"What can I take in place of Coumadin?”

I’m asked that question regularly. The answer is simple: Nothing. Coumadin (warfarin) is a powerful inhibitor of the blood’s clotting ability for which there is no substitute. It is, after all, a highly effective rodent poison that kills rats and mice by causing internal bleeding.

While the dose used to trigger fatal hemorrhages in rodents is much greater than that used in medical treatment, hemorrhages, some fatal, can and do occur in people taking Coumadin as part of their medical regimen.

The question that should be asked is not, "What can I take in place of Coumadin?” but rather, "Is Coumadin Right for Me?” or "Do I need to be taking Coumadin, given my current condition?”

In some conditions the answer is clear: Coumadin is essential to prevent severe or fatal complications. These would include the presence of a blood clot in the deep veins of the leg or when a mechanical heart valve is present.

The majority of individuals on long-term Coumadin therapy, however, have conditions in which the risk of hemorrhage or other side effects of the medication may equal or exceed the risks it is meant to address. The two most common conditions in which long term Coumadin therapy is prescribed are atrial fibrillation (a fluttering of the upper heart chambers) and myocardial infarction (heart attack). Statistical studies support the use of Coumadin in these conditions, but the statistics may not dictate the best decision for each individual.

The case for placing individuals who have had a heart attack on a combination of aspirin and coumadin is based upon the (WARIS-II study 23rd Congress of the European Society of Cardiology (ESC) Stockholm, Sweden; September 2001). In this study approximately 1200 Norwegians who had experienced a heart attack were placed on either aspirin alone, warfarin alone, or a combination of aspirin and warfarin. Over a four year period, 20 % of those receiving aspirin alone, 16.7 % of those receiving warfarin alone, and 15 % of those receiving both aspirin and warfarin experienced a second heart attack or a stroke.

The CHAMP study (Circulation 105: 557-563, 5 Feb 2002), which looked at 5012 U.S. Veterans, failed to show any difference in outcome between those given aspirin alone or warfarin in combination with aspirin. Those on both warfarin and aspirin hemorrhaged 1.7 times more often than those on aspirin alone.

It could be argued that someone who has had a heart attack needs to decide which study to believe – the WARIS study or the CHAMP study. This is not the case, however. The studies themselves are seriously flawed.

There is no indication that the WARIS investigators made any effort to assure that other known risk factors, such as cigarette smoking, were equally divided among the three groups in the study. Having failed to do so, there is no way to assure that the individuals in the aspirin only group were at the same risk of a second event as those in the warfarin groups. Neither study made any attempt to reduce the risk of a second heart attack or stroke by preventing oxidation of LDL cholesterol or by lowering homocysteine to a safe level.

Individuals who address these factors cannot meaningfully compare their risk of a second event with those who simply take drugs to prevent their blood from clotting effectively. The fact that 51 % of the participants in the WARIS study experienced a second cardiovascular event within 4 years and 34 % of those in the CHAMP study within 2.7 years should lead to the conclusion that anticoagulation is not an effective strategy to prevent second events. That such studies are being used to promote one method of anticoagulation over another is a tragedy of monumental proportions.

The case for the using warfarin in atrial fibrillation is similarly muddy. Because blood is not being actively pumped out of the upper heart chambers it can pool and, because it is stagnant, clot. Portions of these clots can then break off and be sent through the arterial circulation, causing strokes. The numbers that are widely quoted to support long-term warfarin administration in those with atrial fibrillation are that aspirin reduces the risk of stroke by 36 % and warfarin by 68 %.

The studies showing the benefit of warfarin were done in academic centers, however. These centers tend to treat the sickest people in the population, those with serious or multiple health challenges.

Researchers at Washington University in St. Louis have demonstrated that the risk of stroke rises rapidly when other conditions such as congestive heart failure, high blood pressure, or diabetes are present. Therefore, addressing these conditions appropriately may be significantly more effective than taking warfarin in preventing a stroke.

This position is supported by a study of people receiving care from community physicians (BMJ October 9, 1999; 319:958-64). This study found that the rate of stroke was 1 % in those less than 78 years of age and 4 percent in older individuals regardless of whether aspirin or warfarin was used. The rate of a major hemorrhage was 1.2 % and of a minor hemorrhage was 2.7 % in both groups.

Individuals taking warfarin must be monitored with regular blood work, typically at 2 week intervals. In addition to the risk of hemorrhage, side effects of Coumadin include abdominal pain and cramping, allergic reactions, diarrhea, fatigue, feeling cold and chilled, feeling of illness, fever, fluid retention and swelling, gassiness and bloating, hepatitis, hives, itching, lethargy, liver damage, hair loss, nausea, gangrene, pain, purple toes, rash, severe or long-lasting inflammation of the skin, taste disturbances, vomiting, and yellow skin and eyes.

Warfarin therapy should not be a one-size-fits-all proposition. The decision to take Coumadin on an on-going basis should be an individual one. Known risks of cardiovascular disease should be addressed. Personal risk based upon one’s age and the presence of concurrent conditions should be determined. The cost and inconvenience of monitoring and the potential for drug side effects should also be considered.

Someone who has had a heart attack should aggressively address the factors that triggered the initial attack. Doing so should drop the risk of a second cardiovascular event much more dramatically than relying upon aspirin and Coumadin.

An individual with atrial fibrillation who has reached the age of 78, who has a past history of stroke, and who has concurrent congestive heart failure, hypertension and diabetes can clearly decrease his or her risk of stroke by taking Coumadin. The person who is younger than 78 and has no concurrent conditions may legitimately conclude that his or her risks from taking Coumadin are greater than the risk of an atrial fibrillation associated stroke.

Addendum:  Since this article was written in 2006 other anti-clotting drugs, such as Pradaxa and Xarelto, have appeared on the scene.  While they do not require the regular monitoring of Coumadin, they carry similar risks of hemorrhage.  If bleeding occurs while on Pradaxa or Xarelto there is no antidote available to reverse the effect of the drug and stop the bleeding. 

 Nattokinase, an enzyme that helps the body dissolve small clots before they become big ones, may be an alternative to Coumadin for some individuals.  Unfortunately, there are no medical studies demonstrating its effectiveness in preventing blood clots or strokes, so it is impossible to compare a regimen of omega-3 fatty acids and nattokinase with one of the anti-clotting drugs.  If it is determined that Coumadin is not right for you supplementing omega-3 oils and nattokinase should be considered as a way to potentially reduce the risk of a clot-related event.