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.

Monday, November 16, 2020

Prior antiplatelet therapy in patients undergoing endovascular treatment for acute ischemic stroke: Results from the MR CLEAN Registry

In plain words I have no fucking clue what this means.

Prior antiplatelet therapy in patients undergoing endovascular treatment for acute ischemic stroke: Results from the MR CLEAN Registry

First Published August 14, 2020 Research Article Find in PubMed 

Antiplatelet therapy may increase the risk of symptomatic intracranial hemorrhage after endovascular treatment for ischemic stroke but may also have a beneficial effect on functional outcome. The aim of this study is to compare safety and efficacy outcomes after endovascular treatment in patients with and without prior antiplatelet therapy.

We analyzed patients registered in the MR CLEAN Registry between March 2014 and November 2017, for whom data on antiplatelet therapy were available. We used propensity score nearest-neighbor matching with replacement to balance the probability of receiving prior antiplatelet therapy between the prior antiplatelet therapy and no prior antiplatelet therapy group and adjusted for baseline prognostic factors to compare these groups. Primary outcome was symptomatic intracranial hemorrhage. Secondary outcomes were 90-day functional outcome (modified Rankin Scale), successful reperfusion (extended thrombolysis in cerebral infarction score ≥2B) and 90-day mortality.

Thirty percent (n = 937) of the 3154 patients were on prior antiplatelet therapy, who were matched to 477 patients not on prior antiplatelet therapy. Symptomatic intracranial hemorrhage occurred in 74/937 (7.9%) patients on prior antiplatelet therapy and in 27/477 (5.6%) patients without prior antiplatelet therapy adjusted odds ratio 1.47, 95% confidence interval 0.86–2.49. No associations were found between prior antiplatelet therapy and functional outcome (adjusted common odds ratio 0.87, 95% confidence interval 0.65–1.16), successful reperfusion (adjusted odds ratio 1.23, 95% confidence interval 0.77–1.97), or 90-day mortality (adjusted odds ratio 1.15, 95% confidence interval 0.86–1.54).

We found no evidence of an association of prior antiplatelet therapy with the risk of symptomatic intracranial hemorrhage after endovascular treatment, nor on functional outcome, reperfusion, or mortality. A substantial beneficial or detrimental effect of antiplatelet therapy on clinical outcome cannot be excluded. A randomized clinical trial comparing antiplatelet therapy versus no antiplatelet therapy is needed.

Approximately 50% of patients with ischemic stroke do not recover to functional independence after endovascular treatment (EVT).1 (That is absolutely appalling. What is your solution to change that to 100% recovery?)Although pre-stroke disability and large baseline infarct core are known causes of these poor outcomes, incomplete microvascular reperfusion—a potentially reversible process—might contribute to these poor outcomes as well. One of the causes of incomplete microvascular reperfusion is the formation of microthrombi occluding the distal capillary bed. These microthrombi are abundantly present after focal cerebral ischemia in the distal vascular territory. The formation of microthrombi might be promoted by vessel wall damage caused by EVT.2,3 Use of antiplatelet drugs could potentially reduce periprocedural formation of microthrombi by inhibiting platelet aggregation and inflammation of the vessel wall, which could ultimately improve microvascular reperfusion.3 On the other hand, one randomized trial showed that antiplatelet therapy increases the risk of symptomatic intracranial hemorrhage (sICH) when administered early—within 90 min—after intravenous treatment with alteplase.4 However, this trial did not focus on the subpopulation of patients with ischemic stroke caused by a large vessel occlusion undergoing EVT. In these patients, the beneficial effect of platelet inhibition could counterbalance the detrimental effects of increase risk of sICH. As interventionists are familiar with periprocedural use of antiplatelet agents during non-stroke neurovascular procedures (i.e. stenting), this treatment might be an easily applicable therapy of adjunctive value in EVT for stroke. However, as antiplatelet agents are not administered systematically during EVT for acute ischemic stroke and current evidence is limited to small observational studies investigating the association of prior antiplatelet therapy with sICH risk and functional outcomes, there are conflicting results.5 The evaluation of risks and benefits of prior antiplatelet therapy in a large cohort of patients treated with EVT could provide useful information for clinical practice. The aim of this study is to compare safety and efficacy outcomes, after EVT of patients with and without prior antiplatelet therapy.

 

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