The Question Still Arises - How Long Should I take Plavix after Coronary Artery Stent Placement?
Written by:
Hector Fontanet, M.D., FACC
Joan Stelzner, ARNP

Plavix (Clopidogrel) is a medication that is given to patients, along with aspirin, following coronary artery stent placement to prevent blood clot formation on the newly implanted stent. Currently, there is controversy regarding the optimal length of Plavix therapy following coronary artery stenting. Since there are two types of stents, drug-eluting stents (stents coated with a medication designed to prevent re-narrowing of the stented blood vessel as the body heals) and bare metal stents (stents without any coating) there are also two different recommendations regarding length of Plavix therapy.

The American Heart Association in conjunction with the American College of Cardiology issued a statement published in the January 15, 2007 issue of Circulation regarding length of Plavix therapy following coronary artery stenting. The recommendation for Plavix therapy following drug-eluting stent (coated stent) placement is currently one full year. For bare metal stents (non-coated stents), the recommendation for Plavix is at least one month. In other words, if you have received a drug eluting stent, continue Plavix for one year. If you receive a bare metal stent, do not stop taking Plavix for at least one month after implant.

Additionally, patients should never stop Plavix without first checking with their cardiologist and/or cardiology care provider. Interrupting Plavix therapy prematurely can lead to clot formation on the stent resulting in heart attack or even death.

In certain situations, Plavix therapy may need to be interrupted before the recommended length of therapy has been completed. These situations, however, are rare and only your cardiologist and/or cardiology care provider should make this determination on your behalf.

Sources:
http://circ.ahajournals.org/

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Prevention of Atherosclerosis – It’s not just about Lowering Cholesterol
Hector Fontanet, MD, FACC
Marie Cheine, Medical Writer

It is not new news that atherosclerosis is a leading cause of death from heart attack and stroke. This occurs when there is an excess of cholesterol that builds up fatty areas in blood vessels called plaques. These plaques can break up and cause blood clots in the blood vessels, causing sudden interruption of flow to the heart (heart attack), which can be fatal. Lowering cholesterol levels (the cholesterol your body manufacturers as opposed to dietary cholesterol) has long been known to reduce the risk of cardiovascular events. But it is not just about lowering cholesterol, but about prevention of heart attacks and stroke and prevention of damage and inflammation to the lining of the blood vessels.

The medical community has been treating elevated cholesterol levels with a class of drugs known as statins for over 25 years. Statins have proven to be effective in slowing the progression of plaque build up in the blood vessels. In early 2004, results from the multi-national trial (PROVE IT – TIMI 22) demonstrated that lowering a patient’s LDL or “bad” cholesterol to less than 70 mg per deciliter helped prevent recurrent heart attack and death, even in patients with normal cholesterol levels.

That is why in the recent years the medical community has been examining the relationship between cardiac events and inflammation. Inflammation occurs in the body in response to infection and injury. Current views are that exposure to high cholesterol is responsible for inflammation of the blood vessel linings, resulting in plaque build up and disease progression.

The results of PROVIE IT-TIMI 22 and other major clinical trials found that intensive treatment with statins also lowers C-reactive protein (CRP), a marker of inflammation in the body. A decrease in levels of CRP correlated with significantly slower rates of progression of coronary disease. In fact, in a recent study published in the New England Journal of Medicine, Dr. Nissen and associates showed that patients with the largest reductions in CRP levels actually had regression of plaque build-up in the blood vessels (www.nejm.org).  Furthermore, achieving a target CRP level of <2 mg/l is associated with better outcomes (less risk of heart attacks and strokes) for patients regardless of the DL level achieved with statin treatment.

These recent studies provide strong evidence that inflammation plays an important role in heart and vascular disease. Furthermore, the reduction of inflammation after a myocardial infarction may improve cardiovascular outcomes and alter the atherosclerotic processocess.

In summary, statin therapy is a widely used drug that is successful in lowering LDL cholesterol and CRP levels in the blood stream. Large-scale clinical trials have shown the overwhelming positive results of statin therapy in patients who have suffered a heart attack.
As a class, these medications are safe for most. However, in a small percentage of people, the drugs can cause muscle pain or fatigue and can affect liver function. Careful monitoring while on statin therapy is imperative and side effects are easily detected. The benefits of this class of drugs far outweigh the risks. Recent findings that statins have a dual benefit of reducing LDL cholesterol and CRP levels suggests that aggressive statin treatment results in the best outcomes for patients.

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