Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,793 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
1. Department of Neurology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China
2. Guilin Municipal People's Hospital, Guangxi Zhuang Autonomous Region, Guilin, China
Abstract
Background:
Although successful recanalization of the occluded artery is achieved, no-reflow phenomenon (NRP) becomes a main contributor to poor prognosis in patients with acute ischemic stroke. There are some laboratory results to represent biomarkers of the no-reflow phenomenon. However, few studies have characterized the metabolomic signature of NRP. Using high-performance liquid chromatography–tandem mass spectrometry (LC–MS)-based method, this study aims to characterize the plasma metabolites associated with NRP.
Methods:
A total of 34 patients with acute large vessel occlusion in anterior circulation who underwent successful thrombectomy with final angiographic expanded Treatment in Cerebral Infarction score of 2c-3 score were enrolled (19 without NRP and 15 with NRP). Fasting venous blood collected 24 h after the procedure was centrifuged and subjected to metabolomic analysis.
Results:
We identified 29 differentially expressed plasma metabolites, the majority of which were phosphatidylcholine (PC) species. Among them, PC(20:4(5Z,8Z,11Z,14Z)/P-16:0) showed the most significant alteration and exhibited robust predictive performance (AUC = 0.846). The most prominently disrupted metabolic pathway was glycerophospholipid metabolism, particularly PC-mediated pathways, which appeared to play a central role in the association with of NRP.
Conclusion:
This study depict the plasma metabolic profile of NRP patients following stroke thrombectomy, and discover that phosphatidylcholine-dominated metabolites and related pathways may play a potential role in the occurrence of NRP. These metabolic biomarkers demonstrate promising discriminative ability and may help identify high-risk patients at an early stage, providing new targets for mechanism research and therapeutic intervention.
Previous studies have found that the use of intravenous thrombolysis (IVT) before endovascular treatment (EVT) could mitigate the “no‐reflow” phenomenon in large‐vessel occlusion of the anterior circulation. However, the effect of preoperative IVT on reducing the “no‐reflow” phenomenon in vertebrobasilar artery occlusion (VBAO) is still uncertain. This study aimed to compare the outcomes of IVT before EVT versus EVT alone in patients with VBAO with complete reperfusion (mTICI [Modified Thrombolysis in Cerebral Infarction] 3).
Methods
We performed a retrospective analysis of patients with acute VBAO at 65 stroke centers in China. Patients with complete reperfusion after EVT were included. These patients were divided into 2 groups on the basis of whether IVT was used before EVT, and propensity score matching was applied to balance the groups. The primary outcome was favorable functional outcome, defined as a modified Rankin Scale score of 0 to 3 at 90 days. Secondary outcomes were functional independence (modified Rankin Scale score of 0–2 at 90 days) and modified Rankin Scale shift at 90 days. Safety end points included symptomatic intracranial hemorrhage and death at 90 days.
Results
Of the 2422 patients with VBAO who received EVT, 1452 patients achieved complete reperfusion. Among these, 273 patients received IVT before EVT. After propensity score matching, 268 patients treated with IVT before EVT were compared with 519 patients without IVT. In the matched cohort, the group that received IVT before EVT showed a higher rate of favorable functional outcome (modified Rankin Scale score, 0–3) (adjusted odds ratio, 1.40 [95% CI, 1.03–1.91]; P=0.033) and a lower mortality rate at 90 days (adjusted odds ratio, 0.72 [95% CI, 0.52–0.99]; P=0.044) compared with the EVT alone group.
Conclusions
Our study indicates that IVT before EVT could improve favorable functional outcomes and reduce death in patients with VBAO who achieve complete reperfusion.
In real-world clinical practice, a substantial number of ischemic
stroke patients fail to achieve functional independence, even after
technically successful thrombectomy with excellent angiographic
reperfusion scores (TICI 2C-3). This discordance has been described as
futile recanalization and may be attributable to a phenomenon referred
to as “no-reflow.” This has been conceptualized as the failure of
downstream microvascular reperfusion at the tissue level despite
successful macrovascular recanalization. Several mechanisms including
microvascular obstruction by microthrombi, edema-related microvascular
compression, and pericyte-induced capillary contraction may be at play.1
Its clinical relevance is magnified in the context of recent trials
expanding thrombectomy to patients with large core infarcts and
perfusion mismatch — groups where optimizing tissue-level perfusion may
be especially crucial. Prior research supports use of CTP imaging as a
better predictor of outcomes following successful recanalization than CT
angiogram alone and was even utilized as an indicator of therapeutic
success in recent thrombolytic trials.
The authors Rivet et al. aimed to investigate the clinical impact of
this no-reflow mechanism on functional outcomes by comparing patient
characteristics between patients with “no-reflow” mechanism on perfusion
imaging and varying degrees of angiographic recanalization (TICI
scores). They conducted a post hoc analysis on the data from three
clinical trials: EXTEND-IA (Endovascular Therapy for Ischemic Stroke
with Perfusion-Imaging Selection) and EXTEND-IA TNK (Tenecteplase Versus
Alteplase Before Thrombectomy for Ischemic Stroke) part 1 and 2 trials.
Both qualitative and quantitative evidence of tissue perfusion
evaluation for “no-reflow” were evaluated in a two-step process through
application of commercially available fully automated software (RAPID;
iSchemaView, Menlo Park, CA) on post-thrombectomy follow-up 24-hour
perfusion imaging (CTP or MR Perfusion). The authors identified 2
distinct regions of interest (ROI) which were superimposed into
perfusion maps and excluded signals associated with hemorrhagic
transformation of infarct. No-reflow was defined when both qualitative
and quantitative criteria were met — that is, visually demonstrable
reduced intralesional rCBV or rCBF and >15% interside reduction in
median rCBV or rCBF value2 (Figure 1). It is
worth noting that since the primary studies were not primarily designed
to evaluate for this phenomenon, not all patients had both MRP and CTP.
Figure 1. Imaging analysis method.
They compared both clinical and radiological characteristics of
patients with combinations of no-reflow or completeFlow with different
levels of angiographic success (full-TICI 2c3, partial-2b,
unsuccessful-0-2a). No significant difference in the rate of no-reflow
detection according to imaging modality (CT perfusion 13.6% [n=9/66]
versus MRP 25.0% [n=21/84]; P=0.10) was observed. No-reflow
mechanism occurred more frequently in successful angiographic
recanalization (TICI 3) (n=17/30, 56.7%). Among patient characteristics
across varying degrees of technical success, it is worth noting a
statistically significant difference among time of onset and proportion
of patients receiving thrombolytic (alteplase or tenecteplase).
The primary outcome of functional independence (mRS score of 0–2) was
achieved in 43.33% (n=13/30) of patients with eTICI 2c3–NoReflow,
versus 67.50% (n=81/120) of patients with eTICI 2c3–CompleteFlow, 63.03%
(n=150/238) of patients with eTICI 2b and 50.00% (n=34/68) of patients
with unsuccessful thrombectomy. In unadjusted analysis, patients with
no-reflow were less likely to experience functional independence
despite technical success, TICI 2c-3 compared to completeFlow (odds
ratio [OR], 0.37 [95% CI, 0.16–0.83]; P=0.02) or those with eTICI 2b (OR, 0.45 [95% CI, 0.21–0.97]; P=0.04) but had similar rate to patients with unsuccessful thrombectomy (OR, 0.76 [95% CI, 0.32–1.82]; P=0.54).
When adjusted for age, premorbid mRS, baseline NIHSS, and baseline core
volume, multivariable analysis confirmed lower odds of functional
independence with no-reflow and full/partial recanalization, and similar
odds of functional independence with unsuccessful thrombectomy.
Furthermore, exploratory analysis of functional infarct volumes (FIV)
showed that despite similar volumes, patients with no-reflow had worse
outcomes despite full recanalization compared to partial recanalization.
These findings suggest that “no-reflow” phenomenon negates benefit of
macrovascular recanalization in achieving favorable clinical outcome.
The authors further caution that no-reflow mechanism tends to occur more
frequently with prolonged periods of ischemic injury, suggesting that
this prevalence could be underestimated by this study given the
inclusion of patients within the 4.5-hour time window. Their major
strength includes use of prospectively collected data from clinical
trials. As we push the boundaries of thrombectomy eligibility, tackling
the no-reflow phenomenon may be the next frontier in improving
patient-centered outcomes — representing a crucial step not only in
restoring macrovascular blood flow but also in minimizing downstream
ischemic injury, thereby broadening the therapeutic benefit for patients
with acute ischemic stroke.
Just maybe you've rediscovered Capillaries that don't open due to pericytes September 2011. What the fuck is your solution to that problem? Describing a problem with NO solution is grounds for firing! My God, the amount of absolute stupidity in stroke is appalling!
Hypoperfusion is a term that describes "a reduced amount of blood flow".
Tissue-level
hypoperfusion (no-reflow) persists in 30% of patients with seemingly
successful upstream angiographic recanalization at thrombectomy. We
investigated the clinical impact of the no-reflow phenomenon by
comparing patients with no-reflow versus patients with varying degrees
of angiographic recanalization.
METHODS:
In
a post hoc pooled analysis of the EXTEND-IA (Endovascular Therapy for
Ischemic Stroke With Perfusion-Imaging Selection) and EXTEND-IA TNK
(Tenecteplase Versus Alteplase Before Thrombectomy for Ischemic Stroke)
part 1 and 2 trials, clinical and radiological outcomes were compared
between patients with (1) full angiographic recanalization with
no-reflow (expanded Treatment in Cerebral Ischemia [eTICI]
2c3–NoReflow), defined as >15% reduction in relative cerebral blood
flow or Volume within the infarct relative to a contralateral homolog on
24-hour-follow-up perfusion computed tomography or magnetic resonance
imaging despite eTICI grade 2c-3 angiographic recanalization, (2) full
angiographic recanalization and tissue reperfusion (eTICI
2c3–CompleteFlow), (3) partial angiographic recanalization (eTICI 2b),
and (4) unsuccessful thrombectomy (eTICI 0-2a). The primary outcome,
functional independence at 90 days, was investigated using a mixed
effect logistic regression model, both unadjusted and adjusted for a
priori-selected covariates, namely age, premorbid modified Rankin Scale,
baseline National Institutes of Health Stroke Scale, and baseline core
volume.
RESULTS:
Among
537 patients from the overall pooled cohort, 456 patients were included
in the analysis. The mean age of the included patients was 71 years
old, and 54% were male. A favorable outcome (90-day modified Rankin
Scale score of 0–2 or return to baseline modified Rankin Scale) was
observed in 43.33% (n=13/30) of patients with eTICI 2c3–NoReflow, 67.50%
(n=81/120) of eTICI 2c3–CompleteFlow, 63.03% (n=150/238) of eTICI 2b,
and 50.00% (n=34/68) of unsuccessful thrombectomy. In multivariable
analysis, patients with eTICI 2c3–NoReflow had lower odds of favorable
outcome compared with those with eTICI 2c3–CompleteFlow (adjusted odds
ratio, 0.31 [95% CI, 0.12–0.77]; P=0.01) and eTICI 2b (adjusted odds ratio, 0.40 [95% CI, 0.17–0.96]; P=0.04) but not unsuccessful thrombectomy (adjusted odds ratio, 1.02 [95% CI, 0.38–2.73]; P=0.97). Patients with eTICI 2c3–NoReflow had similar follow-up infarct volume to unsuccessful thrombectomy (β=−8.26 [95% CI, −27.38 to 10.86]; P=0.40) and eTICI 2b (β=9.38 [95% CI, −7.33 to 26.09]; P=0.27) but had larger infarcts compared with eTICI 2c3–CompleteFlow (β=18.85 [95% CI, 1.16–36.54]; P=0.04).
CONCLUSIONS:
When
no-reflow occurred, clinical and radiological outcomes in patients with
full angiographic recanalization were similar to patients with
unsuccessful thrombectomy. Preventing or reversing no-reflow has the
potential to augment the clinical benefit of reperfusion treatment in
ischemic stroke.
Endovascular
reperfusion therapy is the primary strategy for acute ischemic stroke.
No-reflow is a common phenomenon, which is defined as the failure of
microcirculatory reperfusion despite clot removal by thrombolysis or
mechanical embolization. It has been reported that up to 25% of ischemic
strokes suffer from no-reflow, which strongly contributes to an
increased risk of poor clinical outcomes. No-reflow is associated with
functional and structural alterations of cerebrovascular
microcirculation, and the injury to the microcirculation seriously
hinders the neural functional recovery following macrovascular
reperfusion. Accumulated evidence indicates that pathology of no-reflow
is linked to adhesion, aggregation, and rolling of blood components
along the endothelium, capillary stagnation with neutrophils, astrocytes
end-feet, and endothelial cell edema, pericyte contraction, and
vasoconstriction. Prevention or treatment strategies aim to alleviate or
reverse these pathological changes, including targeted therapies such
as cilostazol, adhesion molecule blocking antibodies, peroxisome
proliferator-activated receptors (PPARs) activator, adenosine, pericyte
regulators, as well as adjunctive therapies, such as extracorporeal
counterpulsation, ischemic preconditioning, and alternative or
complementary therapies. Herein, we provide an overview of
pathomechanisms, predictive factors, diagnosis, and intervention
strategies for no-reflow, and attempt to convey a new perspective on the
clinical management of no-reflow post-ischemic stroke.
Acute
ischemic stroke (AIS) afflicts millions of individuals worldwide.
Despite the advancements in thrombolysis and thrombectomy facilitating
proximal large artery recanalization, the resultant distal
hypoperfusion, referred to “no-reflow” phenomenon, often impedes the
neurological function restoration in patients. Over half a century of
scientific inquiry has validated the existence of cerebral “no-reflow”
in both animal models and human subjects. Furthermore, the correlation
between “no-reflow” and adverse clinical outcomes underscores the
necessity to address this phenomenon as a pivotal strategy for enhancing
AIS prognoses. The underlying mechanisms of “no-reflow” are
multifaceted, encompassing the formation of microemboli, microvascular
compression and contraction. Moreover, a myriad of complex mechanisms
warrant further investigation. Insights gleaned from mechanistic
exploration have prompted advancements in “no-reflow” treatment,
including microthrombosis therapy, which has demonstrated clinical
efficacy in improving patient prognoses. The stagnation in current
“no-reflow” diagnostic methods imposes limitations on the timely
application of combined therapy on “no-reflow” post-recanalization. This
narrative review will traverse the historical journey of the
“no-reflow” phenomenon, delve into its underpinnings in AIS, and
elucidate potential therapeutic and diagnostic strategies. Our aim is to
equip readers with a swift comprehension of the “no-reflow” phenomenon
and highlight critical points for future research endeavors.
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