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jinianIn which tPA makes strokes much less dangerous and awful: http://elisem.livejournal.com/1661214.html
As the American Heart Association would really like you to know, tissue plasminogen activator (tPA) dissolves blood clots. In ischemic stroke (estimated 80% of all strokes) there's blockage of blood flow to part of the brain, and if that goes on the cells in the blocked area will die. If blood clots are broken up, the cells get oxygen back before they die. It should be pretty clear why this is a better outcome.
Doctors can only give tPA within three hours of the onset of symptoms, because if they do it later the risk of causing dangerous bleeding outweighs the possible benefits. You're a high priority in the ER if you go in with heart or brain symptoms, but diagnosis still takes time, so get down there as soon as you can. Those cells are suffocating and the treament window's closing.
The good news? Elise is, as far as scans and doctors can tell, totally fine. That's why she's asked that people spread the word. More stroke victims can be totally fine in the future.
I wondered about the mechanism for tPA's action, and it looks like there's an enzyme called plasminogen running around in the bloodstream all the time. When tPA and fibrin (what blood clots are made of) get together with plasminogen, you get plasmin, which degrades blood clots. Plasmin also does other cool things like degrade the Graafian follicle leading to ovulation, which makes me wonder if there's an effect on female fertility after a tPA stroke treatment; probably not a lot of overlap in patient groups there, though. Normally tPA is produced in the cells lining blood vessels, which can presumably sense clots through pressure or gas exchange mechanisms and move the enzyme to where it'll be useful. So putting a bunch of tPA into a person's bloodstream just jump-starts the process, allowing plasmin to be produced immediately from a precursor that's always around rather than waiting for the blood-vessel cells to move their own tPA to a surface where it might contact the bloodstream or just jam up against a clot. Result: more plasmin faster.
As far as how tPA can cause new bleeding, it seems to affect cell integrity in a way that's not totally clear. I found a grant application for people to study a signaling cascade in mice, but that's all I got for now. If it does turn out that some of their mutant mice are more susceptible to bleeding, we may be able to genetically profile people (in advance) and determine whether they're more or less likely to have adverse effects from tPA treatment on that basis. Few things in genomic medicine have been immediately beneficial so far, but if we can build up evidence like that to affect people's chances of getting treatments that will work for them, especially on time-sensitive stuff like this, benefits are going to start accumulating faster and faster.
As the American Heart Association would really like you to know, tissue plasminogen activator (tPA) dissolves blood clots. In ischemic stroke (estimated 80% of all strokes) there's blockage of blood flow to part of the brain, and if that goes on the cells in the blocked area will die. If blood clots are broken up, the cells get oxygen back before they die. It should be pretty clear why this is a better outcome.
Doctors can only give tPA within three hours of the onset of symptoms, because if they do it later the risk of causing dangerous bleeding outweighs the possible benefits. You're a high priority in the ER if you go in with heart or brain symptoms, but diagnosis still takes time, so get down there as soon as you can. Those cells are suffocating and the treament window's closing.
The good news? Elise is, as far as scans and doctors can tell, totally fine. That's why she's asked that people spread the word. More stroke victims can be totally fine in the future.
I wondered about the mechanism for tPA's action, and it looks like there's an enzyme called plasminogen running around in the bloodstream all the time. When tPA and fibrin (what blood clots are made of) get together with plasminogen, you get plasmin, which degrades blood clots. Plasmin also does other cool things like degrade the Graafian follicle leading to ovulation, which makes me wonder if there's an effect on female fertility after a tPA stroke treatment; probably not a lot of overlap in patient groups there, though. Normally tPA is produced in the cells lining blood vessels, which can presumably sense clots through pressure or gas exchange mechanisms and move the enzyme to where it'll be useful. So putting a bunch of tPA into a person's bloodstream just jump-starts the process, allowing plasmin to be produced immediately from a precursor that's always around rather than waiting for the blood-vessel cells to move their own tPA to a surface where it might contact the bloodstream or just jam up against a clot. Result: more plasmin faster.
As far as how tPA can cause new bleeding, it seems to affect cell integrity in a way that's not totally clear. I found a grant application for people to study a signaling cascade in mice, but that's all I got for now. If it does turn out that some of their mutant mice are more susceptible to bleeding, we may be able to genetically profile people (in advance) and determine whether they're more or less likely to have adverse effects from tPA treatment on that basis. Few things in genomic medicine have been immediately beneficial so far, but if we can build up evidence like that to affect people's chances of getting treatments that will work for them, especially on time-sensitive stuff like this, benefits are going to start accumulating faster and faster.
no subject
Date: 2011-01-10 05:37 am (UTC)