Deans' stroke musings: How Do You “STOP” a Stroke in the Setting of Cervical Artery Dissection?

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.

Thursday, March 21, 2024

How Do You “STOP” a Stroke in the Setting of Cervical Artery Dissection?

Really disappointed they excluded recent head/neck trauma like chiropractic adjustments or beauty parlor strokes.

The goal is to solve ALL problems in stroke, not just the easier ones to research. Leaders solve problems, so I guess there are NO leaders in this bunch!

How Do You “STOP” a Stroke in the Setting of Cervical Artery Dissection?

Maryam Zulfiqar, MD @MaryamZulfiqar_

Originally published March 19, 2024 10.1161/blog.20240319.906242

Yaghi S, Shu L, Mandel DM, Leon Guerrero CR, Henninger N, Muppa J, Affan M, Ul Haq Lodhi O, Heldner MR, Antonenko K, et al. Antithrombotic Treatment for Stroke Prevention in Cervical Artery Dissection: The STOP-CAD Study. Stroke. 2024.

Cervical artery dissection is an uncommon stroke etiology and mostly affects a younger patient population. The treatment of cervical artery dissection varies across different practices and is based on the treating clinician’s experience. Since the mechanism of stroke is deemed to be artery-to-artery emboli, treating it with antithrombotic is an important decision to make.

The TREAT-CAD trial concluded non-inferiority of aspirin compared to vitamin K antagonist (VKA) while reporting less ischemic events on VKA. Another trial, CADISS, did not report any significant differences in outcome between antiplatelet and anticoagulation treatment groups. Both trials were based on a smaller sample size.

The current study aims to compare the risks of ischemic stroke and hemorrhages (symptomatic intracranial hemorrhage and extracranial hemorrhage) between antiplatelets and anticoagulation groups in patients with cervical artery dissection, within 30 and 180 days. It is important to note that this was a large international multicenter retrospective study. Patients with chronic dissection, recent head or neck trauma, dissecting aneurysm causing SAH and of iatrogenic etiology were excluded from the analysis. A total of 3,636 patients were included in the study. Two thousand four hundred and fifty-three patients had received single and dual antiplatelet (DAPT), 402 had received anticoagulation (VKA or direct oral anticoagulants, DOAC, or parenteral anticoagulants), and 781 received both treatments. Most of the patients were followed up to 180 days. A total of 162 patients had ischemic strokes, and 28 patients had hemorrhages. Patients on anticoagulation had lower rates of ischemic stroke (1.5% vs 3.3 %, p = 0.059) and slightly higher rates of hemorrhage (0.7% vs 0.5%, p = 0.484), although the results were non-significant. In addition, hemorrhage on anticoagulation was reported to occur more on 180-day follow-up (HR = 5.56), less on 90-day follow-up (HR 1.64), and even less on 30 days (HR 1.39).

While the study results were not significant, it does provide a trend towards the use of anticoagulation to prevent ischemic strokes in the setting of cervical artery dissection. Anticoagulation may be safer to use for a smaller duration (like 30 days) to prevent higher risk of hemorrhage. Similarly, a shorter course of DAPT might be better for high-risk TIA or minor stroke compared to a prolonged duration, which may lead to increased risk of bleeding. This study does provide a framework for prospective clinical trials to compare the type of antiplatelet or anticoagulation used in dissection. Future studies can potentially look at how soon a treatment can be initiated and if longer duration of treatment poses more risk of hemorrhages. Another potential area of study could be the type of antiplatelet used for long-term management of dissection.