Acute development of collateral circulation and therapeutic prospects in ischemic stroke

In acute ischemic stroke, collateral circulation plays an important role in maintaining blood flow to the tissue that is at risk of progressing into ischemia, and in increasing the successful recanalization rate without hemorrhagic transformation. We have reported that well-developed collateral circulation is associated with smaller infarct volume and better long-term neurological outcome, and it disappears promptly once the effective recanalization is achieved. Contrary to the belief that collateral vessels develop over time in chronic stenotic condition, there exists a phenomenon that collateral circulation develops immediately in acute stenosis or occlusion of the arteries and it seems to be triggered by fluid shear stress, which occurs between the territories of stenotic/occluded arteries and those fed by surrounding intact arteries. We believe that this acute development of collateral circulation is a target of novel therapeutics in ischemic stroke and refer our recent attempt in enhancing collateral circulation by modulating sphingosine-1-phosphate receptor 1, which is a known shear-stress mechanosensing protein.

[1]  M. Tomita,et al.  Significance of Development and Reversion of Collaterals on MRI in Early Neurologic Improvement and Long-Term Functional Outcome after Intravenous Thrombolysis for Ischemic Stroke , 2015, American Journal of Neuroradiology.

[2]  H. Mizusawa,et al.  Sphingosine-1-Phosphate Receptor-1 Selective Agonist Enhances Collateral Growth and Protects against Subsequent Stroke , 2015, PloS one.

[3]  F. Shi,et al.  Combination of the Immune Modulator Fingolimod With Alteplase in Acute Ischemic Stroke: A Pilot Trial , 2015, Circulation.

[4]  R. Ransohoff,et al.  Sphingosine 1-phosphate signaling at the blood-brain barrier. , 2015, Trends in molecular medicine.

[5]  M. Hoehn,et al.  Poststroke angiogenesis, con: dark side of angiogenesis. , 2015, Stroke.

[6]  R. Anne Stetler,et al.  Vascular remodeling after ischemic stroke: Mechanisms and therapeutic potentials , 2014, Progress in Neurobiology.

[7]  J. Szostak,et al.  Physical training and hypertension have opposite effects on endothelial brain-derived neurotrophic factor expression. , 2013, Cardiovascular research.

[8]  P. Barber,et al.  Failure of Collateral Blood Flow is Associated with Infarct Growth in Ischemic Stroke , 2013, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[9]  M. Tomita,et al.  Posterior Cerebral Artery Laterality on Magnetic Resonance Angiography Predicts Long-Term Functional Outcome in Middle Cerebral Artery Occlusion , 2013, Stroke.

[10]  MasahikoIchijo,et al.  Posterior Cerebral Artery Laterality on Magnetic Resonance Angiography Predicts Long-Term Functional Outcome in Middle Cerebral Artery Occlusion , 2013 .

[11]  D. Liebeskind,et al.  Imaging Evaluation of Collaterals in the Brain: Physiology and Clinical Translation , 2013, Current Radiology Reports.

[12]  S. Olindo,et al.  Fluid-attenuated inversion recovery vascular hyperintensity: an early predictor of clinical outcome in proximal middle cerebral artery occlusion. , 2012, Archives of neurology.

[13]  S. Rafii,et al.  Flow-regulated endothelial S1P receptor-1 signaling sustains vascular development. , 2012, Developmental cell.

[14]  D. Liebeskind,et al.  Collateral Flow Averts Hemorrhagic Transformation After Endovascular Therapy for Acute Ischemic Stroke , 2011, Stroke.

[15]  S. Schwab,et al.  Characteristics and Outcome of Patients with Early Complete Neurological Recovery after Thrombolysis for Acute Ischemic Stroke , 2010, Cerebrovascular Diseases.

[16]  C. Levi,et al.  The independent predictive utility of computed tomography angiographic collateral status in acute ischaemic stroke. , 2009, Brain : a journal of neurology.

[17]  W. Schaper,et al.  Trpv4 induces collateral vessel growth during regeneration of the arterial circulation , 2009, Journal of cellular and molecular medicine.

[18]  D. Liebeskind,et al.  Occurence and variability in acute formation of leptomeningeal collaterals in proximal middle cerebral artery occlusion. , 2008, Journal of vascular and interventional neurology.

[19]  F Viñuela,et al.  Impact of collateral flow on tissue fate in acute ischaemic stroke , 2007, Journal of Neurology, Neurosurgery, and Psychiatry.

[20]  上村 昭博.  Prominent laterality of the posterior cerebral artery at three-dimensional time-of-flight MR angiography in M1-segment middle cerebral artery occlusion , 2007 .

[21]  J. Pearlman,et al.  Impact of Mouse Strain Differences in Innate Hindlimb Collateral Vasculature , 2005, Arteriosclerosis, thrombosis, and vascular biology.

[22]  David A. Schultz,et al.  A mechanosensory complex that mediates the endothelial cell response to fluid shear stress , 2005, Nature.

[23]  S. Windecker,et al.  Is There Functional Collateral Flow During Vascular Occlusion in Angiographically Normal Coronary Arteries? , 2003, Circulation.

[24]  Jess Li,et al.  Vascular endothelial cells synthesize and secrete brain‐derived neurotrophic factor , 2000, FEBS letters.

[25]  M. Hennerici,et al.  Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. , 1998, Archives of neurology.

[26]  J. Cooke,et al.  Fluid shear stress induces endothelial transforming growth factor beta-1 transcription and production. Modulation by potassium channel blockade. , 1995, The Journal of clinical investigation.