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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  68 Ga-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  68 Ga-NOTA-PRGD2 uptake in the peri-infarct, subcortical, and periventricular regions of the lesioned side, with a higher  68 Ga-NOTA-PRGD2 SUV max  compared to that in the contralateral hemisphere (0.15 vs. 0.06, p=0.001). The  18 F-FDG PET SUV max  was significantly lower on the lesioned side (11.28 vs. 13.92, p=0.001). Subgroup analyses revealed that the recent group ( 6 months) (6.73 vs. 2.36, p&lt;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.

journal of cerebral blood flow and metabolism

Imaging angiogenesis using <sup>68</sup>Ga-NOTA-PRGD2 positron emission tomography/computed tomography in patients with severe intracranial atherosclerotic disease

Imaging angiogenesis using 68Ga-NOTA-PRGD2 positron emission tomography/computed tomography in patients with severe intracranial atherosclerotic disease

Imaging angiogenesis using ⁶⁸Ga-NOTA-PRGD2 positron emission tomography/computed tomography in patients with severe intracranial atherosclerotic disease