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training of the staff involved. Ambulance personnel must be trained to recognize ischaemic symptoms, administer oxygen when appropriate, secure intravenous (i.v.) access, effectively relieve pain, administer fibrinolysis when indicated, and provide basic life support.142 Ambulance staff should record an ECG as soon as possible for diagnostic purposes and either interpret the ECG or transmit it so that it can be reviewed by experienced staff to establish or refute a working diagnosis of STEMI. Regular and structured training of ambulance staff is mandatory for a high-quality pre-hospital service. 4.1.4 General practitioners In some countries, primary care clinicians (general practitioners) play an important role in the early care of patients with suspected ACS and may provide the FMC. Education and training of general practitioners in emergency, pre-hospital care is essential for the delivery of optimal pre-hospital care in this setting. The responsibilities of the primary care clinicians may include diagnosis, activation of the EMS, risk stratification, and initiation of pre-hospital treatment. However, in most settings, consultation with a general practitioner instead of a direct call to the EMS will increase the pre-hospital delay. Therefore, the public should be educated to call the EMS directly rather than a primary care physician for symptoms suggestive of ACS. 4.1.5 Organization of ST-elevation myocardial infarction treatment in networks It is recommended that a regional reperfusion strategy is established to maximize the efficiency of care for patients with a working diagnosis of STEMI.143 The optimal treatment of patients with a working diagnosis of STEMI should be based on the implementation of networks between hospitals with various levels of clinical service provision (the ‘hub and spoke’ model), linked by a prioritized and efficient ambulance service. A PCI centre is a multidisciplinary acute care centre that provides emergency invasive management 24/7 for patients presenting with suspected STEMI. This centre should also provide intensive care facilities, and more advanced centres should offer cardio-thoracic services, advanced haemodynamic support, and surgery. The goal of STEMI networks is to provide optimal care while minimizing delays, thereby improving clinical outcomes. Cardiologists should actively collaborate with all stakeholders, particularly emergency physicians, in establishing such networks. The main features of such a network are detailed in Supplementary data online, Table S6. It is recommended that the EMS should transport patients with a working diagnosis of STEMI to hospitals with a 24/7 service for PCI, bypassing non-PCI-capable hospitals.144 Further information on this topic is provided in the Supplementary data online. Geographic areas where the expected transfer time to the primary PCI centre makes it impossible to routinely achieve the maximal allowable delays indicated in the recommendations should develop protocols for rapid fibrinolysis at the place of STEMI diagnosis, with the aim of treatment within 10 min of FMC, followed by immediate transfer to a centre with 24/7 service for PCI. Such networks increase the proportion of patients receiving reperfusion with the shortest possible treatment delay.145–147 The quality of care, time delays, and patient outcomes should be measured and reported to the healthcare professionals contributing to the EMS. 4.2 Emergency care 4.2.1. Initial diagnosis and monitoring Management of ACS starts from the point of FMC, when a working diagnosis of ACS is established. The working diagnosis of ACS is usually based on symptoms consistent with myocardial ischaemia and the signs on a 12-lead ECG (see Section 3.2). It is recommended to initiate ECG monitoring as soon as possible in all patients with suspected ACS in order to detect life-threatening arrhythmias and to allow prompt defibrillation if indicated. 4.2.2 Acute pharmacotherapy 4.2.2.1. Oxygen Oxygen supplementation is recommended in ACS patients with hypoxaemia (oxygen saturations <90%). Oxygen supplementation in patients who are not hypoxic (oxygen saturations >90%) is not associated with clinical benefits and is therefore not recommended.148,149 4.2.2.2 Nitrates Sublingual nitrate may be helpful to relieve ischaemic symptoms. However, a reduction in chest pain after nitroglycerine administration can be misleading and is not recommended as a diagnostic manoeuvre.150 In patients with an ECG compatible with ongoing STEMI and symptom relief after nitroglycerine administration, it is recommended to obtain another 12-lead ECG. Complete normalization of ST-segment elevation, along with relief of symptoms, after nitroglycerine administration is suggestive of coronary spasm, with or without associated MI. Nitrates should not be given to patients with hypotension, marked bradycardia or tachycardia, RV infarction, known severe aortic stenosis, or phosphodiesterase 5 inhibitor use within the previous 24–48 h. 4.2.2.3 Pain relief Intravenous opioids (e.g. morphine 5–10 mg) should be considered for the relief of severe chest pain. Other forms of pain relief (e.g. nitrous oxide/oxygen plus i.v. acetaminophen/paracetamol) have been reported to be inferior to morphine.151 However, morphine may enhance nausea and vomiting and slow the gastrointestinal absorption of oral medicines, which may delay the onset of action of orally administered antiplatelet therapy.152,153 Evidence from small-scale trials suggests that i.v. morphine may also reduce myocardial and microvascular damage when given to patients with ongoing acute coronary artery occlusion, though co-administration with metoclopramide appears to negate this effect. Conversely, morphine has also been reported to reduce antiplatelet activity after administration of ticagrelor, though this effect was rescued by metoclopramide administration.154,155 The positive effects of morphine on myocardial damage may potentially be related to reduced oxygen consumption as a result of decreased preload and negative inotropy and chronotropy. Platelet inhibition induced by oral P2Y12 receptor antagonists may be delayed in patients with ongoing MI. Morphine may also further reduce absorption, delay the onset of action, and decrease the antiplatelet effect of oral P2Y12 receptor inhibitors in MI patients, although this effect may vary between the different P2Y12 inhibitors.153,156– 158 Further research is ongoing in this area, but at present it should be noted that currently available clinical data have not demonstrated any increase in the risk of adverse clinical outcomes as a result of any interaction between morphine and antiplatelet agents in the setting of ACS.159–161 4.2.2.4 Intravenous beta-blockers Few RCTs testing early i.v. beta-blockers have been performed in the era of invasive management for patients with a working diagnosis of STEMI. Not all beta-blockers appear to exert the same Downloaded from academic.oup.com/eurheartj/article/44/38/3720/7243210 by guest on 07 October 2026