Role of Computational Fluid Dynamics for Predicting Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage: Study Protocol for a Multicenter Prospective Study

2019 ◽  
pp. 161-164
Author(s):  
Masato Shiba ◽  
◽  
Fujimaro Ishida ◽  
Fumitaka Miya ◽  
Tomohiro Araki ◽  
...  
Keyword(s):  
Fluid Dynamics ◽  
Computational Fluid Dynamics ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Prospective Study ◽  
Study Protocol ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Multicenter Prospective Study

scholarly journals Role of Endothelin-1 in Human Aneurysmal Subarachnoid Hemorrhage: Associations with Vasospasm and Delayed Cerebral Ischemia

2011 ◽  
Vol 15 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Bhavani P. Thampatty ◽  
Paula R. Sherwood ◽  
Matthew J. Gallek ◽  
Elizabeth A. Crago ◽  
Dianxu Ren ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Endothelin 1

scholarly journals Role of ABO blood type in delayed cerebral ischemia onset and clinical outcomes after aneurysmal subarachnoid hemorrhage in an ethnic minority urban population

2020 ◽  
Vol 11 ◽  
pp. 108
Author(s):  
Santiago René Unda ◽  
Tarini Vats ◽  
Rafael De la Garza Ramos ◽  
Phillip Cezaryirli ◽  
David J. Altschul
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Clinical Outcomes ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Univariate Analysis ◽  
Delayed Cerebral Ischemia ◽  
Blood Type ◽  
Academic Center ◽  
Abo Blood Type

Background: In recent years, the role of ABO blood type moved into focus through the discovery of different hemostaseologic properties with importance in many diseases including subarachnoid hemorrhage (SAH). However, the role of ABO blood type in delayed cerebral ischemia (DCI) onset, clinical progress, and outcome after SAH is to date largely unexplored. Our aim was to explore the role of ABO blood group in DCI and clinical outcomes after aneurysmal SAH (aSAH). Methods: A retrospective analysis was made with data collected from patients who presented aSAH at our single- academic center from 2015 to 2018. We included demographic, clinical, and imaging variables in the univariate analysis and in the subsequent multivariate analysis. Results: A total of 204 patients were included in this study. About 17.9% of “O” type patients developed a DCI while DCI was reported in only 8.2% of non-O type patients (P = 0.04). “O” type was an independent risk after in the logistic regression after adjusting for significant factors in the univariate analysis (OR=2.530, 95% CI: 1.040- 6.151, P = 0.41). Compared to “non-O” type patients, “O” type patients had a trend to have poorer outcomes at discharge (25.5% vs. 21.3%, P = 0.489) and at 12–18 months (21.1% vs. 19.5%, P = 0.795). However, there were no significant differences. Conclusion: Our study evidenced that patients with “O” blood type have higher risk of DCI onset after aSAH. Although these findings need to be confirmed, they may aid to improve DCI prevention and outcome predictions.

scholarly journals The Role of the Glycocalyx in the Pathophysiology of Subarachnoid Hemorrhage-Induced Delayed Cerebral Ischemia

2021 ◽  
Vol 9 ◽  
Author(s):  
Hanna Schenck ◽  
Eliisa Netti ◽  
Onno Teernstra ◽  
Inger De Ridder ◽  
Jim Dings ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurovascular Unit ◽  
Delayed Cerebral Ischemia ◽  
Treatment Strategies ◽  
Early Brain Injury

The glycocalyx is an important constituent of blood vessels located between the bloodstream and the endothelium. It plays a pivotal role in intercellular interactions in neuroinflammation, reduction of vascular oxidative stress, and provides a barrier regulating vascular permeability. In the brain, the glycocalyx is closely related to functions of the blood-brain barrier and neurovascular unit, both responsible for adequate neurovascular responses to potential threats to cerebral homeostasis. An aneurysmal subarachnoid hemorrhage (aSAH) occurs following rupture of an intracranial aneurysm and leads to immediate brain damage (early brain injury). In some cases, this can result in secondary brain damage, also known as delayed cerebral ischemia (DCI). DCI is a life-threatening condition that affects up to 30% of all aSAH patients. As such, it is associated with substantial societal and healthcare-related costs. Causes of DCI are multifactorial and thought to involve neuroinflammation, oxidative stress, neuroinflammation, thrombosis, and neurovascular uncoupling. To date, prediction of DCI is limited, and preventive and effective treatment strategies of DCI are scarce. There is increasing evidence that the glycocalyx is disrupted following an aSAH, and that glycocalyx disruption could precipitate or aggravate DCI. This review explores the potential role of the glycocalyx in the pathophysiological mechanisms contributing to DCI following aSAH. Understanding the role of the glycocalyx in DCI could advance the development of improved methods to predict DCI or identify patients at risk for DCI. This knowledge may also alter the methods and timing of preventive and treatment strategies of DCI. To this end, we review the potential and limitations of methods currently used to evaluate the glycocalyx, and strategies to restore or prevent glycocalyx shedding.

Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage

2021 ◽  
pp. 0271678X2110208
Author(s):  
Ari Dienel ◽  
Peeyush Kumar T ◽  
Spiros L Blackburn ◽  
Devin W McBride
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Blood Vessel ◽  
Vascular Function ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Aneurysm Rupture ◽  
Large Artery ◽  
Major Contributor

Aneurysmal subarachnoid hemorrhage (aSAH) patients develop delayed cerebral ischemia and delayed deficits (DCI) within 2 weeks of aneurysm rupture at a rate of approximately 30%. DCI is a major contributor to morbidity and mortality after SAH. The cause of DCI is multi-factorial with contributions from microthrombi, blood vessel constriction, inflammation, and cortical spreading depolarizations. Platelets play central roles in hemostasis, inflammation, and vascular function. Within this review, we examine the potential roles of platelets in microthrombi formation, large artery vasospasm, microvessel constriction, inflammation, and cortical spreading depolarization. Evidence from experimental and clinical studies is provided to support the role(s) of platelets in each pathophysiology which contributes to DCI. The review concludes with a suggestion for future therapeutic targets to prevent DCI after aSAH.

scholarly journals The Role of Cortical Spreading Depolarizations in Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage

2018 ◽  
Vol 22 (1) ◽  
pp. 45-53
Author(s):  
Norberto Andaluz ◽  
Mario Zuccarello ◽  
Jens P. Dreier ◽  
Jed A. Hartings
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Cortical Lesions ◽  
Regional Cerebral Blood ◽  
Arterial Spasm ◽  
Energy Substrates ◽  
Ischemic Complications

Delayed cerebral ischemia (DCI) is the leading potentiallytreatable cause of mortality and disability in patients with aneurysmal subarachnoid hemorrhage (SAH). However, to date there is no effective treatment for this entity. The recently demonstrated lack of clinical response to pharmacologic reversal of arterial spasm as a result of SAH has spurred a reassessment of the pathophysiological concepts on DCI that follows SAH. DCI was long believed the consequence of the angiographically visible arterial spasm observed in patients with SAH. Since the measurement of cortical spreading depolarizations (CSD) in patients with SAH, increasing evidence has suggested a role for these phenomena in the pathophysiology of DCI. When inducedin a healthy brain, CSDs are associated with an increasein regional cerebral blood flow that facilitates the delivery ofthe necessary energy substrates for cellular repolarization. In a brain that has been injured, however, CSDs can induce microvascular constriction, or cortical spreading ischemia. This inverse hemodynamic response to CSD was first discovered in an animal model replicating the conditions following SAH, and later demonstrated in patients with SAH. The spreading ischemia leads to energy substrates shortage and hypoxia, resulting in cortical lesions, and may explain similar lesion patterns which occur in SAH patients. This review describes the salient characteristics of CSD and its potential relevance in the pathophysiology, monitoring, and treatment of ischemic complications following SAH.

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