Basics
Blood thinners are colloquially referred to as all drugs that interfere with blood clotting in various ways. However, the blood does not become thinner, it just coagulates more heavily. Clotting is an essential function of the blood and ensures that the bleeding is quickly stopped when injuries occur.
In some situations, however, a targeted inhibition of coagulation is desired, so that the use of blood thinners is useful here. The aim is therefore always to prevent the formation of a blood clot (thrombus), from which there are basically two dangers. One is acute vascular occlusion, especially of arteries.
The other is the risk of thrombi being carried from veins and closing a vessel elsewhere. Blood thinners are currently taken by about 1 million people in Germany on a permanent basis and by many more for short periods of time, e.g. after a medical intervention. Within blood thinners, one can differentiate between different active substances with different mechanisms and areas of application. Blood thinners are mainly used prophylactically to prevent dreaded complications in certain diseases, but also acutely, for example in the case of a heart attack, to inhibit the growth of the blood clot that has formed. Medical terms for blood thinners are anticoagulants or thrombocyte aggregation inhibitors.
Mode of action
In order to understand the mechanism of action of blood thinners, it is necessary to briefly consider the coagulation system of the blood in a simplified form. It can be activated by injuries, disturbances of the blood flow in the vessels and pre-damaged vessel walls. Arteriosclerosis, i.e. the calcification of vessels, plays a major role in this process.
Blood coagulation can be divided into two parts. First, the blood platelets (thrombocytes) play the main role. They are activated when required by certain signals, attach themselves to the vessel wall and stick together.
By releasing messenger substances, they activate further platelets, which expand the network. This leads to the first blood clot (white thrombus), which is intended to provide a temporary cover for the leak. Certain receptors and messenger substances play a decisive role in the activation and adhesion.
A main group of blood thinners, known as platelet aggregation inhibitors, act on these receptors and messengers. The name reveals that these blood thinners inhibit the attachment and adhesion of the blood platelets and thus prevent the formation of the clot. The best known blood thinner of this type is acetylsalicylic acid, better known as ASA or aspirin. It prevents the formation of an important messenger substance to activate the blood platelets. Also widely used is clopidogrel, which blocks a receptor on the surface of the blood platelets so that it cannot be activated.
Secondary/plasmatic coagulation
The other part of blood clotting is carried by certain proteins in the blood, the clotting factors. This is somewhat slower, but ensures better cross-linking and forms a more stable red thrombus. The blood thinners that intervene here work on a total of 13 coagulation factors.
The best-known and most widely used agent in this context is Marcumar® . It is a vitamin K antagonist which inhibits the formation of four coagulation factors – factors 2,7,9 and 10 – and thus effectively suppresses the system. Another agent with the same mechanism is warfarin.
For several years now, other blood thinners have been on the market that intervene in plasmatic coagulation elsewhere. These are direct inhibitors of a coagulation factor: Dabigatran, which blocks Factor 2, and Rivaroxaban, an inhibitor of Factor 10. In addition, there is heparin, which is also often used, but is only used for a short period of time for the treatment of vascular occlusion or as a prophylactic against it.
It works by increasing the effectiveness of a protein (antithrombin 3) in the body by a factor of 1000, which controls the coagulation. The complex of antithrombin 3 and heparin is thus a competent anticoagulant. Which of the above-mentioned agents is used as a blood thinner depends on the indication and the individual situation of the patient.
