Positron Emission Tomographic Imaging in Stroke: Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke

Ramesh Sahathevan; Thomas Linden; Victor L Villemagne; Leonid Churilov; John V Ly; Christopher Rowe; Geoffrey Donnan; Amy Brodtmann

doi:10.1161/STROKEAHA.115.010528

Positron Emission Tomographic Imaging in Stroke: Cross-Sectional and Follow-Up Assessment of Amyloid in Ischemic Stroke

Stroke. 2016 Jan;47(1):113-9. doi: 10.1161/STROKEAHA.115.010528. Epub 2015 Nov 17.

Authors

Ramesh Sahathevan¹, Thomas Linden¹, Victor L Villemagne¹, Leonid Churilov¹, John V Ly¹, Christopher Rowe¹, Geoffrey Donnan¹, Amy Brodtmann²

Affiliations

¹ From the Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia (R.S., T.L., L.C., J.V.L., G.D., A.D.); University of Melbourne, Victoria, Australia (R.S., V.L.V., L.C., J.V.L., C.R., G.D., A.D.); Universiti Kebangsaan Malaysia Medical Centre, Bangi, Malaysia (R.S.); Gothenburg University, Gothenburg, Sweden (T.L.); and Austin Hospital PET Centre, Melbourne, Victoria, Australia (V.L.V., C.R.).
² From the Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia (R.S., T.L., L.C., J.V.L., G.D., A.D.); University of Melbourne, Victoria, Australia (R.S., V.L.V., L.C., J.V.L., C.R., G.D., A.D.); Universiti Kebangsaan Malaysia Medical Centre, Bangi, Malaysia (R.S.); Gothenburg University, Gothenburg, Sweden (T.L.); and Austin Hospital PET Centre, Melbourne, Victoria, Australia (V.L.V., C.R.). agbrod@unimelb.edu.au.

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.

Keywords: Alzheimer disease; follow-up studies; positron emission tomography; risk factors.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Aged
Amyloid beta-Peptides / metabolism*
Brain Ischemia / diagnostic imaging*
Brain Ischemia / metabolism*
Cross-Sectional Studies
Female
Follow-Up Studies
Humans
Male
Middle Aged
Positron-Emission Tomography / trends*
Risk Factors
Stroke / diagnostic imaging*
Stroke / metabolism*

Substances

Amyloid beta-Peptides