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.

Friday, September 2, 2022

Shortening the delay to anticoagulation initiation after ischemic stroke

Anticoagulation initiation time is an invalid measurement, it is not measuring recovery.   You're going to have to deliver tPA in the ambulance. CAN YOU DO THAT?

In this research in mice the needed time frame for tPA delivery is 3 minutes. That's for full recovery NOT the intermediate step of reperfusion. If your hospital is touting reperfusion you don't have a functioning stroke hospital.

Electrical 'storms' and 'flash floods' drown the brain after a stroke

The latest here:

Shortening the delay to anticoagulation initiation after ischemic stroke

By Michele Romoli, MD, PhD, FEBN – Neurology and Stroke Unit, Bufalini Hospital, Cesena, Italy

Follow Michele Romoli on Twitter: @MicheleRomoli

Anticoagulation with direct oral anticoagulants (DOACs) started early after acute ischemic stroke (IS) or transient ischemic attack (TIA) related to nonvalvular atrial fibrillation (NVAF) is critical to reduce the risk of recurrent stroke and systemic embolism.1 The optimal timing to start anticoagulation, however, remains elusive.

A 1-3-6-12 rule has been largely adopted in clinical practice, with early DOAC initiation in TIA and later initiation (12 days or more) in severe stroke.1 Such a timing, proposed on the basis of observational data and consensus/opinions, lacks support from (ongoing) randomized trials. In the meantime, stroke specialists are further shortening the timing for DOAC initiation, with the aim of reducing as much as possible the risk of stroke recurrence and systemic embolism.2 This strategy has to take into account the risk of haemorrhagic transformation, which may have several contributors, such as the ischemic volume.2

In a recent paper in Stroke, Kimura and colleagues pooled data from several observational studies to define safety and efficacy of shortening the interval between index stroke and DOAC initiation.3 In a derivation cohort including mainly Japanese patients, they compared an early (n=785) and late (n=1012) DOAC initiation strategy for ischemic and bleeding outcomes across four stroke groups: TIA, mild stroke with, moderate stroke, and severe stroke. The early initiation strategy consisted in a 1-2-3-4 day DOAC initiation rule according to increasing severity of stroke. In the derivation cohort, the rate of recurrent ischemic stroke dropped from 3.9% with late initiation to 1.9% with early initiation (adjusted hazard ratio 0.50 [95% CI, 0.27–0.89]). Major bleeding occurred in six (0.8%) in the early group and 10 (1.0%) in the late group (aHR 0.81 [0.28–2.19]). In the external validation cohort (n=2063), ischemic stroke occurred in 13 patients (2.4%) of the early group and 33 (2.2%) of the late group (aHR 1.07 [95% CI, 0.54–2.00]. ICH occurred in one (0.2%) in the early and nine (0.6%) in the late initiation group (aHR 0.31 [0.02–1.65]).3

Overall, the results of this large collaborative studies suggest that a shorter delay of anticoagulation initiation (1-2-3-4 rule vs 1-3-6-12 rule according to stroke severity) could be feasible and may not carry an increase in risk of bleeding, with a potential higher efficacy among Japanese people.3

At the moment, the timing of anticoagulation resumption is investigated in four ongoing randomized trials (TIMING, OPTIMAS, ELAN, and START, Clinical trials identifier NCT02961348, NCT03759938, NCT03148457, NCT03021928, respectively), which differ in timing of randomization to DOAC initiation. Indeed, in TIMING and OPTIMAS anticoagulation is initiated no earlier than four days, while a severity-based timing is proposed in ELAN and START. Results from these trials are critically needed, as shorter initiation timing might benefit stroke patients.

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