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.

Wednesday, May 18, 2022

Association of Systolic Blood Pressure and Cerebral Collateral Flow in Acute Ischemic Stroke by Stroke Subtype

So we still have NO FUCKING CLUE what a blood pressure management protocol is. Hope you don't mind dying because of the cesspools of incompetence of the complete stroke medical world.  Unless YOU hold your stroke hospital's feet to the fire you are allowing your children and grandchildren to die or become disabled from their strokes.

5 years and still incompetent leadership in stroke.

 

Association of Systolic Blood Pressure and Cerebral Collateral Flow in Acute Ischemic Stroke by Stroke Subtype

 

  • Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea

Background and Purpose: Collateral flow in acute ischemic stroke is known as a predictor of treatment outcome and long-term prognosis. However, factors determining the initial collateral flow remain unclear. We investigated factors related to collateral flow in patients with acute ischemic stroke caused by large vessel occlusion (AIS-LVO) and further analyzed the results according to stroke etiology.

Methods: This was a retrospective study using prospective stroke registry data from a single university hospital from October 2014 to May 2021. AIS-LVO with middle cerebral artery M1 occlusion identified by pre-treatment multiphasic computed tomography angiography was included. Collateral flow score was graded on a 6-point ordinal scale according to pial arterial filling.

Results: A total of 74 patients [cardioembolism (CE): 57; large artery atherosclerosis (LAA): 17] was included. The mean age of all patients was 72.2 ± 11.7 years, and 37.8 % (n = 28) were men. Multivariate regression analysis showed that initial SBP [odds ratio (OR): 0.994; 95% confidence interval (CI): 0.990–0.998; p = 0.002] and stroke etiology (OR: 0.718; 95% CI: 0.548–0.940; p = 0.019) were independent factors of the collateral flow grade. Collateral flow grade was independently associated with initial SBP in the CE group (OR: 0.993; 95% CI: 0.989–0.998; p = 0.004) but not in the LAA group (OR: 0.992; 95% CI: 0.980–1.004; p = 0.218). Initial SBP was significantly correlated with NIHSS score in the CE group but not in the LAA group (r2= 0.091, p = 0.023; r2 = 0.043, p = 0.426, respectively).

Conclusions: Elevated initial SBP was associated with poor cerebral collateral flow and more severe symptoms in the CE group, but not in the LAA group in patients with AIS-LVO. These findings suggest differential effects of initial SBP elevation on collateral flow by stroke subtypes.

Introduction

Collateral flow is an important feature of cerebral circulation when major arteries are occluded, which varies depending on individuals. Collateral flow in acute ischemic stroke is known as a predictor of acute thrombolytic and endovascular therapy outcome as well as long-term prognosis (15). Patients with a cervical large artery atherosclerosis (LAA) have a more extensive cerebral collateral circulation and a better functional outcome at 90 days than those with a cardioembolic (CE) stroke (6). Previous studies have also suggested that LAA stroke is associated with better collateral flow than CE stroke (69). Theoretically, LAA in humans develops over decades, which might promote the gradual development of cerebral collateral flow. For example, patients with a severe (71–99%) stenosis have a better collateral flow than those with a moderate (51–70%) stenosis (6). In contrast, since CE stroke is not accompanied by chronic cerebral hypoperfusion, the chances of collateral artery formation and recruitment are less likely to occur in these patients.

Although the importance of collateral flow has attracted more attention over the past decade, studies on the factors which determine collateral flow are not well understood. The potential relationship of collateral flow with history of cardiovascular risk factors, such as hypertension, congestive heart failure, hyperlipidemia, and diabetes might exhibit complex interactions. Calleja et al. have reported that diabetes is significantly associated with poorer collateral flow on admission (1).A history of hypertension has also been more frequently found among patients with poor collateral flow (2, 10, 11). Menon et al. have found that metabolic syndrome, hyperuricemia, and age are associated with poor collateral flow in patients with acute ischemic stroke (12). In case of coronary collateral flow, eGFR is an independent affecting factor (13).

We hypothesize that factors related to collateral flow in patients with acute ischemic stroke caused by large vessel occlusion (AIS-LVO) are different according to stroke etiology. In this study, we investigated the extensive physiologic, laboratory, and imaging parameters which have been reported to be possibly related with collateral flow in patients with AIS-LVO. We further analyzed the results according to stroke etiology with the assumption that stroke subtype may influence the collateral development.

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