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- Sahathevan, R., et al.
(author)
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Positron Emission Tomographic Imaging in Stroke Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke
- 2016
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In: Stroke. - : Ovid Technologies (Wolters Kluwer Health). - 0039-2499 .- 1524-4628. ; 47:1, s. 113-119
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Journal article (peer-reviewed)abstract
- Background and Purpose Cardiovascular risk factors significantly increase the risk of developing Alzheimer disease. A possible mechanism may be via ischemic infarction-driving amyloid deposition. We conducted a study to determine the presence of -amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger -amyloid deposition, with deposition over time. Methods Patients were recruited within 40 days of acute ischemic stroke and imaged with computed tomographic or magnetic resonance imaging and Pittsburgh compound B (11C-PiB) positron emission tomographic scans. Follow-up positron emission tomographic scanning was performed in a subgroup 18 months after the stroke event. Standardized uptake value ratios for regions of interest were analyzed after coregistration. Results Forty-seven patients were imaged with C-11-PiB positron emission tomography. There was an increase in C-11-PiB accumulation in the stroke area compared with a reference region in the contralesional hemisphere, which was not statistically significant (median difference in standardized uptake value ratio, 0.07 [95% confidence interval, -0.06 to 0.123]; P=0.452). There was no significant increase in the accumulation of C-11-PiB in the peri-infarct region or in the ipsilesional hemisphere (median difference in standardized uptake value ratio, 0.04 [95% confidence interval, -0.02 to 0.10]; P=0.095). We repeated C-11-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of C-11-PiB between regions of interest (median difference in standardized uptake value ratio, -0.08 [95% confidence interval, -0.23 to -0.03]; P=0.04). Conclusions There was no significant increase in C-11-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric C-11-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased -amyloid deposition 18 months after stroke.
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