Hao Jiang1, Juan F Toscano2, Michael Schiraldi3, Shlee S Song4, Konrad H Schlick5, Oana M Dumitrascu6, Raymond Liou7, Patrick D Lyden8, Jianwei Pan9, Renya Zhan10, Jeffrey L Saver11, Nestor R Gonzalez12. 1. Department of Neurosurgery, Gonzalez Neurovascular Laboratory, Cedars-Sinai Medical Center, Los Angeles, California; Department of Neurosurgery, The First Affiliated Hospital of Zhejiang University-School of Medicine. Hangzhou, China. Electronic address: neurosurg_jh@163.com. 2. Department of Neurosurgery, Gonzalez Neurovascular Laboratory, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Juan.Toscano@cshs.org. 3. Department of Neurosurgery, Gonzalez Neurovascular Laboratory, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Michael.Schiraldi@cshs.org. 4. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Shlee.Song@cshs.org. 5. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Konrad.Schlick@cshs.org. 6. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Oana.Dumitrascu@cshs.org. 7. Stanford University, School of Medicine, Palo Alto, California. Electronic address: rliou@stanford.edu. 8. Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Patrick.Lyden@cshs.org. 9. Department of Neurosurgery, The First Affiliated Hospital of Zhejiang University-School of Medicine. Hangzhou, China. Electronic address: swordman_pan@aliyun.com. 10. Department of Neurosurgery, The First Affiliated Hospital of Zhejiang University-School of Medicine. Hangzhou, China. Electronic address: zyyyzry@163.com. 11. Department of Neurology, University of California Los Angeles, Los Angeles, California. Electronic address: JSaver@mednet.ucla.edu. 12. Department of Neurosurgery, Gonzalez Neurovascular Laboratory, Cedars-Sinai Medical Center, Los Angeles, California; Department of Neurology, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Nestor.Gonzalez@cshs.org.
Abstract
BACKGROUND: Vascular endothelial growth factor-A165 (VEGF-A165) has been identified as a combination of 2 alternative splice variants: proangiogenic VEGF-A165a and antiangiogenic VEGF-A165b. Intracranial atherosclerotic disease (ICAD) and moyamoya disease (MMD) are 2 main types of intracranial arterial steno-occlusive disorders with distinct capacities for collateral formation. Recent studies indicate that VEGF-A165 regulates collateral growth in ischemia. Therefore, we investigated if there is a distinctive composition of VEGF-A165 isoforms in ICAD and MMD. METHODS: Sixty-six ICAD patients, 6 MMD patients, and 5 controls were enrolled in this prospective study. ICAD and MMD patients received intensive medical management upon enrollment. Surgery was offered to 9 ICAD patients who had recurrent ischemic events, 6 MMD patients, and 5 surgical controls without ICAD. VEGF-A165a and VEGF-A165b plasma levels were measured at baseline, within 1 week after patients having surgery, and at 1, 3, and 6 months after treatment. RESULTS: A significantly higher baseline VEGF-A165a/b ratio was observed in MMD compared to ICAD (P = .016). The VEGF-A165a/b ratio increased significantly and rapidly after surgical treatment in ICAD (P = .026) more so than in MMD and surgical controls. In patients with ICAD receiving intensive medical management, there was also an elevation of the VEGF-A165a/b ratio, but at a slower rate, reaching the peak at 3 months after initiation of treatment (baseline versus 3 months VEGF-A165a/b ratio, P = .028). CONCLUSIONS: Our study shows an increased VEGF-A165a/b ratio in MMD compared to ICAD, and suggests that both intensive medical management and surgical revascularization elevate the VEGF-A165a/b ratio in ICAD patients.
BACKGROUND:Vascular endothelial growth factor-A165 (VEGF-A165) has been identified as a combination of 2 alternative splice variants: proangiogenic VEGF-A165a and antiangiogenic VEGF-A165b. Intracranial atherosclerotic disease (ICAD) and moyamoya disease (MMD) are 2 main types of intracranial arterial steno-occlusive disorders with distinct capacities for collateral formation. Recent studies indicate that VEGF-A165 regulates collateral growth in ischemia. Therefore, we investigated if there is a distinctive composition of VEGF-A165 isoforms in ICAD and MMD. METHODS: Sixty-six ICADpatients, 6 MMDpatients, and 5 controls were enrolled in this prospective study. ICAD and MMDpatients received intensive medical management upon enrollment. Surgery was offered to 9ICADpatients who had recurrent ischemic events, 6 MMDpatients, and 5 surgical controls without ICAD. VEGF-A165a and VEGF-A165b plasma levels were measured at baseline, within 1 week after patients having surgery, and at 1, 3, and 6 months after treatment. RESULTS: A significantly higher baseline VEGF-A165a/b ratio was observed in MMD compared to ICAD (P = .016). The VEGF-A165a/b ratio increased significantly and rapidly after surgical treatment in ICAD (P = .026) more so than in MMD and surgical controls. In patients with ICAD receiving intensive medical management, there was also an elevation of the VEGF-A165a/b ratio, but at a slower rate, reaching the peak at 3 months after initiation of treatment (baseline versus 3 months VEGF-A165a/b ratio, P = .028). CONCLUSIONS: Our study shows an increased VEGF-A165a/b ratio in MMD compared to ICAD, and suggests that both intensive medical management and surgical revascularization elevate the VEGF-A165a/b ratio in ICADpatients.
Authors: T Takahashi; C Kalka; H Masuda; D Chen; M Silver; M Kearney; M Magner; J M Isner; T Asahara Journal: Nat Med Date: 1999-04 Impact factor: 53.440
Authors: Miguel D Quintero-Consuegra; Juan F Toscano; Robin Babadjouni; Peyton Nisson; Mohammad N Kayyali; Daniel Chang; Eyad Almallouhi; Jeffrey L Saver; Nestor R Gonzalez Journal: Neurosurgery Date: 2021-03-15 Impact factor: 4.654