Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, June 24, 2023

Inflammation in stroke: initial CRP levels can predict poor outcomes in endovascularly treated stroke patients

You do realize predicting failure to recover doesn't do a damn bit of good in getting survivors recovered? Or are you that fucking clueless? Survivors want recovery, do the research that gets there!

Inflammation in stroke: initial CRP levels can predict poor outcomes in endovascularly treated stroke patients

Tom Finck1*, Philipp Sperl1, Moritz Hernandez-Petzsche1, Tobias Boeckh-Behrens1, Christian Maegerlein1, Silke Wunderlich2, Claus Zimmer1, Jan Kirschke1 and Maria Berndt1
  • 1Department of Diagnostic and Interventional Neuroradiology, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany
  • 2Department of Neurology, School of Medicine, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany

Background and purpose: Inflammation has been linked to poor prognoses in cardio- and cerebrovascular conditions. As it is known to increase after ischemia, C-reactive protein (CRP) may serve as a surrogate for systemic inflammation and thus be a hallmark of increased tissue vulnerability. The question arises whether CRP in the acute phase of ischemic stroke, prior to mechanical thrombectomy (MT), might help predict outcomes.

Materials and methods: A single-center collective of patients with large-vessel occlusion, who were treated via MT, was analyzed in this observational case–control study. Univariate and multivariate models were designed to test the prognostic value of inflammatory markers (CRP and leukocytosis) in predicting clinical outcomes (modified Rankin score >2) and all-cause mortality 90 days after MT.

Results: A total of 676 ischemic stroke patients treated with MT were included. Of these, 313 (46.3%) showed elevated CRP levels (≥5 mg/l) on admission. Poor clinical outcome and mortality at 90 days occurred in 113 (16.7%) and 335 (49.6%) patients and significantly more frequently when initial CRP levels were elevated [213 (64.5%) vs. 122 (42.1%), p < 0.0001, and 79 (25.2%) vs. 34 (9.4%), p < 0.0001, respectively]. CRP levels were highly predictive for impaired outcomes, especially in patients with atrial fibrillation, in both univariate and multivariate models. Interestingly, patients with initially elevated CRP levels also showed more pronounced increases in CRP post-MT.

Conclusion: Poor outcome and death occur significantly more often in stroke patients with elevated CRP levels before MT. Our findings suggest that stroke patients with atrial fibrillation and elevated inflammatory markers are of particular risk for poor outcomes.

Introduction

Outcomes in ischemic stroke have improved greatly over the last decades in large part due to the wider availability of specialized stroke units as well as the establishment of endovascular therapy as the standard of care for patients who present with acute large-vessel occlusions (LVOs) (15). In recent years, the indication for mechanical thrombectomy (MT) has been extended, e.g., to later time windows and smaller vessels, with procedural techniques being continuously improved (6, 7).

Nonetheless, ischemic stroke continues to pose a significant burden as it remains a main cause of morbidity and mortality worldwide and accounts for a large proportion of quality-adjusted life years lost (8). Many multiparametric models for predicting good clinical outcomes after endovascularly treated stroke include obvious confounders, such as time to treatment or the success of revascularization. However, despite successful reperfusion in good time windows, the long-term clinical trajectory is not always as favorable as expected. Some mechanisms conveying adverse outcomes remain ill-explained, especially as complex markers such as neuronal damage serum proteins may also play an important and yet poorly understood role in influencing outcomes (9, 10).

Pro-inflammatory systemic environments have recently been identified to independently predict poor outcomes in a panoply of conditions, from ischemic heart disease to carotid atherosclerosis progression, as well as ischemic stroke treated via intravenous thrombolysis (1115). Moreover, the more delayed cellular inflammation conveyed by leukocytosis has been shown to correlate with poor outcome after MT (16). All these observations are hinting at the role that neuro-inflammation could have in post-ischemic brain remodeling.

High-sensitivity C-reactive protein (CRP) is an accessible serum protein known to be a reliable marker for systemic inflammation but also mediate pro-inflammatory downstream cascades, making it a suitable candidate to assess the level of intra-individual inflammation (17, 18). Moreover, the observation that most stroke patients showcase high-CRP levels is noteworthy given that activation of the secondary complement system and subsequent secondary brain damage through CRP has been shown experimentally (19).

It remains unclear whether CRP is elevated in response to ischemia-induced neuronal damage or whether pro-inflammatory mechanisms themselves are causing a time-delayed injury of ischemic brain tissue, analogous to phenomena seen after thermic tissue shock (20). As inflammatory markers have been associated with atrial fibrillation and thromboembolic complications, it may also be conceivable that inflammation influences the pathogenesis of ischemic stroke (21).

Our assumption is that CRP levels in the very-early stage of ischemic stroke could be a hallmark of systemic inflammation and increase the ad hoc vulnerability of the brain tissue to ischemic stress as well as promote subsequent neuronal damage through mediation of a post-ischemic ischemia-inflammation cascade. Identification of this association would add to current knowledge in stroke care, identify patients at risk benefitting from the most intensified and early anti-inflammatory therapy regimes, and advocate for future interventional studies (22).

To address those questions, the present study aims to investigate an association of inflammatory blood markers (CRP and leukocytosis) with neurological outcome and mortality in a large cohort of ischemic stroke patients with LVO treated with MT.

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