The immediate management of patients with acute coronary syndrome

An overview of acute coronary syndrome

Acute coronary syndrome (ACS) refers to a spectrum of conditions usually caused by thrombus formation within the coronary arteries.¹ ACS varies in severity and includes:^{1, 2}

• ST-segment-elevation myocardial infarction (STEMI)
• Non-ST-segment-elevation acute coronary syndromes (NSTEACS):
  • Non-ST-segment-elevation myocardial infarction (NSTEMI)
  • Unstable angina

Less commonly, ACS may be caused by myocardial infarction with no obstructive coronary arteries (MINOCA) or spontaneous coronary artery dissection (SCAD).³

Patients may present to general practice currently experiencing chest pain, or they may report recent symptoms, e.g. from the previous evening. In most cases, chest pain is unlikely to be caused by ACS, however, all patients with symptoms consistent with a cardiac origin require prompt assessment and treatment as indicated (see: “Take a focused history and perform a clinical examination”).² If the patient has ACS, additional interventions, e.g. intravenous (IV) fibrinolysis, may be appropriate in primary care depending on the type of ACS, location of the practice, transport time to hospital and medicines availability. Having a practice protocol that all staff can initiate for patients with suspected cardiac chest pain may streamline management.

For information on the management of stable angina, see: bpac.org.nz/2025/angina.aspx

Investigating patients with possible cardiac chest pain

Most patients with ACS present with chest discomfort, described as either pain, pressure, tightness, heaviness or a burning sensation in the chest.^{2, 4} Other common symptoms include shoulder, arm, jaw and upper abdominal pain.^{2, 6} Patients can also present with non-specific symptoms such as dyspnoea, nausea, vomiting and sweating; these symptoms are reported more frequently in patients who are older, female or who have diabetes or chronic inflammatory conditions.^{2, 7} In severe presentations, patients may display symptoms or signs of cardiogenic shock, haemodynamic instability, acute heart failure or cardiac arrest.^{4, 7}

Have a high clinical suspicion for ACS in patients who present with:^{5, 7}

• Chest pain and/or pain in areas such as the upper arms, back or jaw, that lasts longer than 15 minutes
• Chest pain and nausea, vomiting, sweating or dyspnoea (particularly a combination of these symptoms)
• New-onset chest pain, or a sudden deterioration in previously stable angina, with chest pain episodes lasting longer than 15 minutes, recurring frequently and following little or no exertion

Take a focused history and perform a clinical examination

A team response involving multiple clinical staff may be required when a patient presents with suspected ACS in primary care. Depending on the patient’s condition, the following steps may occur concurrently, or the order may differ, e.g. an ECG may prioritised before detailed history taking and physical examination.

Take a focused history. Consider pain characteristics, including the nature, onset, duration, location, radiation, precipitating and relieving factors and any associated symptoms.⁶ Also ask about any history of ischaemic heart disease, cardiovascular risk factors and prior investigations/treatments for chest pain.⁵ If a patient has a history of cardiovascular disease, it is likely their symptoms have a cardiac origin. However, patient history can also suggest other causes of chest pain, such as gastroesophageal reflux disease or that there is an underlying musculoskeletal origin (Table 1).^{2, 6} Have a higher index of suspicion for ACS in patients of Māori, Pacific and South Asian ethnicity presenting with characteristic symptoms and signs as these groups are at increased risk of cardiovascular disease, e.g. myocardial infarction.^{8, 9}

Perform a physical examination. This should include assessment of pulse, heart rate and rhythm (including change in rhythm, e.g. new-onset atrial fibrillation), measurement of blood pressure and oxygen saturation, and auscultation of the chest.^{2, 4} Assess for signs of heart failure or circulatory compromise.⁴

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Table 1. Examples of clinical features that may differentiate ACS from other causes of chest pain.

	Clinical features	Increases suspicion of ACS	Suggestive of another cause
Character	How is the sensation described?	Pain, pressure, tightness, heaviness or burning sensation in the chest4, 6	Sharp shooting pain or pain only felt on inspiration5, 10
	Are there any associated symptoms?	Dyspnoea, nausea, vomiting, sweating, dizziness, syncope2, 7	Difficulty swallowing5
Cause	What is the patient doing when symptoms begin?	Discomfort at rest or with minimal exertion5, 7	Physical exertion, emotional stress5 Reproducible with palpation6, 10 Positional discomfort6, 10
Duration	How long do symptoms last?	Longer than 15 minutes5, 7	A few seconds or hours/days5, 10
Location	Where is the discomfort felt?	Predominantly in the chest5, 7	Right upper quadrant of the abdomen or epigastrium6, 10
	Does it radiate to other parts of the body?	Shoulder, arm, jaw or upper abdomen2, 6	Lower extremities10

Perform a 12-lead ECG as soon as possible

A 12-lead ECG should be performed as soon as possible for all patients presenting with chest pain with a potential cardiac cause.^{1, 4} The ECG may indicate STEMI, but more commonly, acute ECG changes will be absent which may be consistent with NSTEMI, or the ECG may be inconclusive.^{1, 4} It is also possible that there will be delayed cardiac changes not initially detectable on ECG. Check the patient’s medical records for previous ECG recordings as these can be used as a baseline for comparison.⁶

If ST-segment elevation is detected (≥ 2 mm in at least two leads V1 – 3 or ≥ 1 mm in at least two contiguous leads in another area)¹¹, urgently refer the patient for acute cardiology assessment (check local HealthPathways for the referral protocol in your area).¹² Other changes on ECG indicating possible ACS that should prompt urgent referral include:^{2, 4}

• ST-segment depression
• Pathological Q waves
• T wave changes, especially biphasic T waves or prominent negative T waves (Wellens’ sign)
• New bundle branch block

Referral is also recommended for patients where a cardiac cause cannot be reasonably excluded, regardless of their ECG results, i.e. a normal ECG does not exclude the possibility of a cardiac cause.^{4, 10}

Additional investigations should not delay referral

Laboratory testing has a limited role in primary care for the initial investigation of a patient with suspected ACS, and should not delay referral for acute cardiology assessment.^{10, 12} A blood sample could be collected if there will be significant delay in transporting the patient to hospital or if an opportunity arises, e.g. if inserting an IV line for pain relief (see: “Acute treatment in primary care while awaiting transfer”).

Testing may also be considered if the situation is less urgent, e.g. patients:¹²

• Who have been symptom-free for over 24 hours
• Presenting with atypical symptoms
• With unexplained chest pain and a normal ECG (see: “Lower suspicion of ACS? Calculate EDACS”)

Cardiac biomarkers, e.g. troponin, are useful for detecting myocardial injury.^{10, 12} Depending on the patient’s clinical condition and circumstances, troponin levels may be assayed urgently in a community laboratory, or the blood sample can be sent with them to hospital. Some rural practices may have access to point-of-care troponin testing. An elevated serum troponin (above the 99^th percentile) is a typical finding in patients with acute myocardial infarction.^{2, 4} Whereas unstable angina can be distinguished from other types of ACS by the absence of significantly elevated serum troponin.^{3, 4} Troponin levels can also be raised due to other reasons, e.g. decreased clearance due to renal dysfunction, pulmonary embolism, myocarditis.²

Additional laboratory tests may be requested as indicated, e.g. full blood count, renal and liver function, C-reactive protein, thyroid function.

Acute treatment in primary care while awaiting transfer

Offer pain relief as soon as possible. Sublingual GTN is often used initially for symptom relief (unless contraindicated: see below).^{5, 7} Administer one to two sprays, repeat in five minutes, and then repeat again in another five minutes if pain persists.^{1, 2} Monitor the patient’s blood pressure as rapid hypotension can occur. In general, a systolic drop of ≥ 30 mmHg can be suggestive of a right ventricular myocardial infarction as these patients are more sensitive to the vasodilatory effects of GTN.

This GTN dosing regimen is appropriate when patients are under the supervision of a clinician and is consistent with guidance from the National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand (2025) and local HealthPathways.² Up to three doses are also recommended in the 2025 American ACS guideline.¹ This differs to the instructions given for patients during an episode of angina, in which up to two doses may be given at five minute intervals before calling an ambulance.¹⁶ Use clinical judgement when assessing the risk (e.g. hypotension) versus benefit of additional GTN doses (i.e. three or more) when managing patients with suspected ACS.

Caution with GTN. There are some scenarios where GTN may not be appropriate to use: caution or avoidance is recommended for patients with haemodynamic instability, phosphodiesterase-type 5 inhibitor (e.g. sildenafil) use within the last 24 – 48 hours or those who have an inferior/right ventricular infarction on ECG (see NZF for a full list of cautions and contraindications).^{1, 16}

IV opioids (e.g. morphine 5 – 10 mg in incremental doses) may be administered for pain if the patient does not respond to GTN, particularly in those with acute myocardial infarction.⁴ Opioids are not routinely recommended for all patients because they can cause nausea and vomiting and delay the onset of action of oral antiplatelets (e.g. ticagrelor) by slowing gastrointestinal absorption.⁴ If administered, an IV antiemetic, e.g. metoclopramide 10 mg, may be given as needed.

Give aspirin 300 mg (dissolved or chewed) as soon as possible unless contraindicated (see NZF), including in patients already taking low-dose aspirin.^{1, 2} Aspirin lowers the risk of further cardiovascular events, e.g. myocardial infarction, stoke, and can reduce STEMI mortality.^{7, 12}

Dual antiplatelet treatment, i.e. aspirin plus ticagrelor (usually preferred)^* or clopidogrel.⁷ The need to give aspirin to all patients with ACS as soon as possible is universally acknowledged. However, whether or not to give an additional antiplatelet in primary care to these patients is more complex and depends on expected transport time to hospital and clinical context.

It is unlikely that most general practices will have ready access to either of these medicines at short notice as neither ticagrelor nor clopidogrel are available on PSO. Furthermore, in most urban areas there should not be significant delays in transporting patients by ambulance to hospital, therefore, the decision regarding dual antiplatelet treatment will usually be made in secondary care. In remote communities where there are often significant delays in transporting patients to hospital, it may be necessary to initiate dual antiplatelet treatment (for patients with STEMI or NSTEACS) and to thrombolyse some patients with ACS (STEMI) in primary care if the medicines are available (see: “If a patient with STEMI cannot be transported to hospital immediately”). Discuss the need for administering dual antiplatelet treatment in the community with the accepting clinician in the department the patient will be transferred to.

* Ticagrelor has shown superior efficacy to clopidogrel in combination with aspirin for patients with ACS, however, it is associated with a higher risk of bleeding^{2, 4} June 2025 – Concerns are emerging about the validity of these studies, watch this space.

Oxygen is not routinely required unless the patient is hypoxic (oxygen saturation < 90 – 93%) or has signs of heart failure or cardiogenic shock.^{1, 7} If oxygen is indicated, do not exceed an oxygen saturation > 96%.² In people who are not hypoxic, oxygen supplementation does not improve outcomes and can cause harm.^{2, 7}

Transfer all relevant information with the patient

Ensure all relevant information from the patient’s record is available to staff upon arrival at hospital. If the patient’s ECG shows ST-segment elevation, alert the on-call cardiologist or emergency department consultant to prevent delays in accessing the catheterisation laboratory. Include the following information where possible:

• Time of symptom onset and duration
• ECGs (current and previous if available)
• Blood pressure, heart rate and oxygen saturation levels
• Co-morbidities
• Medicines given acutely, including time and dose
• Medicines currently prescribed and any over-the-counter products
• Allergies
• Relevant family history and personal details such as an advance care plan

Secondary prevention post-ACS

Most patients post-ACS will be taking additional medicines after being discharged from hospital to reduce the possibility of recurrent events (see: “Pharmacological secondary prevention”).² Lifestyle changes are also a fundamental component of secondary prevention in addition to risk factor modification, e.g. diabetes management (see: “Lifestyle changes to reduce cardiovascular risk”).⁴ Influenza and COVID-19 vaccinations should also be recommended.^{*1, 4}

* Influenza vaccination can reduce mortality risk and major adverse cardiovascular events in people post-ACS.^{1, 4} Data supporting routine administration of other vaccines, e.g. COVID-19, post-ACS are lacking,¹ but are still recommended for eligible patients.

Patients may benefit from referral to a secondary prevention or cardiac rehabilitation service.² For a list of cardiac rehabilitation programmes throughout New Zealand, see: hhdirectory.heartfoundation.org.nz.

A post-ACS checklist guide for healthcare professionals is available from the Heart Foundation New Zealand: www.heartfoundation.org.nz/resources/post-acute-coronary-syndrome-checklist

Pharmacological secondary prevention

Cardiovascular event risk can be reduced with pharmacological intervention.^{2, 4} Patients may be initiated on the following medicines in secondary care; set a recall as a reminder for when a medicine needs to be discontinued:

• Aspirin. Aspirin is usually continued indefinitely after ACS, with regular dosing of 75 – 150 mg per day.^{1, 2, 4} However, there are some clinical situations in which aspirin is discontinued early, e.g. patients with an indication for anticoagulation.¹ A proton pump inhibitor may be needed for patients at increased risk of gastrointestinal bleeding.⁴
• Ticagrelor (usually preferred) or clopidogrel, i.e. dual antiplatelet treatment. In patients who have had ACS, in particular those who have received a stent, dual antiplatelet treatment with aspirin and ticagrelor or clopidogrel is required for up to 12 months.^{1, 2, 4} Ticagrelor is preferred, but clopidogrel may be used in patients with high bleeding risk (e.g. those who are older, taking oral anticoagulants). The choice and duration of dual antiplatelet treatment (or triple antithrombotic treatment if oral anticoagulation is used; see below), should be clearly described on the hospital discharge documents; seek clarification if it is not. Clopidogrel monotherapy may be used for patients taking long-term antiplatelet treatment who do not tolerate aspirin.¹⁷ A proton pump inhibitor may be needed for patients at increased risk of gastrointestinal bleeding.^{2, 4}
  • Patients with an indication for long-term oral anticoagulation, e.g. atrial fibrillation, may be discharged on triple antithrombotic treatment: dual antiplatelets (aspirin and clopidogrel) plus an anticoagulant.^{1, 4} The choice and duration of triple antithrombic treatment is determined by the cardiologist, but in general, triple treatment is continued for up to one month post-ACS, before aspirin is discontinued.^{1, 4} Clopidogrel is usually continued for 12 months and then discontinued, with the patient remaining on the anticoagulant indefinitely.⁴
• Statin, e.g. atorvastatin, rosuvastatin. Patients will either be initiated on a high-intensity statin, or treatment optimised for those already taking a statin, e.g. addition of ezetimibe.^{1, 2} Treatment is usually continued indefinitely.² Aim for a LDL-C target of < 1.4 mmol/L and ≥ 50% LDL-C reduction from baseline.²
• Beta blocker, e.g. bisoprolol, metoprolol.^{2, 4} It has previously been standard practice to prescribe beta blockers to most patients post-ACS, however, newer guidelines now recommend only initiating beta blockers in select patients, e.g. those with reduced left ventricular ejection fraction (LVEF).²
  • Evidence increasingly supports the withdrawal of beta blockers one year post-myocardial infarction in patients with a LVEF ≥ 50%, no (or minor) regional wall motion abnormalities on echocardiogram and no other indications for treatment, e.g. heart failure, arrhythmias, as treatment beyond this period has not been associated with improved cardiovascular outcomes.^{4, 17, 18} A beta blocker is usually required indefinitely for patients with reduced left ventricular ejection fraction or evidence of considerable myocardial damage.¹⁷
• ACE inhibitor/ARB. An ACE inhibitor/ARB is usually initiated and continued long-term in some patients post-ACS, e.g. those with diabetes, hypertension, chronic kidney disease, heart failure (some patients with heart failure may instead be taking an ARNI).^{2, 4}

Additional medicines may be initiated in secondary care depending on patient co-morbidities. For example, a calcium channel blocker for patients with angina or hypertension, a mineralocorticoid receptor antagonist and SGLT-2 inhibitor for patients with heart failure.^{4, 17}

Lifestyle changes to reduce cardiovascular risk

	Body weight. Support patients to achieve and maintain a healthy body weight;17 target a BMI of < 25 kg/m2 or a reduction in waist circumference. For information on weight loss, see: bpac.org.nz/2022/weight-loss.aspx
	Diet.2 Recommend patients follow a Mediterranean-style diet and reduce daily alcohol consumption.4, 17 For information on managing alcohol misuse, see: bpac.org.nz/2018/alcohol.aspx
	Physical activity.2 Patients who were not previously active should reduce sedentary behaviour and gradually introduce regular physical activity based on their clinical condition, co-morbidities and physical capability.4, 17 Resistance (strength) training should also be incorporated, if appropriate.
	Smoking cessation.2 Use behavioural and pharmacological interventions, e.g. nicotine replacement therapy, as needed.4, 17 Patients should also avoid passive exposure to tobacco smoke. For information on smoking cessation, see: bpac.org.nz/2024/smoking.aspx
	Mental health.2 Identify and address any mental health concerns that may influence cardiovascular outcomes.4 Use pharmacological and non-pharmacological management options as appropriate. Experiencing ACS is likely to be traumatic for many patients, and they may need regular mental health and wellbeing check-ins.