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Protimenow

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JK - I'm sure glad that you're here.

Leadville - I just found that paper that equated INR to viscosity -- and I was kind of amazed, too. But it helps to explain why they call anticoagulants Blood Thinners.
 

pellicle

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... - systolic and diastolic are "flipped" between the aortic and mitral valve.
never thought of it, but yes, of course it is.
So can I then extrapolate from this that the sys pressures and diastolc pressures equivalently higher as reported on the BP in terms of the pressure gradients at the Mitral vs Aortic valve?
 

pellicle

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Leadville - I just found that paper that equated INR to viscosity -- and I was kind of amazed, too. But it helps to explain why they call anticoagulants Blood Thinners.
care to share that? Because:
...I saw some papers about the way that they tested INR years ago - and a few methods used tiny magnetic pieces in the reagent,
err ... this is happening during coagulation, so of course it gets thicker ... as the coagulation occurs, this is not something which happens between blood that has not begun coagulation and I'll be surprised if there is any reported viscosity difference between blood from people NOT on AC Therapy and those on AC Therapy.

However if one assumes that coagulation takes longer and "that is why its thinned" one doesn't really need a paper for that does one? I mean its QED really isn't it?

https://en.wikipedia.org/wiki/Prothrombin_time
 
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Protimenow

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I've been looking for the paper. Your point is good - although the researchers measured the time to formation of a clot from the time the blood is added to the reagent. They put iron filings in with the reagent, and had a rotating magnet below the test area, and measured the time until the iron filings stopped moving. They apparently figured that, if it takes longer for the blood to clot, this must because the anticoagulated blood had lower viscosity.

(It's not like we now know - that anticoagulants make it take longer for blood to clot - it's an assumption that the blood's viscosity was lower, so it took longer to form a clot than it does for 'normal' blood).

This is not my conclusion - I'm just repeating what I read - and should have saved the link to the paper. I'll eventually find it again, list a link, and may quote a paragraph or two.
 
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Protimenow

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Someone, somewhere, decided that this was what anticoagulants do.

He (probably) was also looking for terminology that people could sort of understand. 'Blood Thinner' is easier to understand (and spell) than anticoagulant.

I'm not sure how many people (other than those on this forum, and perhaps a few doctors who know what anticoagulants actually do) who chafe at the misuse of the term to describe what anticoagulants actually do..

Yes. It's bad science. But, unfortunately, the term is stickier than blood without platelets.
 

pellicle

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(It's not like we now know - that anticoagulants make it take longer for blood to clot - it's an assumption that the blood's viscosity was lower, so it took longer to form a clot than it does for 'normal' blood).
"we've" known about this for quite some time ... before valve surgery really
https://www.ncbi.nlm.nih.gov/pubmed/2180278
Petit, a surgeon, recognized in the 1730s that clotting was hemostatically important in amputations. Finally, the mechanism of clotting began to be studied by Buchanan (1838), who recognized thrombin; Hammarsten (1875), who purified fibrinogen; and Arthus (1890), who discovered the need for calcium. The fact that platelets existed and had a hemostatic function was developed in the 1800s. Not until the late 1940s did the explosion in the discovery of new clotting factors begin; they now number up to Factor XIII, plus many more that have no Roman numeral designation. Discovery of clotting factors led to their assays. The use of whole blood clotting times was improved by measuring the clotting times of plasma.

(again from that wiki) https://en.wikipedia.org/wiki/Prothrombin_time
The prothrombin time was developed by Armand Quick and colleagues in 1935
 

pellicle

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Poor science, it's maybe how the 'Urban myth' started eh ?
did you just change your avatar?

anyway, Urban Myths in this area are probably started by half schooled clincians (who promptly forgot 90% of that class room nonsence after the exams and just skilled up on the job) attempting to be "Homer Simpson" in front of the patients ... combined with a mix of "dumbed down" (mostly wrong) metaphors for their (usually low requirement) educational capacity and hope that they "got the gist"
 

Protimenow

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I may have overstated a conclusion in the paper that I mentioned. Here's the link to the paper: https://arrow.dit.ie/cgi/viewcontent.cgi?article=1153&=&context=scschbioart&=&sei-redir=1&referer=https%3A%2F%2Fcse.google.com%2Fcse%3Fcx%3Dpartner-pub-2698861478625135%3A7463904445%26ie%3DUTF-8%26q%3D%250D%250Ahemoccult%250D%250A#search="hemoccult".

At the bottom of Page 3, it says: "Mechanical detection also replaced visual detection in which the change in viscosity was detected, for instance by the cessation of the movement of a steel ball in the rotating sample tube which could be detected optically [9]. "

This may have been referring to a change in viscosity of the blood when coagulation is happening. On re-reading this paper, it appears that this method detects the clot, but doesn't specifically say that the viscosity of the blood is higher or lower depending on whether or not a person's blood is anticoagulated.

Still, I can see uninformed researchers concluding that anticoagulated blood must be of lower viscosity than normal blood because it takes longer for the anticoagulated blood to reach the high levels of viscosity when a clot begins to form.

This 2013 paper doesn't otherwise mention viscosity, but it's interesting to consider that someone, somewhere, made the erroneous conclusion that, if it takes longer for anticoagulated blood to clot than normal blood, the reason must be because the anticoagulated blood is 'thinner.'
 

Paul1972

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tom in MO

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A pool of blood gets thicker as it clots, most people used to know this (i.e. killing chickens, hunting, blood sausage, etc.) If your INR is elevated due to warfarin and you bleed out quick, it's because your blood didn't thicken up and clot. Hence warfarin is a blood thinner. It doesn't need to be scientific to make sense :)
 

Protimenow

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No, Tom. Your reasoning is the same as that used by the people who first called it a blood thinner. I suspect that if you are able to test ACTUAL viscosity of blood, there wouldn't be much ddifference between normal and unanticoagulated blood. They equally thick.

The difference is that anticoagulated blood takes longer to clot. This characteristic doesn't make blood thinner - it just makes clotting take longer.

When researchers determined how clots formed, they identified a 'cascade' of processes, ultimately resulting in a clot. One of the steps involves vitamin K1. Warfarin reduces the activity of K1, interrupting the clotting process. (I'm loosely paraphrasing this process - if I don't list the correct order of processes, I would be surprised if Pellicle doesn't provide a link).

It's the processes that are involved in clotting, NOT the viscosity of the blood, that determines the speed of clot formation. Blood viscosity has NOTHING to do with it.
 
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carolinemc

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Someone, somewhere, decided that this was what anticoagulants do.

He (probably) was also looking for terminology that people could sort of understand. 'Blood Thinner' is easier to understand (and spell) than anticoagulant.

I'm not sure how many people (other than those on this forum, and perhaps a few doctors who know what anticoagulants actually do) who chafe at the misuse of the term to describe what anticoagulants actually do..

Yes. It's bad science. But, unfortunately, the term is stickier than blood without platelets.
Even Aspirin is considered a blood thinner. Check it out. Hugs for today. :cool:
 

Protimenow

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Caroline -- this isn't entirely correct. Aspirin and other NSAIDS interfere with clotting, but do something entirely different from Warfarin -- they make platelets more 'slippery.' NSAIDs interfere with clotting, making it possibly take longer for a clot to form. They don't 'thin' the blood - blood is the same thickness before taking Aspirin and after taking it.

When I broke my wrist a few years ago, the doctor tried pushing Norco (a pain reliever with Tylenol and Codeine) - and I didn't want it. I told him I was taking an NSAID. He told me not to, because it interferes with with platelets. It does. But I don't think you can test this using a meter.

But, no, Aspirin is NOT a blood thinner. Neither is Warfarin.



Check it out.
 
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