Development and validation of a nomogram for cerebral hemorrhage in patients with carotid stenosis undergoing stenting: a multicenter retrospective study

Do you not understand, prediction is useless for stroke survivors? It does nothing to get them recovered. There are a lot of mentors and senior researchers that  need to be re-educated on the purpose of stroke research. The only goal in stroke is 100% recovery; not biomarkers, prediction, prognosis or other useless shit! 

Why are you stenting at all? Verify that the Circle of Willis is complete, close up the offending artery and you won't have to deal with all these complications!

My right carotid artery was closed for 10 years and I cognitively functioned quite well with no episodes of fainting.

 Here is why your doctor needs to guarantee NO complications from stenting!

• stenting (22 posts to May 2011)

• carotid stenting (21 posts to May 2016)

• carotid artery stenting (7 posts to November 2021)

 

A nomogram, also called a nomograph, alignment chart, or abac, is a graphical calculating device, a two-dimensional diagram designed to allow the approximate graphical computation of a mathematical function.

 

 Development and validation of a nomogram for cerebral hemorrhage in patients with carotid stenosis undergoing stenting: a multicenter retrospective study

1. Xianjun Zhang1,
2. Xiaoliang Wang2,
3. Teng Ma3,
4. http://orcid.org/0000-0002-3306-1892Wentao Gong4,
5. Yong Zhang1,
6. Naidong Wang1

1. Correspondence to Professor Naidong Wang; wangnaidong163@163.com; Professor Yong Zhang; bravezhang@126.com

Abstract

Background Hyperperfusion-induced cerebral hemorrhage (HICH) is a rare but severe complication in patients with carotid stenosis undergoing stent placement for which predictive models are lacking. Our objective was to develop a nomogram to predict such risk.

Methods We included a total of 1226 patients with carotid stenosis who underwent stenting between June 2015 and December 2022 from three medical centers, divided into a development cohort of 883 patients and a validation cohort of 343 patients. The model used LASSO regression for feature optimization and multivariable logistic regression to develop the predictive model. Model accuracy was assessed via the receiver operating characteristic curve, with further evaluation of calibration and clinical utility through calibration curves and decision curve analysis (DCA). The model underwent internal validation using bootstrapping and external validation with the validation cohort.

Results Older age (OR 1.07, p=0.005), higher degrees of carotid stenosis (OR 1.07, p=0.006), poor collateral circulation (OR 6.26, p<0.001), elevated preoperative triglyceride levels (OR 1.27, p=0.041) and neutrophil counts (OR 1.36, p<0.001) were identified as independent risk factors for HICH during hospitalization. The nomogram constructed based on these predictive factors demonstrated an area under the curve (AUC) of 0.817. The AUCs for internal and external validation were 0.809 and 0.783, respectively. Calibration curves indicated good model fit, and DCA confirmed substantial clinical net benefit in both cohorts.

Conclusion We developed and validated a nomogram to predict(NOT PREVENT!) HICH in patients with carotid stenosis post-stenting, facilitating early identification and preventive intervention in high-risk individuals.

Data availability statement

Data are available upon reasonable request. The data supporting the conclusions of this study are available from the corresponding author upon reasonable request at wangnaidong163@163.com.

https://doi.org/10.1136/jnis-2024-022022

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Nomogram to predict prognosis in patients with posterior circulation acute ischemic stroke after mechanical thrombectomy

 Do you not understand, prognosis is useless for stroke survivors? It does nothing to get them recovered. There are a lot of mentors and senior researchers that  need to be re-educated on the purpose of stroke research. The only goal in stroke is 100% recovery; not biomarkers, prediction, prognosis or other useless shit!

Nomogram to predict prognosis in patients with posterior circulation acute ischemic stroke after mechanical thrombectomy

Jiayang LiJin ZhangChangxin LiJun LiXupeng WuShaoshuai Wang^*

• Department of Neurology, First Hospital of Shanxi Medical University, Taiyuan, China

Purpose: This study aimed to investigate the risk factors of prognosis and hemorrhagic transformation after mechanical thrombectomy (MT) in patients with posterior circulation acute ischemic stroke (PC-AIS) caused by large vessel occlusion. We sought to develop a nomogram for predicting the risk of poor prognosis and symptomatic intracerebral hemorrhage (sICH) in patients with PC-AIS.

Methods: A retrospective analysis was conducted on 81 patients with PC-AIS who underwent MT treatment. We collected clinical information from the patients to assessed sICH and prognosis based on CT results and National Institutes of Health Stroke Scale (NIHSS) scores. Subsequently, they were followed up for 3 months, and their prognosis was assessed using the Modified Rankin Scale. We used the least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression to determine the factors affecting prognosis to construct a nomogram. The nomogram’s performance was assessed through receiver operating characteristic curves, calibration curves, decision curve analysis, and clinical impact curves.

Results: Among the 81 patients with PC-AIS, 33 had a good prognosis, 48 had a poor prognosis, 19 presented with sICH, and 62 did not present with sICH. The results of the LASSO regression indicated that variables, including HPT, baseline NIHSS score, peak SBP, SBP CV, SBP SD, peak SBP, DBP CV, HbA1c, and BG SD, were predictors of patient prognosis. Variables such as AF, peak SBP, and peak DBP predicted the risk of sICH. Multivariate logistic regression revealed that baseline NIHSS score (OR = 1.115, 95% CI 1.002–1.184), peak SBP (OR = 1.060, 95% CI 1.012–1.111), SBP CV (OR = 1.296, 95% CI 1.036–1.621) and HbA1c (OR = 3.139, 95% CI 1.491–6.609) were independent risk factors for prognosis. AF (OR = 6.823, 95% CI 1.606–28.993), peak SBP (OR = 1.058, 95% CI 1.013–1.105), and peak DBP (OR = 1.160, 95% CI 1.036–1.298) were associated with the risk of sICH. In the following step, nomograms were developed, demonstrating good discrimination, calibration, and clinical applicability.

Conclusion: We constructed nomograms to predict poor prognosis and risk of sICH in patients with PC-AIS undergoing MT. The model exhibited good discrimination, calibration, and clinical applicability.

1 Introduction

Acute ischemic stroke (AIS) is the leading cause of disability and mortality, posing a severe threat to human well-being (1). Research on the Chinese population reveals that, in 2020, there were 15.5 million cases of ischemic stroke among adults >40 years, with a prevalence rate of approximately 2.3/100 people (2). Over 30% of AIS cases result from large vessel occlusion (LVO) (3). LVO causes ischemia and hypoperfusion in the affected area, and timely restoration of perfusion to the ischemic area can maintain brain cell activity. Thrombolysis treatment by intravenous recombinant tissue plasminogen activator is accessible within a 4.5 h window from the onset of symptoms. However, it is not always feasible owing to missed time windows or contraindications. In recent years, mechanical thrombectomy (MT) development has provided new treatment options for patients with AIS. MT treatment is safe and effective for patients with anterior circulation AIS (AC-AIS), extending the treatment time to 6–24 h (4).

Compared with AC-AIS, posterior circulation AIS (PC-AIS) occurs in the vertebrobasilar system-supplied area, resulting in a worse prognosis (5). The early symptoms of PC-AIS are mild and unspecific, making identification challenging. Therefore, patients with PC-AIS have a lower rate of benefit from intravenous thrombolysis than those with anterior circulation AIS, with only 1/6 of patients benefiting from this treatment (6). It indicates that MT is an important treatment for patients with PC-AIS. However, the outcome of MT treatment in PC-AIS remains controversial, with significant differences observed in four randomized controlled trials (RCTs). In the BEST and BASIC studies, no significant difference was observed in prognostic outcomes between the MT and drug therapy alone groups.

In contrast, the BAOCHE and ATTENTION studies indicated a more favorable prognosis for patients who underwent MT treatment (7–10). Most patients with PC-AIS can achieve revascularization after MT treatment; however, only 38% experience a good prognosis (11). Therefore, exploring the factors influencing prognosis can help clinicians identify patients at high risk of poor prognosis and provide more timely interventions. There are fewer studies on the factors influencing the prognosis of PC-AIS patients undergoing MT treatment. A meta-analysis revealed that hypertension and diabetes were associated with poor prognosis (12). Gao et al.’s study identified baseline National Institutes of Health Stroke Scale (NIHSS) score, posterior circulation acute stroke prognosis early computed tomography (PC-ASPECT) score, and modified thrombolysis in cerebral infarction (mTICI) classification as independent risk factors affecting patients’ prognosis (13).

Notably, no study investigates the impact of post-operative medical management on the risk of patients’ prognosis, and predictive models for poor prognosis and sICH are yet to be constructed. This study addresses these gaps by investigating factors affecting the prognosis and sICH of patients with PC-AIS undergoing MT and constructs a nomogram applicable to clinical practice. We aimed to guide targeted clinical interventions to improve the management of patients with PC-AIS and enhance their post-treatment prognosis.

Reclassification and risk stratification of embolic stroke of undetermined source by ASCOD phenotyping

So you described something, WHAT THE FUCK DO SURVIVORS DO WITH IT TO PREVENT THE NEXT STROKE? Nothing? Then totally useless research. The mentors and senior researchers need re-education in the point of stroke research.     100% RECOVERY!

Reclassification and risk stratification of embolic stroke of undetermined source by ASCOD phenotyping

Takao Hoshinohttps://orcid.org/0000-0002-2477-9755, Takafumi Mizuno, Ayako Nishimura, Kentaro Ishizuka, Sono Toi, Shuntaro Takahashi, Sho Wako, and Kazuo Kitagawahttps://orcid.org/0000-0002-7669-231X
Background:

 

Common vascular diseases underlying stroke, including atherosclerosis, small-vessel disease (SVD), and cardioembolic pathology, can be present in patients with embolic stroke of undetermined source (ESUS), although these are not direct causes of stroke.
 

Aims: 

 

To describe the frequency and degree of the three major diseases using atherosclerosis, SVD, cardiac pathology, other causes, and dissection (ASCOD) phenotyping and to assess their prognostic implications in ESUS.
 

Methods:

 

 In this prospective observational study, 221 patients with ESUS within 1 week of onset were consecutively enrolled and followed up for 1 year. Vascular diseases associated with stroke were assessed using the ASCOD classification. The primary outcome was a composite of nonfatal stroke, nonfatal acute coronary syndrome, and vascular death.
 

Results:

 

Among 221 patients (mean age, 69.6 years; male, 59.7%), 135 (61.1%), 102 (46.2%), and 107 (48.4%) had any grade of atherosclerosis (A2 or A3), SVD (S3), and cardiac pathology (C2 or C3), respectively. ESUS patients graded as A2 or A3 (i.e. ipsilateral atherosclerotic plaque, contralateral ⩾ 50% stenosis, or aortic arch plaque) were at a significantly higher risk of composite vascular events than those graded as A0 (i.e. no atherosclerotic disease) (adjusted hazard ratio (95% confidence interval), 2.40 (1.01–5.72). No differences were observed in the event risk between patients with S3 (i.e. magnetic resonance imaging evidence of SVD) and S0 (i.e. no SVD) and between those with C2 or C3 (i.e. presence of any cardiac pathology) and C0 (i.e. no cardiac abnormalities).
 

Conclusions:

 

Atherosclerotic diseases corresponding to ASCOD grade A2 or A3 were predictive of recurrent vascular events in ESUS patients. Reclassification of ESUS using ASCOD phenotyping provides important clues for risk prediction and may guide optimal management strategies.

Brain zinc dyshomeostasis and glial cells in ischemic stroke

So you have identified a problem, useless with NO SOLUTION. Your mentors and senior researchers need re-education on the whole point of stroke research. 100% recovery for all.

Brain zinc  and glial cells in ischemic stroke

Higashi Y ¹ , 

Aratake T ¹ , 

Shimizu S ¹ , 

Shimizu T ¹ , 

Saito M ¹  

Affiliations

Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica [01 Jan 2019, 154(3):138-142]

Type: Review, Journal Article (lang: jpn)
DOI: 10.1254/fpj.154.138

Abstract

Zinc, an essential trace element, plays an important role in a large number of biological functions. In mammalian brain, whereas the majority of brain zinc is bound to proteins including metallothionein, about 5-15% is stored in presynaptic vesicles of glutamatergic neurons throughout the forebrain, especially in the hippocampus, in a relatively free state. Thus, free zinc (Zn2+) concentration in the brain is considered to be regulated in order to maintain normal brain functions such as learning and memory. On the other hand, brain Zn2+ dyshomeostasis has been recognized as a mechanism for neuronal injury in brain disorders including Alzheimer's disease and brain ischemia. In particular, after transient brain ischemia, Zn2+ accumulates in hippocampal neurons via a zinc transport system, or via release from cytosolic zinc-binding proteins, which results in neuronal cell death. Recently, it has been demonstrated that Zn2+ dyshomeostasis also occurs in glial cells such as microglia, astrocytes and oligodendrocytes after brain ischemia. In oligodendrocytes, ischemic insult triggers intracellular Zn2+ accumulation, resulting in cell death via mitochondrial dysfunction. Increased extracellular Zn2+ inhibits astrocytic glutamate uptake. In addition, extracellular Zn2+ massively released from ischemic neurons primes microglia to enhance production of pro-inflammatory cytokines in response to stimuli that trigger M1 activation. This review aims to describe the impact of brain Zn2+ dyshomeostasis on alterations in glial cell survival and functions in post-ischemic brains.

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