Oral antiplatelet therapy in the treatment of acute coronary syndrome

In recent years, there have been rapid developments in cardiology, particularly regarding the diagnosis and treatment of acute coronary syndromes (ACS). In this article, we reviewed the position of oral antiplatelet therapy in current guidelines. Since plaque rupture in ACS leads to a contact between atheroma content and platelets, resulting in rapid platelet aggregation and formation of thrombus plug, the ACS treatment must provide an effective inhibition of platelet aggregation. Therefore, dual antiplatelet therapy with aspirin and a P2Y12 inhibitor is the cornerstone of ACS treatment. The fact that the genetic and pharmacokinetic properties of clopidogrel, a P2Y12 inhibitor, cause insufficient antiplatelet efficacy and inadequate offset of action has led to the introduction of new P2Y12 inhibitors such as prasugrel, ticagrelor and cangrelor, which offer an improved antiplatelet efficacy with a bleeding risk within acceptable limits. Prasugrel, which is currently approved in Turkey, is used in ACS only for percutaneous coronary intervention (PCI) in the patients with a known coronary anatomy and without an intended bypass surgery. It has been found prasugrel is found to be efficient in the diabetic patients and for the prevention of subacute thrombus. However, it has limitations such as being contraindicated in the patients with a TIA history, and recommended not to be used (or used with dose reduction) in the patients above the age of 75 years and those with a body weight less than 60 kg. The other approved agent in Turkey is ticagrelor. It allows starting treatment without coronary angiography and can be used in a wide spectrum including PCI and medical treatment, and decreases mortality, all of which are advantages; however, it causes dyspnea in some patients and is dosed twice daily, which are considered as limitations. The widespread use of new P2Y12 inhibitors in daily practice will demonstrate the antithrombotic efficacy, bleeding risk, effect on mortality and patient compliance associated with these drugs.