameter of arterial brain vessels. The same vessels were also measured by LKEB Automated Vessel Analysis (LAVA). We calculated the intraclass correlation coefficient (ICC) of each rater's diameters versus those obtained with LAVA. RESULTS: The ICC between diameters obtained by the general practitioner or the neurology resident compared to LAVA was excellent for both internal carotid arteries (ICA) and Basilar Arteries (BA) (ICC > .80 in all comparisons) in NOMAS. In the Atahualpa Project, ICC between diameters obtained by a vascular neurologist and LAVA was good for both ICA and BA (ICC > .60 in all comparisons). The ICCs for the measurements of the remaining arteries were moderate to poor. CONCLUSION: Results suggest that manual measurements of ICA and BA diameters, but not MCA or ACA, are valid and could be used to identify dilated brain arteries at the bedside and for eventual selection of patients with dolichoectasia into clinical trials.
RESUMO
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 ß = 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.
