![]() ![]() There was no risk stratification of patients admitted to hospital Powered to detect difference in biomarker level Primary endpoint: peak troponin value during hospitalization Time to angiography in delayed group (median + IQR, h) Time to angiography in early group (median + IQR, h) A more delayed approach was based historically on a need for a period of pharmacological passivation followed by coronary angiography. There have been a number of randomized controlled trials (RCTs) ( Table 1) which have attempted to determine the value of an early invasive strategy compared to standard treatment. Randomized controlled trials evaluating timing of coronary intervention in non-ST segment elevation myocardial infarction The aim of this article is address what evidence there is for the timing of intervention, and particularly around issues of very early intervention, in those patients such Class 1A indications highlighted above. ![]() These latter guidelines 6 then break down the timing of intervention into various categories (2–25 h, 25–72 h) according to various criteria, some of which may be based more on clinical opinion than hard evidence. However, we are not debating that those patients who have refractory pain, haemodynamic or electrical instability, should have urgent intervention, which is given Class 1A in both the ESC and AHA guidelines (2014). Our ethos is to address the issues around who should undergo intervention and at what time point after presentation. It is important that the rationale of this article is understood. We will also review the current ESC guideline recommendations, which set out to guide the timing of coronary intervention in NSTEMI patients. We will touch on the mechanistic aspects to explain the potential issues with an early invasive strategy. This review article will evaluate the current evidence that can help determine the timing of invasive coronary angiography and intervention in patients presenting with NSTEMI, and whether immediate or early invasive strategies are more cost-effective. The variations in presentation make decisions around timing of intervention less categoric than with STEMI patients. Patients may suffer chest discomfort or shortness of breath only, with biomarker evidence of myocardial injury or present with acute haemodynamic compromise. 1–3 In contrast, non-ST segment elevation myocardial infarction (NSTEMI), which is defined as presentation with ischaemic chest pain, electrocardiographic changes consistent with ischaemia (ST-segment depression or T-wave inversion) and biomarker elevation indicating myocardial injury, 4 can present in a heterogeneous manner. In ST-elevation myocardial infarction (STEMI), there is complete occlusion of the coronary artery resulting in a need for immediate transfer to the cardiac catheter lab for primary percutaneous coronary intervention (PCI) to achieve reperfusion of the myocardium and improve clinical outcomes. Non-ST-elevation myocardial infarction, Timing, Percutaneous coronary intervention, Delayed intervention, Immediate intervention, Revascularization IntroductionĪcute coronary syndromes (ACS) represent a spectrum of clinical presentations in general caused by acute plaque erosion/rupture and consequent thrombus formation. We will place this current evidence base in the context of evolving therapies including high-sensitivity troponins and other biomarkers, allowing for earlier diagnosis of NSTEMI and also more potent antiplatelet agents. ![]() This article will review the current evidence base and guideline recommendations for timing of coronary intervention in patients presenting with NSTEMI. In contrast, the presence of fresh thrombus overlying acute plaque rupture may potentially result in worse outcomes following very early intervention compared to initial pharmacological therapy with antiplatelet agents and anticoagulant therapy followed by interval PCI. This can result in a heterogenous presentation, with some patients demonstrating higher risk features than others and thus potentially benefitting from earlier intervention. Within NSTEMI there is non-occlusive plaque rupture, resulting in myocardial infarction evidenced by raised biomarkers, specifically troponin, with ischaemic chest pain and electrocardiographic changes. In contrast to St-segment elevation myocardial infarction (STEMI), where immediate coronary revascularization by percutaneous coronary intervention (PCI) for completely-occluded infarct-related artery is a guideline-mandated treatment, in non-ST-segment elevation myocardial infarction (NSTEMI) the optimal timing of coronary intervention is less clear. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |