Antiplatelet Research Paper

Blood platelets are actually fragments of cells – meaning they don’t contain all the necessary cellular equipment. When a person gets a cut or scratch, platelets release thromboxane, a chemical that signals other platelets to “help out.” Without the release of thromboxane, the platelets won’t come (stick) together, no clot will form, and the cut will continue to bleed. If you have a wound, thromboxane is an indispensable self-sealing material; but if you’re a stroke survivor, thromboxane’s ability to round up “help” to form a blood clot becomes potentially life-threatening.

Antiplatelet agents, including aspirin, clopidogrel, dipyridamole and ticlopidine, work by inhibiting the production of thromboxane. Aspirin is highly recommended for preventing
a first stroke, but it and other antiplatelets also have an important role in preventing recurrent strokes.

According to a statement by the American Heart Association, taking aspirin within two days of an ischemic stroke reduces the severity of the stroke.
In some cases, it prevents death. For long-term (meaning for the rest of your life unless otherwise specified by your physician) prevention, antiplatelet therapy is recommended primarily for people who have had a transient ischemic attack (TIA or “mini” stroke) or acute ischemic
stroke.

Despite the potential benefits, antiplatelet therapy is not for everyone. People with a history of liver or kidney disease, gastrointestinal disease or peptic ulcers, high blood pressure, bleeding disorders or asthma may not be able to take aspirin or may require special dosage adjustments.

Anticoagulants

While antiplatelets keep clots from forming by inhibiting the production of thromboxane, anticoagulants target clotting factors, which are other agents that are crucial to the blood-clotting process. Clotting factors are proteins made in the liver. These proteins can’t be created in the liver without Vitamin K – a common vitamin found in cabbage, cauliflower, spinach and other leafy green vegetables. Anticoagulants, such as warfarin (Coumadin) and heparin, slow clot formation by competing with Vitamin K. This inhibits the circulation of certain clotting factors with the exotic names of factors II, VII, IX and X. Within the past 3 years, new anticoagulants have been approved by the FDA: dabigitran, apixaban, and rivaroxaban. All of these are simpler to use and less risky than warfarin (bleeding risk is lower).

The most important and most effective thing a survivor can do is take their health into their own hands.
Anticoagulants are considered more aggressive drugs than antiplatelets. They are recommended primarily for people with a high risk of stroke and people with atrial fibrillation. More than 2.7 million Americans have atrial fibrillation (AF), an-arrhythmia of the heart where the atria (the heart’s pumping chambers) quiver instead of beat. As a result, not all of the blood is pumped out of the heart, allowing pools to collect in the heart chamber, where clots may form.

An embolic stroke is a type of ischemic stroke that occurs when a piece of an atrial blood clot (embolus) is pumped out of the heart, circulates to the brain and becomes lodged in an artery. The American Heart Association recommends that most AF patients over age 65 receive some sort of anticoagulant therapy.

Although anticoagulants tend to be more effective for AF patients, they are generally recommended only for patients with strokes caused by clots originating in the heart. Anticoagulants tend to be more expensive and carry a higher risk of serious side effects, including bruising and skin rash and bleeding in the brain, stomach and
intestines.

When used as directed, however, anticoagulants have proven very effective for AF patients. Although the potential risks seem severe, the life-saving effects give these drugs a bright upside.