Efectos cardioprotectores del ticagrelor

Abstract

The development of platelet P2Y₁₂ receptor inhibitors has made a crucial difference to the treatment of patients with acute coronary syndrome. In recent years, extensive evidence from both laboratory and clinical studies has established that platelet P2Y₁₂ receptor inhibitors have pleiotropic effects as well as antiplatelet properties. One possible explanation is that the P2Y₁₂ receptor is found on a wide variety of cells in addition to platelets and could, therefore, modulate the inflammatory response, endothelial function, vascular tone, and ischemia–reperfusion injury. Studies in various animal models and a number of clinical trials have demonstrated that the cardioprotective potential of platelet P2Y₁₂ receptor inhibitors is mediated by a mechanism involving the activation of signaling pathways associated with endogenous myocardial protection (e.g. ischemic postconditioning). However, ticagrelor, unlike other P2Y₁₂ receptor inhibitors, has been shown to influence an additional cardioprotective pathway involving mechanisms associated with the increased bioavailability of adenosine, a molecule that is mainly produced by endothelial cells in response to ischemia and which has several beneficial cardiovascular effects. This article briefly reviews the different mechanisms of action of various platelet P2Y₁₂ receptor inhibitors and explores the cardioprotective effects exerted by these compounds in addition to their antiplatelet actions, particularly those effects associated with adenosine, which are uniquely induced by treatment with ticagrelor.