Positron Emission Tomographic Imaging in Stroke: Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke. Issue 1 (January 2016)

• Record Type: Journal Article
• Authors: Sahathevan, Ramesh; Linden, Thomas; Villemagne, Victor L.; Churilov, Leonid; Ly, John V.; Rowe, Christopher; Donnan, Geoffrey; Brodtmann, Amy
• Is Part Of: Stroke. Volume 47:Issue 1(2016)
• Publication Date: 2016-01
• Subjects: Alzheimer disease -- follow-up studies -- positron emission tomography -- risk factors; Cerebrovascular disease -- Periodicals; Cerebral circulation -- Periodicals; 616.81
• DOI: 10.1161/STROKEAHA.115.010528
• Languages: English
• ISSNs: 0039-2499

Abstract

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 β-amyloid in infarct, peri-infarct, and hemispheric areas after stroke. We hypothesized that an infarct would trigger β-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 11 C-PiB positron emission tomography. There was an increase in 11 C-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 11 C-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 11 C-PiB positron emission tomography in 21 patients and found a significant reduction in accumulation of 11 C-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 11 C-PiB accumulation in or around the infarct. There was no increase in ipsilesional hemispheric 11 C-PiB accumulation over time. We found no evidence that infarction leads to sustained or increased β-amyloid deposition ⩽18 months after stroke.