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Printer Friendly Print ESC Congress 2003: Blood thinners like aspirin may not be equally effective for everybody to prevent heart attack and stroke

ESC Congress 2003: Blood thinners like aspirin may not be equally effective for everybody to prevent heart attack and stroke

September 01, 2003

IMPORTANT: This press release accompanies both a presentation and an ESC press conference given at the ESC Congress 2003. Written by the investigator himself/herself, this press release does not necessarily reflect the opinion of the European Society of Cardiology

ESC Congress 2003: Clot-busters - do they work for all?




Atherosclerosis is a slow, progressive disease accompanied with sudden dramatic episodes of blood clot formation within arteries. Arteries occluded instantly by clots can not provide enough oxigenated blood to tissues of the heart, brain, or legs, therefore these tissues die. The clinical symptoms related to these events are myocardial infarction, stroke or acute limb ischaemia, respectively. Generation of arterial blood clots is initiated by activated blood platelets. The most common drug that objects the platelet's ability to form blood clot is aspirin, which is a relatively weak, but very useful blood thinner.

Doctors have been ordering aspirin since the sixties to prevent the occurence of heart attack, myocardial infarction, stroke. Aspirin is a cheap and clearly effective drug. It can reduce the risk of vascular catastrophes listed above by at least 25 percent (as an average).

There is no drug with a completely equal effect in every human being. Individuals are different, and - probably even more importantly - the extent of their disease is also different. We, cardiologists learned that in case of a more severe clinical situation, when the inner layer of blood vessels is seriously injured we have to use stronger or combined blood thinners in order to avoid occlusive blood clotting.

These particularly serious situations include chest pain threatening with a heart attack; angioplasty, when doctors actively injure the vessel by dilating its narrowing, or when they buttress the artery with a little metal tube called stent, to keep it open.

The most classical blood thinner is coumadine. When the patient takes coumadine, doctors (must) perform regular blood tests, called INR measurements to avoid bleeding or blood clots. Interestingly enough, we do not test the effect of the most widely used blood thinner, aspirin.

It has been believed, that aspirin therapy does not need any laboratory test to follow. However, clinical evidence appeared indicating that in some people aspirin might not inhibit blood platelets as effectively as in others. This phenomenon is called aspirin resistance. Obviously, it is likely that in these patients sudden occlusive blood clots can not be prevented by aspirin and these patients would not have benefit from taking the ineffective drug further.

Studying 1000 patients from HOPE trial, Dr Eikelboom and others from Professor Yusuf's group elegantly proved the clinical importance of aspirin resistance. Aspirin halts the production of a signaling molecule called thromboxane A2, which is one of the most important chemicals, forcing platelets to stick together and to start forming a blood clot.

Thromboxane A2 is degraded in the body to thromboxane B2, and the latter can be detected in the patients' urine. Aspirin takers, who still urinate a high amount of thromboxan B2 - an indicator of the maintained high thromboxane A2 production - had to face a 3,5 fold risk of cardiovascular death compared to others who had low urine thromboxane B2 concentration.

As a result, we can state that in some people aspirin can not produce as pronounced inhibitory effect as in others. These patients have a higher chance to die from heart attack or stroke and may need alternative, stronger blood thinning treatment. Measuring urine thromboxane B2 level to identify these „drug-resistant" patients is a fairly complicated and expensive method, and is largery confined to research centers. Finding a simple and cheap alternative might be very useful in treating patients with atherosclerosis.

Therefore our team has tried to adapt a simple blood test, called platelet aggregation, to screen aspirin taking patients. Ten centers (invasive cardiovascular university centers, stroke departments, county hospitals) applied the same laboratory method using the same simple instrument measuring platelet reactivity in response to different platelet activators.

First, we collected 150 patients, survivors of a myocardial infarction or stroke who were not treated with any blood thinner and served as our control group. Then we measured the platelet reactivity of the next 2215 patients, who were taking aspirin at a dose of 100-125 mg daily. Aspirin-treated patients, whose platelets remained active and responded to the agonists like not-treated ones, were considered as aspirin resistant.

According to our measurements, the chance of being aspirin resistant among patients taking aspirin for secondary prevention after heart attack or stroke is 26,9 % in Hungary.

The clinical importance of this observation has to be determined by further research. Nevertheless, we hope that we can identify those patients by this method, in whom alternative or combination blood thinner treatment may be beneficial.

Robert Gabor Kiss M.D. Ph.D.
National Center for Health Services, Budapest
Hungary

European Society of Cardiology (ESC)



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