The updated Australasian guidelines for ACS management emphasize rapid diagnosis with high-sensitivity troponin, individualized antithrombotic therapy based on bleeding risk, and the avoidance of routine oxygen therapy in normoxic patients.
Adoption refines ACS pathways with hs-troponin and bleeding-risk antithrombotics; extends prior guidelines by de-emphasizing routine oxygen.
The Heart Foundation's Guidelines for the Management of Acute Coronary Syndromes was first published in 2006,1 with an addendum summarizing new evidence and consequent changes in recommendations published in 2007.2 The current 2011 Addendum3 summarizes clinical trial evidence published since the last addendum that is relevant to the management of acute coronary syndromes (ACS) in the Australasian context, and makes recommendations for practice change to improve patient outcomes. The core writing group was comprised mainly of cardiologists and Heart Foundation staff, but included a lone emergency physician. The process of development of the recommendations was iterative, dynamic and highly interactive over an extended period of meetings and teleconferences. Data were not simply taken at face value; there was often robust discussion of the relative merit of published data, its relevance to the Australasian context and practice, and how to deal with evidence gaps. The final recommendations are evidence-based, with grades of evidence reported according to the current National Health and Medical Research Council classifications.4 This Addendum covers 16 published pages with 58 references.3 The main topics addressed include serum troponin measurement in the diagnosis of ACS, choice of reperfusion therapy for ST elevation myocardial infarction (STEMI), antithrombotic therapy for STEMI and non-ST elevation ACS (non-STEACS), an approach to assessment of bleeding risk in ACS, oxygen therapy for patients with ACS and system factors. A summary of the changes in each of these domains of particularly relevance to emergency medicine will be discussed. Readers are referred to the Addendum for the detailed discussion of the evidence and the full wording of the recommendations.3 New troponin assays are much more sensitive than their predecessors but less specific for the diagnosis of ACS. The nett result is that troponin testing can diagnose potential ACS earlier and can contribute to a faster ‘rule out ACS’ strategy. However, a positive troponin test does not, of itself, diagnose ACS. The evolution of troponin testing makes it of paramount importance that emergency physicians are aware of which test is available in their practice setting(s). The analytical performance of the test will dictate appropriate testing intervals for the reliable detection of ACS. High sensitivity tests might allow an interval as short as 2–3 h, whereas so-called ‘conventional’ tests and most point-of-care tests still require a longer testing interval. The changes to troponin assays are reflected in the new recommendations as follows: In cases of suspected ACS, serum troponin should be measured at ED presentation (unchanged from 2007). The use of high sensitivity troponin assays, where available, is recommended. A high sensitivity troponin result should be interpreted as positive if the level is ≥99th centile, OR there is a change of >50% above baseline. If using a high sensitivity troponin, the interval between tests can be reduced to 3 h, as long as one assay is at least 6 h from symptom onset. A single 6 h test can be used for patients who present >6 h from pain onset. A high sensitivity troponin result should be interpreted as negative if the level is <99th centile, AND there is a change of <50% above baseline. Such a result can form part of an early ‘rule out ACS’ strategy. When using a ‘conventional’ test, if the initial troponin test is negative, it should be repeated at least 8 h after symptom onset (unchanged from 2007). Figure 1 of the Addendum is an algorithm for the use of high sensitivity troponin assays in evaluation of ACS. Unfortunately, it has a number of qualifiers and caveats reflecting the evolving understanding and evidence gaps in this area. Of particular interest are the suggestions on how a positive initial troponin assay should be handled. It recommends a further level is taken 6 h later to measure the change in level. A significant change is considered indicative of likely myocardial infarction (MI), with a lack of change ruling out an early MI (with the caveat that late MI or other cause of troponin elevation should be considered). This has both positive and negative potential impacts for EDs. If a slightly longer period of testing can avoid a patient with an elevated troponin from non-ACS causes being admitted to a coronary care unit (CCU), this should improve CCU access for patients with true ACS. As patients awaiting CCU are significant contributors to access block, this is a positive for EDs. The longer ED or observation time is relatively small compared with current practice, so should have a minimal negative impact. On the down side, rigid application of the algorithm might see patients with clear clinical evidence of ACS being delayed in the ED awaiting a follow-up 6 h test. Close collaboration between ED and cardiology services will be needed to ensure that local processes facilitate the early referral of the higher risk patient. There is also a recommendation that if a troponin result cannot be provided within 60 min, point-of-care testing should be performed. Although this could allow earlier detection of high-risk patients, given the longer testing interval required with current point-of-care testing, it is unclear whether the nett benefit would outweigh the impact on ED flow in most EDs. Since the addendum was finalized, two new papers have been published addressing the question of rapidly ruling out MI. Scharnhorst et al. using the TnI Untra assay, a second generation high sensitivity test, reported that a specimen 2 h after arrival had 100% sensitivity for detection of non-STEACS (95% confidence interval 86–100%), if a rise above the 99th centile or >30% change from baseline was considered a positive result.5 They found myoglobin and creatine kinase MB had no added diagnostic value. A different approach taken was the ASPECT trial.6 This investigated whether an accelerated diagnostic protocol (using Thrombolysis in Myocardial Infarction score, ECG and a multimarker point-of-care test) could identify a cohort of chest pain patients at very low risk of short-term adverse outcomes. Nine point eight per cent (9.8%) of patients were identified as low risk and potentially suitable for early discharge. A major adverse cardiac event occurred in three patients, giving the protocol a sensitivity of 99.3% (95% CI 97.9–99.8) and a negative predictive value of 99.1% (97.3–99.8). Thus, the role, selection and timing of biomarkers in assessment of potential ACS are rapidly evolving with a variety of different approaches to research being investigated. The recommendations in this Addendum are likely to have been superseded by new evidence within a relatively short time. The key change in recommendations regarding reperfusion of relevance to emergency physicians is for early routine angiography and revascularization for patients receiving fibrinolysis, regardless of the success of pharmacologic reperfusion (Grade A recommendation, Evidence level I). This recommendation is of particular relevance to emergency physicians in settings without access to a cardiac catheter laboratory. It will necessitate established relationships and clinical pathways to facilitate early transfer of these cases to centres capable of percutaneous coronary intervention (PCI). Although not included as a recommendation in this section, it was also acknowledged that evidence is growing that the reduction in time to PCI through ambulance triage and early activation of catheterization laboratories improves outcomes. This is further addressed in System factors. The main recommendation of relevance is the use of high-dose clopidogrel for patients undergoing primary PCI for STEMI or revascularization for ACS. A 600 mg oral bolus, 150 mg daily for 7 days and 75 mg/day for at least 12 months is recommended (Grade B recommendation, Evidence level II). The Addendum introduces data regarding two new oral antiplatelet agents recently approved for use in Australia; ticagrelor (a reversible platelet adenosine diphosphate P2Y12 inhibitor) and prasugrel (a P2Y12 receptor antagonist). The recommendations state these agents should be considered as an alternative to clopidogrel for subgroups at high risk of recurrent ischaemic events (Grade B recommendation; Evidence level II). This is balanced by the caveat that bleeding risk should be carefully assessed before using these drugs, as there is evidence that bleeding risk is increased in some patient subgroups. This recommendation might add complexity to clinical pathways and require the addition of bleeding risk assessment to treatment algorithms. It also has the potential for cardiologist preference to require additional consultation. Although potentially of less direct relevance to the ED, the recommendations also now consider the use of bivalirudin as an alternative to heparin and glycoprotein (GP) IIb/IIIa inhibitors. There has been a considerable shift in thinking regarding antithrombotic therapy in non-STEACS, with an increased emphasis on the need to balance ischaemic risk with bleeding risk at the individual patient level. This is based on data showing that major bleeding is associated with increased mortality and that the risk is comparable to recurrent MI. Identified risk factors for bleeding include older age, female sex, a history of bleeding, right heart catheterization, use of GPIIb/IIIa inhibitors, creatinine clearance <60 mL/min, high ischaemic risk, diabetes, heart failure, tachycardia, hypotension and hypertension. It is suggested that the use of clinical risk scores for both future ischaemic events and bleeding might be useful to guide pharmacotherapy. Examples of risk scores are provided. The bleeding risk of the available agents is discussed and the importance of adjusting dose for weight and renal function to minimize bleeding risk is emphasized. The Addendum suggests assigning patients to a management strategy based on their bleeding risk. A ‘standard’ strategy for patients at low bleeding risk would include the use of the most effective agents to control ischaemia rapidly, in combination if necessary. A ‘low bleeding strategy’ would be used for higher-risk patients, including preferential use of lower bleeding risk agents and minimization of the number of agents used. As mentioned previously, although tailored strategies are better for patients, they will add complexity to ACS management pathways initiated in the ED. This is likely to have the largest impact in small centres without early access to cardiology consultation, or where a patient with ACS requires transfer between facilities. Close collaboration and 7 day access to cardiology advice regarding choice of therapy will be necessary to optimize patient care. Of particular relevance to the ED is the change in recommendation regarding the use of oxygen therapy. Based on the lack of evidence regarding benefit and some evidence suggesting potential harm, routine administration of oxygen to chest pain patients is no longer recommended (Grade C recommendation, Evidence level I), with the recommendation that it is reserved for patients with hypoxia (oxygen saturation <93%) and those with evidence of shock (consensus). The importance of system factors is further emphasized in the new Addendum, influenced by increasing evidence that systems of care improve timeliness and effectiveness in the management of ACS, and an increasing recognition of the challenges posed by Australasia's geography and access to specialist and interventional cardiology services. The recommendations in this section emphasize: Locally appropriate, system-based approaches to deliver timely reperfusion The establishment of clinical networks and efficient protocols to maximize the proportion of patients receiving timely reperfusion and early revascularization Where there is not ready access to primary PCI, training and support for local clinicians to initiate fibrinolysis in patients with STEMI Ready access to expert cardiology consultation The importance of audit to assess and improve quality Although work in these areas is well advanced in some jurisdictions, in others there is some way to go. Inclusion as formal recommendations in the Addendum will hopefully stimulate improvements both at health service and at state/regional levels. The 2011 Addendum to the Heart Foundation's Guidelines for the Management of Acute Coronary Syndromes has made changes to the recommendations relating to the clinical care of patients with suspected or proven ACS across the therapeutic continuum. These changes potentially improve the efficiency of some elements (diagnosis/rule out of ACS and improved systems of care) while adding complexity to others (chose of antithrombotic therapy). It is now up to emergency physicians and cardiologists to work together to translate these recommendations into improved patient outcomes. AMK has been a member of the core writing group for the Guidelines for the Management of Acute Coronary Syndromes (2006),1 the 2007 Addendum2 and the 2011 Addendum.3 She is an editorial board member of Emergency Medicine Australasia. She is a member of advisory boards for Merck Sharp and Dohme and Astra Zeneca. Where opinions are expressed, they are her own and do not represent the opinions of the Heart Foundation, the co-authors of the Addendum or Emergency Medicine Australasia.
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Anne‐Maree Kelly (2011) conducted a review in Acute coronary syndromes. 2011 Addendum to Guidelines for the management of acute coronary syndromes was evaluated. The 2011 Addendum to the Heart Foundation's Guidelines updates recommendations for ACS management, including high-sensitivity troponin testing, early angiography, and tailored antithrombotic therapy.
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