[Thrombocyte inhibitors in cardiovascular therapy].
An increased platelet-vessel wall interaction plays an important role in most forms of cardiovascular disease. In healthy arteries, the vascular endothelium prevents platelet adhesion and aggregation. As a mediator of this protective function, the endothelium produces prostacyclin, endothelium-derived nitric oxide and tissue plasminogen activator. Cardiovascular risk factors such as hypertension, hyperlipidemia and diabetes are associated with an increased platelet activation and with decreased antithrombotic properties of the blood vessel wall. The available inhibitors of platelet function interfere only with one of various mechanisms of platelet activation and of the platelet-vessel wall interaction. Prostaglandin inhibitors, such as aspirin and newer, more specific inhibitors, prevent the production and/or the effect of thromboxane A2 on platelets and the blood vessel wall. Other drugs interfere with the effect of adenosine diphosphate on platelets, or they increase intracellular concentration of cyclic GMP or AMP in platelets and vascular smooth muscle cells. The protective effects of platelet inhibitors in primary and particularly in secondary prevention of cardiovascular diseases have been documented in numerous studies. The successful clinical use of these substances, however, requires a selective prescription of the drugs in patients with cardiovascular disease.
Lüscher
T F
TF
Departement Medizin, Abteilung für Kardiologie, Kantonsspital Basel.
Pfisterer
M
M
D000375:Aging / Q000502:physiology; D000789:Angina, Unstable / Q000517:prevention & control; D001792:Blood Platelets / Q000502:physiology; D002318:Cardiovascular Diseases / Q000188:drug therapy*; D003327:Coronary Disease / Q000517:prevention & control; D004730:Endothelium, Vascular / Q000502:physiology; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*
D010975:Platelet Aggregation Inhibitors
Thrombozytenhemmer in der kardiovaskulären Therapie.