Overview #
Key points
– Identify STEMI early and escalate immediately
– Early involvement of Cardiology team
– Early antiplatelet agents are important
– Aim to ensure patient is pain free
– Beware of atypical presentations in women, diabetics and elderly patients
Acute coronary syndrome (ACS):
- STEMI: ST-elevation (STE) myocardial infarction
● ST elevation indicates acute epicardial coronary occlusion1
● Clinical history- typical chest discomfort for >20 minutes (which may have resolved by time of presentations)
● ECG criteria with persistent (>20 minutes) ST segment elevation in >2 contiguous leads of1
○ > 2.5mm ST elevation in leads V2-3 in men <40 years1 or
○ >2.0mm ST elevation in leads V2-3 in men >40 years1 or
○ >1.5mm ST elevation in leads V2-3 in women1or
○ >1.0mm in other leads1or
○ Development of new onset LBBB 1
○ In patients with LBBB modified Sgarbossa1criteria is useful
■ lead ST elevation > 1mm concordant with QRS (5 points)1,2
■ lead ST depression > 1mm in leads V1-3 concordant with the QRS (3 points) 1,2
■ ST elevation >1 mm discordant with QRS (2 points), as defined as >25% of the depth of the preceding S- wave1,2
■ >3 points associated with 98% MI but score of zero does not rule out STEMI 1,2
- NSTEMI: non-ST segment elevation myocardial infarction1
● Clinical features consistent with cardiac ischemia
● Elevated cardiac biomarkers (eg. troponin)
● ECG changes:
- New or presumed new horizontal or down-sloping ST depression >0.5 mm in two anatomically contiguous leads1
- T wave inversion >0.1mm in two anatomically contiguous leads with prominent R wave or R/S ratio >11
- Dynamic ECG changes which as transient ST elevation or ST depression or T wave inversion
● Wellens Syndrome: Suggests high grade left anterior descending or left main lesion3
- Type A – 25%
- Biphasic T waves in anterior leads (while pain free)3
- Paradoxical pseudonormalization of ST segments (during pain)
- Type B – most common (75%)
- Deep symmetrical T wave inversion in lead I and aVL3
- Chest leads showing 1mm of ST elevation3
- Unstable angina
○ Myocardial ischaemia at rest or minimal exertion in the absence of myocardial injury/necrosis4
○ High sensitivity troponin has increased the detection of myocardial ischemia and decreased in the diagnosis of unstable angina.4
Localisation of ischaemia on ECG
o Anterior wall: 2 or more of precordial leads (V1-V6)5
o Anterior septal: leads V1-V35
o Apical or lateral: leads aVL and I, and leads V4-V65
o Inferior wall: leads II, III, aVF5
o Right ventricular wall: right sided precordial leads
o Right sided leads V4R, V4R and V6R should be obtained if there is evidence of inferior wall ischemia with STE in leads II, III, aVF5
o Posterior wall: septal precordial leads V1-V3 and posterior precordial leadso Check posterior leads V7, V8 and V9 if there is evidence of posterior wall ischemia by prominent R waves and ST depression in V1 and V25
Triage #
Triage:
– Immediate review if concerned about ACS – often will be paged about “chest pain” {hyperlink to chest pain guideline}
– Review ECG within 10 minutes1,4,5
– Aspirin load promptly
– Escalate immediately if:
o Patient is hemodynamically unstable
o Patient is having a STEMI
Priorities1:
- Is the patient hemodynamically stable?
- Does the patient have ECG changes consistent with acute STEMI?
- Have other life-threatening conditions (eg. aortic dissection, pulmonary embolus, intracranial bleed) that cause ECG changes and cardiac biomarker elevation been excluded?1
Type of Myocardial Infarction (MI) #
- Type 1 MI
- Most common
- Obstruction of coronary artery blood flow by a thrombus that develops as a result of fissure or erosion of an underlying atherosclerotic plaque4,7.
- Type 2 MI
- Imbalance between myocardial oxygen demand and supply due to other conditions such as hypotension, anaemia, hypoxaemia, coronary artery spasms, spontaneous coronary artery dissection (SCAD) or coronary microvascular dysfunction.2,4
- Type 3 MI
- Cardiac death suggesting MI causing death, but prior to biomarkers being taken2,4
- Type 4 and 5 MI
- Myocardial infarction associated with percutaneous coronary intervention and coronary artery bypass grafting2,4
Clinical features #
History:
o “Typical” chest pain/pressure/discomfort
o Described dull, heavy, tight, or crushing8, non-pleuritic, aggravated by exertion and relieved by rest, relieved by nitrates, not positional, not tender to palpation
o Shoulder, arm, jaw and/or upper abdominal pain
o Shortness of breath
o Nausea/vomiting
o Sweaty/Clammy/Diaphoresis
o Risk factors
o Male
o Medical conditions: diabetes, hypertension, dyslipidaemia
o Cigarette smoking
o Family history of ischaemic heart disease
Note: Beware of “atypical” symptoms in women, diabetics and older adults who may present with dyspnoea, weakness, nausea and vomiting, palpitations and syncope without chest pain4
Examination4
o Initial assessment
– ABC: Assess airway, breathing and circulation
o Look for perfusion/cardiogenic shock5
– hypotension
– tachycardia
– impaired mental state
– cool, clammy, pale, ashen skin
o Look for evidence of heart failure5
– elevated JVP
– new/worsening pulmonary crackles
– hypotension
– tachycardia
– new S3 gallop
– new or worsening MR murmur
o Focused neurological examination: screening neurological exam to assess for focal lesions or cognitive deficits that may prevent thrombolytic therapy
Investigations #
Investigation | Timing | Significance |
12 lead ECG | Within 10 minutes of review. If initial ECG not diagnostic and high clinical suspicion/uncertainty repeat ECG in 15 minutes4,6Serial ECGs every 10-15 minutes until patient is pain free1 Serial ECGs every 4-6 hours with serial troponin | Identify ischemic changes. Look for conduction abnormalities- eg. tachyarrhythmias/bradyarrhythmias, heart block (eg. RCA infarct can affect sinoatrial node) Localise the ischemic changes |
Troponin | Within 30 minutes of review Even if first troponin is negative, if high clinical suspicion of ACS measure repeat troponin in 3-6 hours5 If initial troponin elevated, continue to measure serial troponin every 3-6 hours until levels peak and trenddown.1,4,6 | Elevated indicates myocardial damage Troponin elevate 1-3 hour after AMI and can be elevated for up to 14 days1 CK not useful for initial diagnosis of ACS when troponin available.1,4,6 |
FBE | Within 30 minutes of review | Baseline. Low Hb can worsen ischaemia and patients can have lower transfusion thresholds if they are anaemic5 |
UEC | Within 30 minutes of review | Baseline. Important to be aware of renal function prior to angiography which can potentially cause an AKI. CKD is also a known risk factor for CVD. |
Coagulation profile | Within 30 minutes of review | Baseline. Measure if patients are on anticoagulation or heparin therapy is being considered. |
Fasting lipid profile and HbA1c | Within 24 hours with early morning bloods the next day | Assess cardiovascular risk factors and guide secondary prevention.4,6 |
Chest X-ray | Within 30 minutes of review Should not delay other management decisions if no immediate concerns *Earlier if hypoxic or clinical deterioration | To assess cardiac enlargement and identify non coronary causes of chest pain1, assess for complications of ACS such as pulmonary oedema. |
Management #
Ensure early discussion with Cardiology Team to assist with management
All patients
Assess haemodynamic stability and resuscitate as required
Supplemental oxygen
Use supplemental oxygen if patient hypoxic (i.e oxygen saturation <90-93%)1,6
Supplemental oxygen is NOT required if sats >95%
Patients with COPD and risk of hypercapnia- aim for oxygen saturation 88-92%.
Antiplatelet agent:
Aspirin1,4,6 | Aspirin 300mg PO loading dose immediatelyThen 100mg PO daily |
Dual antiplatelet therapy (DAPT)1
**Discuss with cardiology + check local hospital protocol regarding when to load the second antiplatelet agent
Not recommended routine pre-treatment in patients where coronary anatomy not known and early invasive management is planned, but pre-treatment may be considered if cannot undergo early invasive intervention1
Ticagrelor | 180mg PO loading dose then 90mg BDDo not use ticagrelor for patients who have second- or third-degree atrioventricular (AV) block9 OR |
Clopidogrel | 300mg or 600mg PO loading dose then 75mg daily |
Ticagrelor preferred over clopidogrel unless patient having fibrinolysis, in which case give 300mg clopidogrel with aspirin9
Aim to get the patient pain free and alleviate ischemic symptoms
Nitrates
Avoid if:
Hypotension (BP <100)
Phosphodiesterase-5-inhibtior (sildenafil, vardenafil, tadalafil) have been used within the last 24 hours, or 48 hours with tadalafil6,9
Beware– need to be cautious when giving nitrates in Inferior MI due to possible involvement of the right ventricle. These patients are preload dependent to maintain cardiac output and nitrates can cause severe hypotension5
GTN sublingual | 300-600micrograms PO sublingual every 5 minutes for up to 3 doses and then reassess1 OR |
GTN spray | 400-800micrograms every 5 minutes for up to 3 doses and then reassess1 OR |
GTN patch | *Note can be variable in time of onset and dose delivered, therefore can be used once the patient is pain free to maintain pain free status glyceryl trinitrate 5 mg transdermally, once daily, increasing if required up to 15 mg once daily. Can apply for a maximum of 14 hours in a 24-hour period7 |
If symptoms unrelieved may need GTN infusion and/or alternative therapy
GTN infusion | **Typically only given in ED, ICU or CCU**glyceryl trinitrate 10 micrograms/minute by intravenous infusion, increasing by 10 micrograms/minute every 3 minutes until pain is controlled, providing systolic blood pressure is 95 mmHg or more9 |
Opioids- 2nd line
Morphine5,6 | 2 to 4 mg IV, every 5 -15-minute for chest pain5 |
Fentanyl5 | 25micrograms IV every 5 minutes for chest pain |
Often hospital protocol dictates patients need to be in ED/CCU/ICU to administer IV opioids.
Note: Do not use NSAIDs.6
Beta blockers
Early (typically within 24-72 hours) beta blocker in patients with ongoing ischaemic symptoms2 or patients with NSTEMI with very high or high acute risk start beta blocker unless contraindicated9
Avoid if: clinical heart failure, low output state, risk of cardiogenic shock or other contraindications (eg. PR interval >0.24sec, second or third degree heart block without a cardiac pacemaker, active asthma or reactive airway disease). Avoid IV beta blocker6
Metoprolol | metoprolol tartrate 25 mg orally, twice daily, increasing up to 100 mg twice daily.9 OR |
Atenolol | atenolol 25 mg orally, daily, increasing up to 100 mg daily9 |
Preference for patients with NSTEMI, stabilised heart failure and reduced left ventricular ejection fraction (LVEF): cardio-selective beta blockers such as metoprolol SR, carvedilol, bisoprolol5
High dose statin1,4,6
Start immediately (within 24 hours) and continue indefinitely the highest tolerated dose (unless contraindicated or history of intolerance)
Atorvastatin | 80mg PO daily |
Rosuvastatin | 40mg PO daily |
Simvastatin | 80mg PO daily |
Telemetry
Discuss with cardiology team if telemetry is required
Telemetry recommended for
- STEMI (all patients)
- NSTEMI
o Up to 24 hours or to PCI (whichever comes first) in patients at low risk for cardiac arrhythmias4
o For >24 hours in patients at increased risk for cardiac arrhythmias4
o Unstable angina
o May be considered in the absence of signs of symptoms of ongoing ischeamic in selected patients (i.e suspicion of coronary spasm or associated symptom suggestive of arrhythmic events).4
STEMI #
Call a CODE STEMI- management guided by cardiology team
Reperfusion therapy
If < 12 hours since symptom onset emergency reperfusion therapy with primary percutaneous coronary intervention (PCI) or fibrinolytic therapy is recommended1
Primary PCI is preferred if it can be performed within 90 minutes of first medical contact; otherwise fibrinolytic therapy is preferred for those without contraindications.1
Fibrinolytic therapy
If PCI cannot be performed within 90 minutes proceed to fibrinolysis
Transfer to angiography post fibrinolysis
Among patients treated with fibrinolytic therapy who are not in a PCI-capable hospital, early or immediate transfer to a PCI-capable hospital for angiography, and PCI if indicated within 24 hours1.
Among patients treated with fibrinolytic therapy for those with <50% ST recovery at 60-90 minutes, and/or with haemodynamic instability, immediate transfer for coronary angiography with a view to rescue angioplasty is recommended1
NSTEMI: #
Reperfusion therapy: percutaneous coronary intervention (PCI)1
Timing of reperfusion therapy will be guided by cardiology pending risk stratification of the patient and certain clinical characteristics – see below drop down menu
Very high risk patients1
o Clinical characteristics
o Recurrent or ongoing ischemia- i.e. chest pain refractory to medical treatment
o Dynamic ST or T wave changes particularly with intermittent STE, de Winter T wave changes, or Wellen’s syndrome, or widespread ST elevation in two coronary territories
o Haemodynamic compromise, cardiogenic shock
o Mechanical complications of MI
o Life threatening arrhythmias or cardiac arrest
o Immediate invasive strategy is recommended (i.e. within 2 hours of admission)
High risk patients1
o Clinical characteristics
o Absence of very high risk criteria
o GRACE score >140
o Dynamic ST segment and/or T wave changes on ECG with or without symptoms
o Rise and/or fall in troponin compatible with MI
o Early invasive strategy is recommended (i.e. within 24 hours of admission)
Intermediate risk patients1
o Clinical characteristics
o Absence if high risk criteria
o Recurrent symptoms, or substantial inducible ischemic on provocative testing
o Diabetes mellitus
o Renal insufficiency (eGFR <60)
o LVEF <40%
o Prior revascularisation: PCI or CABG
o GRACE score >109 and <140
o Invasive strategy recommended (i.e. within 72 hours of admission)3
Parenteral anticoagulation9
Given to patients with ACS at intermediate to high risk of ischemic events – guided by cardiology team.
Bivalirudin can also be considered if there is a contraindication to heparin.
Continue the parenteral anticoagulant until the time of coronary angiography or longer, depending on the clinical response.
The dose of LMWH due immediately before a scheduled angiogram may be omitted to minimise the risk of bleeding from the procedure.
1st line: Enoxaparin | CrCl > 30 mL/min: 1 mg/kg subcutaneously, twice dailyCrCl < 30 mL/min: 1 mg/kg subcutaneously, once daily OR |
2nd line: Dalteparin | (CrCl 30 mL/min or more) 120 units/kg (up to 10 000 units) subcutaneously, twice daily. |
OR
1st line:Unfractionated heparin | 60 units/kg (up to 4000 units) intravenous loading dose, followed by 12 units/kg/hour (up to 1000 units/hour) by intravenous infusion, adjusted according to APTT. UFH is used for patients with severe kidney impairment or who have a high risk of active bleeding that may require rapid reversal of anticoagulation OR |
2nd line:bivalirudin | (CrCl 30 mL/min or more) 0.1 mg/kg intravenous bolus, followed by 0.25 mg/kg/hour by intravenous infusion. If invasive management, such as an angiogram, is planned for a patient with a high risk of bleeding, consider bivalirudin. Bivalirudin can also be considered if there is a contraindication to heparin. |
Discharge management and secondary prevention #
Aspirin1
Aspirin | 100mg PO daily ongoing To be continued indefinitely unless it is not tolerated for an indication for anticoagulation becomes apparent *Clopidogrel should be prescribed if aspirin is contraindicated or not tolerated1 |
Dual antiplatelet therapy (DAPT)- aspirin and P2Y12 inhibitor1
Ticagrelor | 90mg PO BD OR |
Clopidogrel | 75mg PO daily |
Continue DAPT for up to 12 months in patients with ACS regardless of whether coronary revascularisation is performed1
Can consider continuing DAPT beyond 12 months if ischemic risk > bleeding risk of P2Y12 inhibitor therapy; or discontinuation if bleeding risk > ischemic risk
Patients on oral anticoagulation (eg. for AF and high CHADSVASC)
After a short period (eg. 1 week to 1 month) of triple therapy (oral anticoagulation and two antiplatelet therapy), dual therapy is recommended using oral anticoagulation and single oral antiplatelet agent (preferable clopidogrel) for 12 months, followed by discontinuation of the antiplatelet at 12 month and continuation of the oral anticoagulation lifelong4.
Triple therapy with ticagrelor may be considered as an alternative to clopidogrel to treatment with aspirin and oral anticoagulation in patients with moderate to high risk of stent thrombosis4
High dose statin (HMG-CoA reductase inhibitor)
Start and continue indefinitely the highest tolerated dose (unless contraindicated or history of intolerance)1. Statin therapy following an acute coronary syndrome reduces premature death, myocardial infarction and other cardiovascular events7.
Aim to reduce LDL by >50% from baseline and to achieve LDL <1.44.
If goal not achieved after 4-6 weeks to start combination of statin and ezetimibe4
If goal still not achieved after another 4-6 weeks to add PCSK9 inhibitor4
Beta blocker
Start beta blockers in patients with reduced LVEF <40% unless contraindicated1,4.
ACE inhibitor
Start and continue ACEi or ARB in patients with evidence of heart failure, LV systolic dysfunction, diabetes, chronic kidney disease, anterior AMI or co-existent hypertension1, to reduce all cause and cardiovascular mortality and morbidity4.
Mineralocorticoid receptor antagonist (MRA)
MRA in all patients with heart failure with reduced LVEF (<40%) to reduce all cause and cardiovascular mortality and cardiovascular morbidity4.
Proton pump inhibitors (PPI)
PPI recommended for patients on aspirin and DAPT at high risk of gastrointestinal bleeding to reduce risk of gastric bleeds4
Cardiac rehabilitationMultidisciplinary exercise based cardiac rehabilitation recommended for all patients with CAD4
References #
- Chew D P, Scott I A, Cullen L et al. NHFA/CSANZ ACS Guideline 2016 Executive Working Group. Heart Lung Circ. 2016 September 25th ; 25: 895-951
- Nickson C. Acute Coronary Syndrome. 2021 [cited 2022 Feb 20th]. Available from: https://litfl.com/acute-coronary-syndromes/
- Nickson C.Wellens Syndrome. 2020 [cited 2022 Feb 20th]. Available from: https://litfl.com/wellens-syndrome/
- Collet J P, Thiele H, Barbato E et al. 2020 ESC Guidelines for the management of acute coronary syndrome in patients presenting without persistent ST-segment elevation. Eur Heart J. 2021; 42: 1289-1367
- Reeder G S, Awtry E, Mahler S A. Initial evaluation and management of suspected acute coronary artery syndrome (myocardial infarction, unstable angina) in the emergency department [Internet]. 2021 [updated 2021; cited 2021 August 29th]. Available from: https://www.uptodate.com/contents/initial-evaluation-and-management-of-suspected-acute-coronary-syndrome-myocardial-infarction-unstable-angina-in-the-emergency-department?search=acute%20coronary%20syndrome&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2
- Amsterdam E A, Wenger N K, Brindis R G et al. 2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes. Circulation. 2014 December 1st; 130: e344-e426
- Cannon C P, Kaski J C, Libby P. Mechanisms of acute coronary syndromes related to atherosclerosis [Internet]. 2020 [updated 2020; cited 2021 August 29th]. Available from: https://www.uptodate.com/contents/mechanisms-of-acute-coronary-syndromes-related-to-atherosclerosis?search=causes%20of%20acute%20coronary%20syndrome&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
- DeVon HA, Rosenfeld A, Steffen AD, Daya M. Sensitivity, specificity, and sex differences in symptoms reported on the 13‐item Acute Coronary Syndrome Checklist. J Am Heart Assoc. 2014; 3:e000586. DOI: 10.1161/JAHA.113.000586.
- Therapeutic Guidelines Ltd. Acute Coronary Syndrome [Internet]. 2018 [updated 2021; cited 2021 August 29th]. Available from: https://tgldcdp.tg.org.au.acs.hcn.com.au/viewTopic?topicfile=acute-coronary-syndromes&guidelineName=Cardiovascular#toc_d1e777
Contributors
Reviewing Consultant/Senior Registrar
Dr Madhuka Wijayarathne
Dr Anita Ng