Why 'thin your Blood'

Aspirin, clopidogrel, warfarin, dabigatran, rivaroxaban - you may have heard of some, or all, of these drugs.  Although colloquially known as “blood thinners”, they do not actually thin the blood at all.  Rather, they prevent blood from clotting so easily, and are used to reduce the risk of illnesses which are caused by blood clotting in the wrong place – strokes, heart attacks and pulmonary embolus, to name but three.  But why are there so many different types of blood thinners, and are they all equivalent?  To answer this fully we need to have a closer look at how blood clots or take a look at this animation which may be somewhat technical but shows very nicely the complexity of the systems at play.

These clotting mechanisms have been honed by thousands of years of evolution to prevent us from bleeding to death when we cut ourselves, and they do this very well.  The trouble is, in certain disease states platelets and clotting factors can be fooled into activating inappropriately, and making blood clots where they are not wanted.  If these clots block an artery or vein, the consequences can be very serious.

Blood clotting in disease – clots where we don’t want them

If blood clots in one of the arteries which supply the heart muscle with blood, part of the heart may be starved of oxygen and die – this is known as a myocardial infarction, or “heart attack”.  If the same thing happens in an artery supplying part of the brain with blood, that part of the brain may die – this is a stroke (see “heart or brain attack resembles aircrash”).  
Blood clots in veins can have similarly dramatic consequences: a clot in one of the deep veins of the leg stops blood from being able to return to the heart, leading to the swollen leg characteristic of deep vein thrombosis.  If part of this clot breaks off and makes its way into the lungs, this is called a pulmonary embolus.  These are characterised by abrupt shortness of breath, or even sudden death.
Now, the important thing to understand when it comes to devising treatments to prevent unwanted blood clots, is that clots in arteries and veins result from slightly different processes.  Remember the two mechanisms by which blood clots – platelets and the coagulation cascade?  When an unwanted clot forms in an artery, it tends to be because platelets have been fooled into activating inappropriately.  In veins, it is the coagulation cascade which is to blame.  
The crucial difference is in the speed of blood flow.  Blood in arteries is propelled by the heart, so it is fast moving and at high pressure.  It flows too fast for the complicated reactions of the clotting cascade to get going – all the molecules get moved on before they can interact with each other.  But platelets can still manage to latch on to breaks in an artery wall even if they are whizzing past, and once one has latched on, it recruits others, so that pretty quickly a plug of platelets has formed, blocking the artery.  And what is it that makes them latch on?  Usually it’s an atheromatous plaque.  These are fatty deposits which build up in the walls of arteries as we age – smoking, diabetes and high cholesterol can make them more likely to form.  These sometimes break through the smooth lining of the artery wall, tricking the platelets into thinking that the artery has been injured, and setting them latching on for all they’re worth.  To recap: atheromatous plaque leads to artery wall damage, which leads to platelet activation, which leads to a platelet plug blocking the artery, which starves the brain of its blood supply and causes a stroke – all in the blink of an eye.
In veins, blood moves much more slowly as it works its way back to the heart.  This can be problematic, since sluggish flow is one of the things which encourages the coagulation cascade to spring into action.  If blood moves too slowly, the clotting factors are fooled into thinking they’ve arrived at the site of an injury, and the cascade is activated, resulting in a clot.  Usually blood moves just about fast enough through veins, propelled by the muscles of our limbs, to avoid clotting.  But if you fall asleep at the back of an 8-hour flight, your blood may stay still for long enough that you wake up with a deep vein thrombosis.

Other resources

Why Blood Clots

Coagulation explained

Warfarin Friend or foe?

Written by

Matthew Rogers is a Haematology Spr


  1. I notice now your flow chart for AF advises not to use antiplatelets as an alternative to warfarin if chadsvasc

  2. user_avatar

    One of the main changes in Stroke prevention in last 18 months is the recommendation that Aspirin alone is NOT effective in preventing thrombus build up in left atrium in people with atrial fibrillation. In essence if your patient has CHADVASC2 greater than 1 its Anticoagulants NOT Aspirin. Aspirin in this group causes as many bleeds as Anticoagulants but offers no or very little protection so should not be given.

    Unfortunately there are a very large number of patients in the groups CHADVASC 2-5 who are still being given Aspirin instead of AC. One of our goals is to get those at risk off Aspirin and onto AC and thereby prevent a great number of Strokes.

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