A study published in November of last year in the New England Journal of Medicine, identified warfarin, insulin, oral antiplatelets and oral hypoglycemics as the drugs that cause 2/3 of emergency admissions for Adverse Drug Events (ADEs) in older Americans.
Let’s take a look at one of these drug categories, antiplatelet drugs.
Antiplatelet drugs can be divided into three categories. Each of the classifications work at a different part of the process the body goes through to make a clot. Without taking you through the complicated physiology of the clotting cascade, let’s review the basics. It takes platelets and fibrin to make a clot. If we view fibrin as the threads and platelets as the filler, the body responds to a vessel injury by forming a “knitting” ball composed of threads of fibrin. The platelets stick to the threads and each other forming a “plug” to stop bleeding. While this process is beneficial if you cut yourself, it is detrimental if the injury is inside the vessels and reoccurs due to a disease process such as Coronary Artery Disease. To stop platelets from sticking to plaque and forming a blockage in the vessel, we give antiplatelet drugs to decrease the “stickiness” of the platelets causing them to float along the vessels instead getting caught on an injured part of the vessel, or making a plaque build up even larger.
Antiplatelet drugs work to prevent thrombus formation in the arteries, unlike their counterparts anticoagulants which work to prevent thrombi in the venous system.
The major uses of these drugs are primary or secondary prevention of the consequences of coronary artery disease; MI ( myocardial infarction), angina, TIA (transient ischemic attacks), CVA (cerebrovascular accidents), and PAD (peripheral artery disease). They are also used in the cardiac cath lab for stent placement and other angioplasty procedures.
Aspirin is the first group of antiplatelet drugs. It is the only drug in the class but what a powerful drug it is. The effects on platelets is seen even in low doses. The effects of aspirin on platelets is irreversible, so a single dose of aspirin decreases the effects of platelet aggregation, or clumping, for the life of the platelet (usually 7-10 days). However, no drug is perfect, so we need to discuss the drawbacks of aspirin. It can cause an allergic reaction in many and there is an increased incidence of GI side effects including bleeding. It can be given with food to decrease the GI effects.
The second group of antiplatelets include ticlopidine (Ticlid), dipyridamole (Persantine), and a familiar one, clopidogrel (Plavix).The first two are older drugs. Ticlid is usually given for stroke prophylaxis if the patient is unable to tolerate aspirin. It is a last resort drug due to serious side effects including neutropenia, agranulocytosis, aplastic anemia and TTP (thrombotic thrombocytopenic purpura). Persantine is used to prevent thromboembolism after heart valve replacement. It is given in conjunction with warfarin (Coumadin).
The effects of Clopidogrel (Plavix) begin two hours after the initial dose and, like aspirin, persist for the life of the platelet. Studies have shown Plavix is slightly more effective than aspirin but costs a lot more. A 1 month supply of aspirin is about $3 where a month’s supply of Plavix about $100. Clopidogrel has also been shown to interact with proton pump inhibitors (PPIs) making the antiplatelet effect less effective.
A relatively new drug in this category you might be seeing is prasugrel (Effient). It is similar in action and effectiveness to Plavix but does not seem to interact with PPIs.
The third category of antiplatlets are used in the cardiac cath lab and given IV. These are used for stent placement and short term prevention in ischemic events. They include tirofiban (Aggrastat), eptifibatide (Integrelin) and abciximab (ReoPro).
In the next post we will discuss the side effects and the nursing implications of administering these drugs.
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