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.

Tuesday, May 3, 2022

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

 EXACTLY HOW IS THIS GETTING SURVIVORS BETTER RECOVERY?

The only goal in stroke is 100% recovery, don't the mentors and senior researchers know that?  All research should be linked to that goal.

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

First Published April 14, 2022 Research Article 

Background:

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 3 major diseases using 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 major adverse cardiovascular events (MACEs).

Results:

Among 221 patients, 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 MACE 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:

ASCOD grade A2 or A3 was predictive of MACE in ESUS patients. Reclassification of ESUS using ASCOD phenotyping provides important clues for risk prediction and may guide optimal management strategies.

 

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