Systemic response of coated-platelet and peripheral blood inflammatory cell indices after aneurysmal subarachnoid hemorrhage and long-term clinical outcome

Ray, Bappaditya; Ross, Stephen R.; Danala, Gopichandh; Aghaei, Faranak; Nouh, Claire Delpirou; Ford, Lance; Hollabaugh, Kimberly; Karfonta, Brittany; Santucci, Joshua; Cornwell, Benjamin O.; Bohnstedt, Bradley N.; Zheng, Bin; Dale, George L.; Prodan, Călin I.

doi:10.1016/j.jcrc.2019.03.003

Cited by 24 publications

(12 citation statements)

References 30 publications

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“…Recently, Ray et al reported a rise and fall of the MPV:PLT ratio in patients with aSAH. They found that the MPV:PLT ratio was independently associated with the development of DCI and functional outcomes (14,28). In our study, a similar trend of the MPV:PLT ratio was observed (see Table 2).…”

Section: Discussionsupporting

confidence: 87%

Dynamic Change in Mean Platelet Volume and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Chen

Zhang

2020

Front. Neurol.

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Background: The mean platelet volume (MPV) has been shown to predict short-term outcomes in patients who have experienced aneurysmal subarachnoid hemorrhage (aSAH). The purpose of this study was to explore the temporal variation of MPV in patients with aSAH and its relationship to the development of delayed cerebral ischemia (DCI).Methods: Data from 197 consecutive aSAH patients who were treated at our institution between January 2017 and December 2019 were collected and analyzed. Blood samples to assess MPV were obtained at 1–3, 3–5, 5–7, and 7–9 d after the initial hemorrhage. Univariate and multivariate analyses were performed to investigate whether MPV was an independent predictor of DCI and the receiver operating characteristic (ROC) curve and area under the curve (AUC) were determined.Results: The MPV values in patients with DCI were significantly higher compared to those without DCI at 1–3, 3–5, 5–7, and 7–9 d after hemorrhage (P < 0.001). The trend for MPV in patients with DCI was increased at first and then decreased. The transition from increases to decreases occurred at 3–5 d after hemorrhage. The optimal cutoff value for MPV to accurately predict DCI was 10.35 fL at 3–5 d after aSAH in our cohort. Furthermore, the MPV observed at 3–5 d was an independent risk factor for DCI [odds ratio (OR) = 4.508, 95% confidence interval (CI): 2.665–7.626, P < 0.001].Conclusions: MPV is a dynamic variable that occurs during aSAH, and a high MPV at 3–5 days after hemorrhage is associated with the development of DCI.

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Section: Discussionsupporting

confidence: 87%

Dynamic Change in Mean Platelet Volume and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Chen

Zhang

2020

Front. Neurol.

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“…SAH causes a systemic inflammatory response syndrome (SIRS) that involves complex interactions amongst immune cells, inflammation, coagulation, sympathoadrenal activation, endothelial cell activation, and dysfunction [ 84 ]. This complex process leads to a procoagulant reaction, tissue hypoperfusion, microthrombosis, and compromised microcirculation, which ultimately leads to multiorgan failure [ 84 , 85 , 86 ]. Release of catecholamines into the systemic circulation following aSAH may cause arrhythmias and neurogenic pulmonary edema.…”

Section: Sirs Following Asahmentioning

confidence: 99%

“…Thus, there is no approved intervention as of yet for treating neuroinflammation following aSAH. Interestingly, it has been shown that using a multimodal monitoring approach can potentially aid the development of therapeutics targeting different aspects of the inflammatory cascade following aSAH [ 85 ]. Last but not least, it would be interesting to look at the effect of anti-inflammatory agents on shunt dependency.…”

Section: Sirs Following Asahmentioning

confidence: 99%

The Pathogenesis of Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage

Kuo

Huang

2021

IJMS

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Hydrocephalus is a common complication of aneurysmal subarachnoid hemorrhage (aSAH) and reportedly contributes to poor neurological outcomes. In this review, we summarize the molecular and cellular mechanisms involved in the pathogenesis of hydrocephalus following aSAH and summarize its treatment strategies. Various mechanisms have been implicated for the development of chronic hydrocephalus following aSAH, including alterations in cerebral spinal fluid (CSF) dynamics, obstruction of the arachnoid granulations by blood products, and adhesions within the ventricular system. Regarding molecular mechanisms that cause chronic hydrocephalus following aSAH, we carried out an extensive review of animal studies and clinical trials about the transforming growth factor-β/SMAD signaling pathway, upregulation of tenascin-C, inflammation-dependent hypersecretion of CSF, systemic inflammatory response syndrome, and immune dysregulation. To identify the ideal treatment strategy, we discuss the predictive factors of shunt-dependent hydrocephalus between surgical clipping and endovascular coiling groups. The efficacy and safety of other surgical interventions including the endoscopic removal of an intraventricular hemorrhage, placement of an external ventricular drain, the use of intraventricular or cisternal fibrinolysis, and an endoscopic third ventriculostomy on shunt dependency following aSAH were also assessed. However, the optimal treatment is still controversial, and it necessitates further investigations. A better understanding of the pathogenesis of acute and chronic hydrocephalus following aSAH would facilitate the development of treatments and improve the outcome.

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“…The findings of Tao et al also supported these results, as they found that an increased NLR was an independent factor that predicted the occurrence of DCI, with a sensitivity of 87.3% and a specificity of 48.4% ( 81 ). Ray et al carried out further studies on the dynamics of the NLR and found that NLR trends showed a significant initial decline followed by a gradual rise among those without DCI, whereas the NLR was persistently low in those patients that developed DCI in an early immune-depressed state after aSAH ( 76 ).…”

Section: Clinical Evidencementioning

confidence: 99%

“…The challenge is how to predict the occurrence of DCI and then formulate effective preventive strategies to reverse the development of DCI in advance ( 108 ). At present, four clinical studies have proven that the NLR is an independent prognostic factor for the occurrence of DCI with strong sensitivity and specificity ( 74 , 76 , 77 , 81 ). This implies that the NLR is promising as a new predictor for DCI to help classify patients and direct preventive treatment to those who are most likely to benefit.…”

Section: Practice Prospectsmentioning

confidence: 99%

The Role of the Blood Neutrophil-to-Lymphocyte Ratio in Aneurysmal Subarachnoid Hemorrhage

et al. 2021

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Aneurysmal subarachnoid hemorrhage (aSAH) is an important type of stroke with the highest rates of mortality and disability. Recent evidence indicates that neuroinflammation plays a critical role in both early brain injury and delayed neural deterioration after aSAH, contributing to unfavorable outcomes. The neutrophil-to-lymphocyte ratio (NLR) is a peripheral biomarker that conveys information about the inflammatory burden in terms of both innate and adaptive immunity. This review summarizes relevant studies that associate the NLR with aSAH to evaluate whether the NLR can predict outcomes and serve as an effective biomarker for clinical management. We found that increased NLR is valuable in predicting the clinical outcome of aSAH patients and is related to the risk of complications such as delayed cerebral ischemia (DCI) or rebleeding. Combined with other indicators, the NLR provides improved accuracy for predicting prognosis to stratify patients into different risk categories. The underlying pathophysiology is highlighted to identify new potential targets for neuroprotection and to develop novel therapeutic strategies.

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Systemic response of coated-platelet and peripheral blood inflammatory cell indices after aneurysmal subarachnoid hemorrhage and long-term clinical outcome

Cited by 24 publications

References 30 publications

Dynamic Change in Mean Platelet Volume and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Dynamic Change in Mean Platelet Volume and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

The Pathogenesis of Hydrocephalus Following Aneurysmal Subarachnoid Hemorrhage

The Role of the Blood Neutrophil-to-Lymphocyte Ratio in Aneurysmal Subarachnoid Hemorrhage

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