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Could you explain blood thinning therapy and what role aspirin plays?
I am a 63 year old white male, 5'7" 168 lbs who exercises regularly. I take 25mg of atenolol daily for high blood pressure. I have recently been diagnosed with atrial fibrillation (2 to 3 episodes per week). I was offered a choice of Pradaxa and another drug for blood thinning, or ablation. I take a baby aspirin and fish oil daily. If blood thinning drugs are routinely prescribed for this condition what, in fact, is the target viscosity for your blood with blood thinning therapy? Why isn't aspirin a recognized therapy for afib? It seems to me to be an obvious and logical question that if a physician wants to put me on blood thinners, there should be an optimum viscosity that we are trying to achieve. Further, it seems that this should be measured prior to the beginning of blood thinning therapy. Please explain this whole concept and why blood viscosity measurements are not taken.
submitted by Patrick from San Antonio, Texas on 11/6/2012
by Texas Heart Institute cardiologist, Michael J. Mihalick, MD
Dear Patrick: From the tone of your questions I get the impression that you have an engineering background. Although you may have heard your primary physician and possibly your cardiologist refer to anticoagulation as 'thinning the blood', this is really not true and is used as an oversimplification of the process of anticoagulation. Blood is a complex fluid and its viscosity (or more accurately its rheology) does not follow the simple rules that apply to other more homogeneous liquids such as motor oil. Blood viscosity is related to a number of factors. One of these is the concentration of red and/or white blood cells. For example, there is a threshold of red cell content beyond which blood viscosity becomes suddenly and significantly increased and can predispose the affected individual to stroke. This is most commonly seen in patients with cyanotic congenital heart disease. Periodic removal of blood cells and replacement with saline may be necessary to decrease the risk of stroke. If you're interested, you can Google key words such as polycythemia or rheology of blood for further information.
Anticoagulation and viscosity are two separate phenomena. Blood clotting occurs when a chain reaction is triggered that results in blood clot formation. There are proteins circulating in the blood called clotting factors which, when activated, form a clot. This is obviously desirable in the case of trauma and is what keeps us from bleeding to death from a minor cut or nosebleed. This clotting process can be activated inappropriately by exposure of the inner lining of blood vessels to the circulating blood in diseases such as arteriosclerosis. Slow, stagnant blood flow can also trigger clotting. This frequently occurs in the upper heart chambers when they are not normally contracting as in atrial fibrillation. It turns out that atrial fibrillation is a major cause of stroke. Large studies both here and in Europe have shown that the incidence of stroke can be significantly decreased if the patient is anticoagulated with Coumadin (warfarin). Aspirin has not been shown to have this protective effect in AF patients although it is effective in preventing clotting on the arterial side of the circulation (arteries). Clots that form in the veins and heart chambers require coumadin-like anticoagulants for their prevention.
For over 50 years, warfarin was the only such drug available. It interferes with the clotting reaction by blocking the clotting factors that require vitamin K for their production. Unfortunately, many foods and drugs can affect the vitamin K level in the body. That is why the individual's dose has to be customized to his/her particular diet and drug regimen. A clotting test called the prothrombin time or 'pro time' is used. Recently a number called the INR (International Normalized Ratio) has been used to standardize the prothrombin time test among laboratories. A number between 2.0 and 4.0 is desired and we aim for 2.5 for AF patients. More recently drugs that work on factors not dependent on vitamin K have been developed and marketed. They work quickly (in hours) and wear off in 24-48 hours. Although there are some compounds available to treat bleeding complications with these drugs, specific antidotes are not yet available. These new drugs have been shown neither inferior nor superior to warfarin. They have a similar bleeding risk except that the incidence of brain hemorrhage is much less. This is thought to be due to a more stable level of anticoagulant effect. They have only been approved for use in patients with atrial fibrillation and for the prevention and treatment of leg vein clots (phlebitis). They are not currently approved for use in patients with mechanical heart valves.
Whether or not your cardiologist recommends anticoagulation in your specific situation depends on his assessment of your particular stroke risk weighed against your particular bleeding risk. There are several scoring formulas to assess the risk of stroke in atrial fibrillation, one of which is the CHADS-2 score. Your cardiologist will be happy to discuss this with you. I hope this has been helpful.
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Updated November 2012