By Nicholas Tullo, MD

Atrial fibrillation (AF) is a common heart rhythm disturbance that can affect as many as 20% of the population.  In general, patients with atrial fibrillation have five times the risk of having a stroke as someone without AF. Blood thinners are often used to reduce the risk of stroke in patients with atrial fib, but does every person with atrial fibrillation need a blood thinner?  This article will help you to understand what atrial fibrillation is, who is at risk of having a stroke, and how doctors make the decision of whether you might need to be on blood thinners. 

What Is Atrial Fibrillation?

In a healthy cardiovascular system, the heart contracts and relaxes at a regular rate. The contraction of the heart muscle is controlled by the heart’s electrical system, and we can analyze the electrical activity of the heart with a test called an electrocardiogram (referred to as ECG or EKG).  Atrial fibrillation is diagnosed when the electrical signals that control the top chambers of the heart become disturbed in a very rapid and disorganized manner. This chaotic electrical activity causes the atria to beat in an ineffective manner… the muscle just quivers instead of squeezing in a coordinated fashion. The rapid electrical impulses cause the heart to beat irregularly, which affects the flow of blood from your heart to the rest of your body.

Symptoms of Atrial Fibrillation

People with atrial fibrillation may have symptoms of palpitations, weakness, lightheadedness, shortness of breath, or exercise intolerance.  When these symptoms occur, AF can adversely affect a person’s quality of life. However, many patients have AF with no symptoms at all. In fact, some patients are diagnosed by accident because they happen to be having atrial fibrillation during a doctor visit, or it may be picked up by chance on a heart monitor. 

Atrial fibrillation comes in two versions.  One type of AF is known as “Paroxysmal AF,” and is characterized by periods of atrial fibrillation that come and go. These episodes can last from minutes to days, but they resolve on their own and a normal rhythm eventually resumes.  The other type of AF is known as “Persistent AF.”  As the name implies, this type of AF does not go away. Once it occurs, it will persist until a doctor intervenes to get rid of it. The most common procedure designed to eliminate persistent AF is known as “electrical cardioversion.”  In this procedure a very brief electrical jolt is applied to the chest under deep sedation. The shock stops the atrial fibrillation and allows the normal rhythm to take over again.  Sometimes a high dose of a certain “antiarrhythmic” medication may be effective in getting persistent AF to stop.  Either way, antiarrhythmic medication is usually needed to help the patient stay in a normal rhythm afterwards.

Why Does Stroke Occur In AF Patients?

Although we know AF is associated with an increased risk of stroke, the exact mechanism is controversial. The rapid electrical disturbance that occurs with atrial fibrillation adversely affects the contraction of the atrial muscle. This can lead to slowing of the blood flow within the atrial chamber, particularly the left atrial appendage, which is a large outpouching of the left atrium that is part of everyone’s normal anatomy. If the movement of blood within the left atrial appendage slows sufficiently, then the blood might sit there and form a clot. Theoretically, if that blood clot breaks off into the circulation, it can be swept by the arterial blood flow up to the brain. Even a small blood clot that gets lodged up in the cerebral (brain) circulation can cause havoc, potentially damaging a large part of the brain by depriving it of oxygen and nutrients. Patients who experience a large “cardioembolic” stroke are often severely affected, can suffer from severe weakness or paralysis of half their body, and 50% of those patients don’t live more than a year after such an event.

The purpose of blood thinners is to make the blood less likely to form a clot within the heart. The blood isn’t actually thinner… it just takes longer to clot. The beneficial effects of blood thinners are well known – they can reduce the risk of stroke in patients with atrial fibrillation as much as 80%.  However, the term “blood thinner” is often misused, and not all medications referred to as blood thinners actually have such a beneficial effect in patients with AF. 

Normal versus Abnormal Clotting

blood thinners
Most people don’t understand our body’s clotting function. It turns out that there are two substances normally found in our blood that are designed to keep us from bleeding to death every time we cut ourselves shaving.  One is our platelets and the other is the coagulation proteins.

Platelets.  You can separate whole blood into two components… the cells and the straw-colored liquid that the cells are floating in, called plasma. The cellular portion consists of red blood cells that carry oxygen, white blood cells that mostly fight infection, and platelets. Platelets are microscopic fragments of cells that are made in the bone marrow and are released constantly into the bloodstream. Platelets are very sensitive to materials that are released when a blood vessel gets injured. The injury “activates” the platelets, causing them to stick to the lining of the blood vessel and also to clump together, forming a “plug” that can cork off any small hole in a blood vessel.  Platelets are vitally important in stopping bleeding from smaller blood vessels. Unfortunately, platelets can be activated by any injury, In fact, coronary artery disease can lead to injury of the inner lining of those coronary arteries that feed the heart muscle, and platelet activation within the coronary artery is felt to be the cause of a heart attack. Medications such as aspirin, clopidogrel (Plavix®), ticagrelor (Brilinta®), and prasugrel (Effient®) prevent platelets from being activating and are used to prevent heart attacks. However, they don’t have much of an effect on preventing strokes in atrial fibrillation.

Coagulation Proteins.  In the last paragraph, I mentioned plasma, which is the liquid portion of the blood. Dissolved in the plasma are many substances, including special coagulation proteins, which are manufactured by the liver. These coagulation proteins can undergo a complex chain of chemical reactions in response to injury, resulting in the formation of microscopic fibers made of a protein called fibrin. The strands of fibrin get tangled together and act like cheesecloth, trapping great numbers of cells and material in a gel-like matrix or “thrombus” (clot).  These coagulation proteins can become activated during atrial fibrillation and that seems to lead to the clots that cause strokes. Medications that inhibit the clotting proteins are known as “anticoagulants,” and the oldest medication in that class is warfarin (Coumadin®), which has been around since the 1950s. Unfortunately, warfarin is very unpredictable in its effects, so patients have to have a blood test called an I.N.R. at least once a month (sometimes as often as twice a week) to make sure that the warfarin dose is appropriate.  Too much and people can bleed excessively, but not enough warfarin and the protective effects will be inadequate. 

In the last 8 years or so, several new anticoagulation medications have become available in the U.S.  These “novel oral anticoagulants” are referred to as “NOACs” and have become a popular replacement for warfarin. They include dabigatran (Pradaxa®), rivaroxaban (Xarelto®), apixaban (Eliquis®), and edoxaban (Savaysa®). NOACs do not require constant monitoring of the blood since they work more consistently. They are much easier to take and they generally do a better job of preventing strokes than warfarin, often with a lower risk of side effects like major bleeding.

Do You Need An Anticoagulant?

There are a number of risk factors that are known to increase the chance of a person with atrial fibrillation of having a stroke. These risk factors include age over 65 years (especially over 75 years), hypertension, diabetes, heart failure or weakened heart muscle, vascular or coronary disease, and especially a history of a prior stroke.  Being female increases the risk slightly if you are over age 65.  The more risk factors you have, the higher the chances of having a stroke and the more you could benefit from anticoagulation. If you have NO risk factors (under age 65 with none of the medical problems listed) then your risk of stroke should be less than 1% per year. In that case, there is no measurable benefit to using anticoagulation, and so it is not recommended. Some patients with no risk factors are advised to take aspirin, but even that is controversial since aspirin is known to cause stomach problems.  Anyone with two or more risk factors should be started on anticoagulation according to published guidelines. Anyone who needs to undergo cardioversion, regardless of how many risk factors they have, should be on anticoagulation for at least three weeks prior to the procedure. There are exceptions to these guidelines, so you need to discuss all of the issues with your doctor.   

In summary, patients with atrial fibrillation need to have a detailed and extensive discussion with their doctor, or possibly a cardiologist (heart specialist), to determine their potential stroke risk and to discuss the possible benefits of blood thinners to prevent a stroke. There are no hard-and-fast rules – everyone needs to be evaluated individually and the risks and benefits of blood thinners need to be weighed for every patient and adjusted as the patient gets older.   

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