I'D HAVE ALL OF YOU FIRED FOR EXTREME INCOMPETENCY IN NOT SOLVING STROKE; just useless descriptions/predictions of problems!
Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? Your patients need an explanation of why you aren't trying to get survivors recovered.
Why isn't your 'professional' solving stroke?
Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!
Evaluating predictive models for hemorrhagic transformation post-mechanical thrombectomy in acute ischemic stroke
Jiaxuan Wang1,2†, Jianyou You1†, Hui Yang1,2, Zhongbin Xia1, Xiangbin Wu1, Moxin Wu2,3, Xiaoping Yin1,2* and Zhiying Chen1,2*
1Department of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China
2Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China
3Department of Medical Laboratory, Affiliated Hospital of Jiujiang University, Jiujiang, Jiangxi, China
Edited by
Tao-Ran Li, Nanjing Medical University, China
Reviewed by
Diyang Lyu, Beijing University of Chinese Medicine, China
Archana Hinduja, The Ohio State University, United States
*Correspondence
Xiaoping Yin, xiaopingbuxiao@126.com
Zhiying Chen, zychenjj@jju.edu.cn
†These authors have contributed equally to this work
Received 02 January 2025
Accepted 09 June 2025
Published 25 June 2025
Citation
Wang J, You J, Yang H, Xia Z, Wu X, Wu M, Yin X and Chen Z (2025) Evaluating predictive models for hemorrhagic transformation post-mechanical thrombectomy in acute ischemic stroke. Front. Neurol. 16:1549057. doi: 10.3389/fneur.2025.1549057
Acute ischemic stroke (AIS), a condition defined by a decrease in cerebral blood flow, is primarily treated through mechanical thrombectomy (MT) for blockages in major anterior circulation arteries. Approaches encompass stent retrieval, suction thrombectomy, or a combination of both. MT is increasingly recognized for its rapid revascularization, low hemorrhagic transformation (HT) rate, and extended therapeutic time window. Nonetheless, multiple risk factors lead to post-MT HT through different mechanisms, resulting in adverse outcomes such as increased mortality and morbidity. Therefore, assessing the relevant risks based on predictive models for post-MT HT is necessary. These predictive models incorporate a series of risk factors and conduct statistical analyses to generate corresponding assessment scales, which are then used to evaluate the risk of postoperative bleeding. As this is a rapidly developing field, there is still controversy over which model is more effective than another in improving clinical efficacy, and there is a lack of consensus on the comparison of these data. In this paper, we assess the accuracy of these predictive models using receiver operating characteristic (ROC) curves and the concordance C-index. Determining the most accurate predictive model for post-MT HT is crucial for improving the prediction of patient outcomes and for the development of tailored treatment plans, thereby enhancing clinical relevance and applicability.
Keywords
acute ischemic stroke, mechanical thrombectomy, hemorrhagic transformation, symptomatic intracranial hemorrhage, predictive methods
1 Introduction
Stroke is the leading cause of death and disability worldwide (1). Acute ischemic stroke (AIS) is the predominant type of stroke, constituting more than 80% of all strokes (2). AIS is characterized by an acute episode marked by the occlusion of arterial vessels that supply blood to the brain tissue (3). The onset of the disease results in ischemic blood flow and oxygen deprivation to the brain tissues, manifesting as neurological deficit symptoms (4). Thrombosis is a common underlying mechanism of AIS, and the blockage of cerebral blood flow leads to a series of pathophysiological changes (5) and is also a major cause of morbidity and mortality (6). Effective thrombus management is central to stroke treatment, and advances in thrombus research are helping to improve the efficacy of AIS therapy (7). Studies have shown that the process of thrombus formation involves platelet and coagulation factor pathways (8). After endothelial injury, exposed collagen promotes platelet activation and adhesion to the vessel wall (8), releasing adenosine diphosphate (forming platelet thrombi) (9) and thromboxane A2 (further promoting aggregation) (10). Concurrently, thrombin converts fibrinogen into fibrin (11), while tissue factor from injured vessels activates coagulation factors (FVII, FX, FIX, FII), resulting in fibrin formation (12). In addition, immune mediators are involved, with neutrophils releasing neutrophil extracellular traps and monocytes contributing to red blood cell (RBC) recruitment and fibrin formation (13) (Figure 1). Research shows thrombi have a dense outer shell of fibrin, vascular hemophilic factor, and platelets, with an inner core of erythrocytes, fibrin fibers, and platelets (14). The heterogeneous nature of thrombi is also confirmed by Senna's work (15). Thrombus removal via thrombolysis or mechanical thrombectomy (MT) is limited by factors like time window and thrombus composition (16). RBC-rich thrombi, with low viscosity and high RBC/platelet concentrations (17–20), are more prone to migration (21). Rapidly restoring cerebral blood flow is critical for focal cerebral ischemia. New experimental discoveries, such as targeting pyruvate kinase M2 (22) and using the elastase inhibitor peptide ShSPI (derived from the venom of Scolopendra hainanum), show promise in improving AIS outcomes (23). However, these findings have not been validated by large randomized clinical controlled trials, and therefore thrombolysis remains the mainstay of current treatments, with MT being more widely used. Intravenous injection alteplase or tenecteplase within 4.5 h of AIS shows comparable thrombolytic efficacy and improves 3–6 month functional outcomes. However, due to the strict time window and relatively low recanalization rate, fewer than 5% of AIS patients currently benefit from this treatment (24–26). Emerging evidence indicates that endovascular thrombus extraction within 24 h post-AIS onset (3), i.e., MT, can significantly improve the rate of favorable prognosis and reduce disability. Anterior circulation large vessel occlusion (aLVO) is an important cause of AIS (27). Thereby obstructing blood flow to the anterior part of the brain and precipitating AIS. Numerous randomized clinical trials have established MT as the standard therapy for AIS due to aLVO, with a high reperfusion rate of up to 80% and advantages such as rapid reperfusion, low bleeding conversion rate, and an extended treatment time window (28–32). It is gradually becoming more widely used in clinical treatment.
FIGURE 1
After the endothelial injury, exposed collagen triggers platelet adhesion to the vessel wall. These activated platelets release ADP and TXA2, leading to platelet aggregation and plug formation. They also release thrombin, which converts fibrinogen to fibrin. The injured vessel introduces tissue factors, starting a coagulation cascade that activates several coagulation factors and results in fibrin formation. Immune cells like neutrophils and monocytes play a role, with neutrophils releasing NETs and monocytes aiding in RBC recruitment and fibrin formation. TXA2, thromboxane A2; ADP, adenosine diphosphate; PAR, protease-activated receptor; GP, glycoprotein; VWF, von Willebrand factor; NET, neutrophil extracellular trap; RBC, red blood cell; TLR, toll-like receptor; PSGL-1, P-selectin glycoprotein ligand-1. Created with biorender.
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