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“Everyone is entitled to their own opinion, but not their own facts.” Senator D Moynihan
Modern management of patients with acute coronary syndromes (ACS) in the UK is informed by a rapidly expanding envelope of clinical trial data. Thus, we have witnessed rapid evolution in the assessment and treatment of this patient group over the last decade, with routine and universal application of troponin measurement, early angiography and revascularisation in non-ST elevation myocardial infarction and immediate primary angioplasty for ST-elevation myocardial infarction (STEMI) being the key examples. Interventional cardiologists are inevitably at the centre of care pathways that are dominated by percutaneous coronary intervention (PCI).
Although there is evidence for the benefit of dual antiplatelet therapy (DAPT) as a medical treatment in its own right in ACS, the requirement for DAPT is much stronger following coronary stent placement during PCI.1 Specifically, the spectre of stent thrombosis and other ischaemic complications following PCI in patients with ACS demands appropriate and effective DAPT. Traditionally, the platform upon which DAPT is delivered in patients with ACS is based upon suppression of thromboxane A2 production by aspirin, to which a P2Y12 receptor inhibitor, which blocks ADP-mediated platelet activation, is added. Standard doses of both drugs are then prescribed to all patients without any assessment of individual response. Since clopidogrel took over the role as the default P2Y12 inhibitor from ticlopidine in the 1990s, it has held this position unchallenged until recently. However, in the last couple of years there has been a meteoric uptake of newer P2Y12 inhibitors (prasugrel and ticagrelor) to displace clopidogrel as the default P2Y12 inhibitor in ACS, particularly for primary PCI. But how well does this radical change in clinical practice bear forensic scrutiny? Specifically, we should ask the following questions. Is the switch to prasugrel/ticagrelor clinically appropriate? Is …
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