scholarly journals The Role of Urine F2-isoprostane Concentration in Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Haemorrhage—A Poor Prognostic Factor

Diagnostics ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 5
Author(s):  
Karol Wiśniewski ◽  
Marta Popęda ◽  
Bartłomiej Tomasik ◽  
Michał Bieńkowski ◽  
Ernest J. Bobeff ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Haemorrhage ◽  
Oxidative Stress Biomarkers ◽  
Poor Prognostic Factor ◽  
Non Invasive ◽  
Clinical Conditions

Background: The pathophysiology of delayed cerebral ischemia (DCI) remains unclear. One of the hypotheses suggests that reactive oxygen species play a role in its onset. Thus, we studied F2-isoprostanes (F2-IsoPs)—oxidative stress biomarkers. Our goal was to improve the early diagnosis of DCI in a non-invasive way. Methods: We conducted a prospective single center analysis of 38 aneurysmal subarachnoid hemorrhage patients. We assessed urine F2-IsoP concentration using immunoenzymatic arrays between the first and fifth day after bleeding. A correlation between urine F2-IsoP concentration and DCI occurrence was examined regarding clinical conditions and outcomes. Results: The urine F2-IsoP concentrations were greater than those in the control groups (p < 0.001). The 3rd day urine F2-IsoPs concentrations were correlated with DCI occurrence (p < 0.001) and long term outcomes after 12 months (p < 0.001). Conclusions: High levels of urine F2-IsoPs on day 3 can herald DCI.

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 Inflammation, Cerebral Vasospasm, and Evolving Theories of Delayed Cerebral Ischemia

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Kevin R. Carr ◽  
Scott L. Zuckerman ◽  
J Mocco
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Primary Role ◽  
Inflammatory Cascade ◽  
Exact Etiology ◽  
Intracellular Calcium Dynamics ◽  
Insight Into

Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific research has promulgated the theory that cerebral vasospasm plays a primary role in the pathology of DCI and subsequently delayed ischemic neurological decline (DIND). Approximately 70% of patients develop CVS after aSAH with 50% long-term morbidity rates. The exact etiology of CVS is unknown; however, a well-described theory involves an antecedent inflammatory cascade with alterations of intracellular calcium dynamics and nitric oxide fluxes, though the intricacies of this inflammatory theory are currently unknown. Consequently, there have been few advances in the clinical treatment of this patient cohort, and morbidity remains high. Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline. In this review, we discuss current theories implicating the inflammatory cascade in the development of CVS and potential treatment targets.

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.

scholarly journals Angiographic Findings in Refractory Delayed Cerebral Ischemia

2019 ◽  
Vol 38 (03) ◽  
pp. 157-165
Author(s):  
Nicolás González ◽  
Alvaro Ruiz ◽  
Jorge Mura
Keyword(s):  
Retrospective Study ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Anterior Communicating Artery ◽  
Microsurgical Clipping ◽  
Angiographic Vasospasm ◽  
Transit Times ◽  
Angiographic Findings

Background Delayed cerebral ischemia (DCI) follows a refractory course in a subgroup of patients with aneurysmal subarachnoid hemorrhage (SAH), leading to diffuse ischemic injury. The role of angiographic vasospasm (AV) is unknown. Our goal is to study the angiographic alterations and the clinical profile of refractory DCI patients. Methods Retrospective study of patients with SAH who presented with DCI treated with medical and endovascular therapy, with a refractory evolution, defined as multiple ischemic infarction and brain death. Results Out of a cohort of 336 patients, 7 (2%) developed refractory DCI. The median age of the patients was 48 (38–60) years old. Five patients had ruptured anterior communicating artery (ACoA) aneurysms. Four patients were treated with coil embolization, and three with microsurgical clipping. Angiographic vasospasm was classified as severe in 5 cases. Compromise of bilateral circulation was detected in six patients. Distal circulation vasospasm occurred in five cases. Slow circulatory transit times were observed in three patients. Conclusion Angiographic findings such as bilateral circulatory compromise and distal vasospasm were frequent alterations. Further studies are required to establish the association of these findings with the clinical outcomes.

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.

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