Deans' stroke musings: Interactions among COX-2, GPIIIa and P2Y1 variants are associated with aspirin responsiveness and adverse events in patients with ischemic stroke

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.

Saturday, December 24, 2016

Interactions among COX-2, GPIIIa and P2Y1 variants are associated with aspirin responsiveness and adverse events in patients with ischemic stroke

You probably need to discuss with your doctor if you are susceptible to aspirin resistance.

Interactions among COX-2, GPIIIa and P2Y1 variants are associated with aspirin responsiveness and adverse events in patients with ischemic stroke

Xingyang Yi, Zhao Han, Qiang Zhou, Jing Lin, Chun Wang

First Published December 1, 2016 research-article

Abstract

Background:

The effect of gene variants and their interactions on response to aspirin and clinical adverse outcomes after an acute ischemic stroke (IS) is not fully understood. The aim of this study was to investigate the association of aspirin-relevant gene variants and their interactions with clinical adverse outcomes in IS patients taking aspirin.

Methods:

A total of 14 variants from six genes encoding COX enzymes (COX-1, COX-2), platelet membrane receptors (TXAS1, P2Y1, P2Y12) and glycoprotein receptor (GPIIIa) were examined in 850 acute IS patients. Gene–gene interactions were analyzed using generalized multifactor dimensionality reduction (GMDR) analysis. All patients were followed up for 1 year after admission. Primary outcome was a composite of recurrent ischemic stroke (RIS), myocardial infarction (MI) and death.

Results:

The primary outcome occurred in 112 (13.5%) patients (81 RIS, 16 MI and 15 deaths). There were no significant differences in the frequencies of the genotypes of the 14 variants between the patients with and without primary outcome using single-locus analytical approach. However, there was significant gene–gene interaction among rs20417, rs1371097 and rs2317676. The high-risk interactive genotypes of rs20417, rs1371097 and rs2317676 were independently associated with primary adverse outcome of RIS, MI, and death after acute IS.

Conclusion:

The three-loci interactions are associated with sensitivity of IS patients to aspirin and aspirin-induced adverse clinical events. The combinatorial analysis used in this study may be helpful to elucidate complex genetic risk of aspirin resistance (AR).

Clinical trial registration:

The study described here is registered at http://www.chictr.org/ (unique identifier: ChiCTR-OCH-14004724).

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