期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 37, 期 10, 页码 3401-3408出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X17696322
关键词
Angiogenesis; Ga-68-NOTA-PRGD2 PET/CT; chronic ischemia; severe intracranial atherosclerosis disease; collaterals
资金
- National Natural Science Foundation of China [81471246]
- Beijing Natural Science Foundation [7152121]
Angiogenesis is a critical compensation route, which has been demonstrated in the brain following ischemic stroke; however, few studies have investigated angiogenesis in chronic intracranial atherosclerosis disease (ICAD). We used Ga-68-NOTA-PRGD2 positron emission tomography/computed tomography based imaging to detect angiogenesis in chronic ICAD and to explore the factors that may have affected it. A total of 21 participants with unilateral severe chronic ICAD were included in the study. Of the 21 participants, 19 were men; the mean (SD) age was 52 (15) years. In 18 participants, we observed elevated Ga-68-NOTA-PRGD2 uptake in the peri-infarct, subcortical, and periventricular regions of the lesioned side, with a higher Ga-68-NOTA-PRGD2 SUVmax compared to that in the contralateral hemisphere (0.15 vs. 0.06, p=0.001). The F-18-FDG PET SUVmax was significantly lower on the lesioned side (11.28 vs. 13.92, p=0.001). Subgroup analyses revealed that the recent group (<6 months) had a higher lesion-to-contralateral region ratio SUVmax than the remote group (>6 months) (6.73 vs. 2.36, p<0.05). Our results provide molecular imaging evidence of angiogenesis in patients with severe chronic ICAD. Furthermore, the extent of angiogenesis in chronic ICAD may be affected by the post-qualified event time interval, and not by infarction itself or the severity of the arterial lesion.
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