Jose Gutierrez1, James Goldman2, Lawrence S Honig3, Mitchell S V Elkind4, Susan Morgello5, Randolph S Marshall3. 1. Department of Neurology, College of Physicians and Surgeons, Columbia University Medical Center, NY, USA. Electronic address: jg3233@columbia.edu. 2. Department of Pathology and Cell Biology, College of Physicians and Surgeons, Columbia University Medical Center, NY, USA. 3. Department of Neurology, College of Physicians and Surgeons, Columbia University Medical Center, NY, USA. 4. Department of Neurology, College of Physicians and Surgeons, Columbia University Medical Center, NY, USA; Department of Epidemiology, Mailman School of Public Health, Columbia University Medical Center, NY, USA. 5. Department of Neurology, Icahn School of Medicine at Mount Sinai, NY, USA.
Abstract
OBJECTIVE: It is hypothesized that outward remodeling in systemic arteries is a compensatory mechanism for lumen area preservation in the face of increasing arterial stenosis. Large brain arteries have also been studied, but it remains unproven if all assumptions about arterial remodeling can be replicated in the cerebral circulation. METHODS: The sample included 196 autopsied subjects with a mean age of 55 years; 63 % were men, and 74 % non-Hispanic whites. From each of 1396 dissected cadaveric large arteries of the circle of Willis, the areas of the lumen, intima, media, and adventitia were measured. Internal elastic lamina (IEL) area was defined as the area encircled by this layer. Stenosis was calculated by dividing the plaque area by the IEL area and multiplying by 100. RESULTS: Plotting stenosis against lumen area or stratified by arterial size showed no preservation of the lumen in the setting of growing stenosis. We could not find an association between greater IEL proportion and stenosis (B = 0.44, P = 0.86). Stratifying arteries by their size, we found that smaller arteries have greater lumen reduction at any degree of stenosis (B = -23.65, P ≤ 0.0001), and although larger arteries show a positive association between IEL proportion and stenosis, this was no longer significant after adjusting for covariates (B = 6.0, P = 0.13). CONCLUSIONS: We cannot confirm the hypothesis that large brain arteries undergo outward remodeling as an adaptive response to increasing degrees of stenosis. We found that the lumen decreases proportionally to the degree of stenosis.
OBJECTIVE: It is hypothesized that outward remodeling in systemic arteries is a compensatory mechanism for lumen area preservation in the face of increasing arterial stenosis. Large brain arteries have also been studied, but it remains unproven if all assumptions about arterial remodeling can be replicated in the cerebral circulation. METHODS: The sample included 196 autopsied subjects with a mean age of 55 years; 63 % were men, and 74 % non-Hispanic whites. From each of 1396 dissected cadaveric large arteries of the circle of Willis, the areas of the lumen, intima, media, and adventitia were measured. Internal elastic lamina (IEL) area was defined as the area encircled by this layer. Stenosis was calculated by dividing the plaque area by the IEL area and multiplying by 100. RESULTS: Plotting stenosis against lumen area or stratified by arterial size showed no preservation of the lumen in the setting of growing stenosis. We could not find an association between greater IEL proportion and stenosis (B = 0.44, P = 0.86). Stratifying arteries by their size, we found that smaller arteries have greater lumen reduction at any degree of stenosis (B = -23.65, P ≤ 0.0001), and although larger arteries show a positive association between IEL proportion and stenosis, this was no longer significant after adjusting for covariates (B = 6.0, P = 0.13). CONCLUSIONS: We cannot confirm the hypothesis that large brain arteries undergo outward remodeling as an adaptive response to increasing degrees of stenosis. We found that the lumen decreases proportionally to the degree of stenosis.
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