Last week, we discussed a class of medications called “statins.” This week, I’d like to discuss an even broader class: “blood thinners,” a term that reflects how physicians often use non-medical words to describe medications or medical conditions. Blood thinners refers generally to a variety of drugs that alter the tendency of blood to clot and includes antiplatelet agents and anticoagulants (also known as antithrombotics). We call these agents blood thinners because—in decreasing the tendency of blood to clot—they make the blood seem thinner when a person is bleeding.
In actuality, the blood is not thinned by these agents as it flows through the blood vessels inside the body. But when a person has a cut or has blood drawn, the blood doesn’t thicken as quickly. It comes out of the body no “thinner” than a person who is not on these agents, but it stays liquid longer, as it is more difficult for clot to form. This is how these agents prevent bad things from happening—like heart attacks, strokes or pulmonary emboli (clots in the lungs).
Another misconception is that a person feels colder when they are on these drugs, believing that the “thin” blood is not as warm. But the body temperature doesn’t change in people who take blood thinners and, as discussed above, the blood isn’t actually thinner (inside the body) in the first place.
Antiplatelet agents make platelets less “sticky,” less likely to clump together, decreasing the tendency for clot to form. Platelets float around in the bloodstream as small little sacks of various molecules. They don’t do anything until they are activated, generally due to injury to a blood vessel, at which point they attach to one another, forming a kind of dam. Antiplatelet agents include one of the oldest drugs still in use: aspirin. In addition, clopidogrel (former brand name Plavix™), prasugrel (brand name Effient™) and ticagrelor (brand name Brilinta™) are all antiplatelet agents.
Anticoagulants work on another part of the clotting system—the clotting factors. These are molecules that are in the blood and, like platelets, become activated when a blood vessel is injured. Anticoagulants include warfarin (common brand name Coumadin™), apixaban (brand name Eliquis™), rivaroxaban (brand name Xarelto™), and dabigatran (brand name Pradaxa™). IV anticoagulants include heparin and enoxaparin (brand name Lovenox™).
One way to look at these two systems is to think of clotting factors as the scaffolding of the clot, with the platelets being the cement. Because different medical conditions that lead to clot formation involve the clotting factors versus platelets to a greater or lesser extent, we have found that antiplatelet agents and antithrombotics work better for one condition versus another. Antithrombotic agents are used to treat or prevent clot in the veins (deep vein thrombosis or “DVT”) and lungs (pulmonary embolism). They are also used to prevent strokes in patients who have atrial fibrillation. On the other hand, antiplatelet drugs are commonly used in people who have had heart attacks or stents, lowering the risk of recurrent heart attacks or clot from forming in the stent and closing it off. Of note, it is very important for anyone who has a stent never to stop their antiplatelet medication without discussing it with their cardiologist. Aspirin and Plavix are also used to lower the risk of strokes in people who have had one in the past. But they are minimally effective in reducing strokes caused by atrial fibrillation.
All these drugs are quite potent and can cause bleeding problems. The challenge that we face is to use the right combination and right doses to maximize their ability to prevent harm and minimize the possibility of causing harm. We continue to gather information in clinical trials to optimize this balance. But, as I have emphasized time and again in these blogs, the art of medicine plays an important role.
Greg Koshkarian, MD, FACC