Early inhibition of thromboxane A2, adenosine diphosphate, and thrombin is the ultimate goal of antithrombotic treatments prescribed for patients with acute coronary syndrome (ACS) to prevent the extent of coronary plaque thrombosis and to avoid peri-interventional myocardial infarction (MI). Intravenous administration of aspirin and anticoagulation allows an immediate biological effect whereas the mandatory oral intake and metabolization P2Y12 inhibitors delay their onset of action. To overcome this limitation, a strategy of pre-treatment, defined as the administration of an oral P2Y
12 inhibitor with aspirin to all patients with suspected ACS irrespective of knowledge of the coronary anatomy and possible lesions of the individual patient, has been developed. Although widely adopted for ST-elevated MI undergoing primary percutaneous coronary intervention, this approach has been debated for more than 20 years in the setting of non–ST-elevated acute coronary syndrome (NSTE-ACS) and is now challenged by recent data. Indeed, a more aggressive platelet inhibition does not necessarily lead to less peri-interventional MI and has never been associated with any ischemic benefit, whereas more bleedings in patients with NSTE-ACS undergoing CABG surgery1 or without underlying obstructive coronary artery disease has been established.
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The 20-year-long tale of whether pretreatment should be used in NSTE-ACS is important because it reflects on the too long process of implementation of evidence-based medicine in scientific guidelines and whether interventional cardiologists are able to update their practices. The meta-analysis by Dawson et al is an important step further: pretreatment is associated with harm and does not reduce ischemic events and it is time to change.
