Acute Coronary Syndrome (ACS)
Acute coronary syndrome (ACS) describes the spectrum of conditions caused by sudden reduction in coronary blood flow, including unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). It is a medical emergency requiring rapid diagnosis and treatment to reduce myocardial damage and improve survival.
This UKMLA guide explains the causes, diagnosis and acute management of ACS, based on NICE guideline [NG185] Acute coronary syndromes.
Background Information
Definition
ACS is the acute manifestation of coronary artery disease. This umbrella term includes the spectrum of STEMIST elevation myocardial infarction , NSTEMInon-ST elevation myocardial infarction , and unstable angina. [Ref]
| Unstable angina | NSTEMI | STEMI | |
|---|---|---|---|
| Pathogenesis | Partial occlusion → ischemia WITHOUT infarction | Partial occlusion → partial thickness (subendocardial) infarction | Complete occlusion → full-thickness (transmural) infarction |
| ECG findings | No ST elevation
Other ECG changes may be present:
ECG maybe normal |
ST elevation in at least 2 contiguous leads (see below for full criteria) | |
| Cardiac troponin (T/I) | <99th centile | Rise and/or fall AND >99th centile | |
Risk Factors
Major risk factors: [Ref]
- Age (>65 y/o)
- Male
- Cardiovascular risk factors- History of smoking - Diabetes - Hypertension - Dyslipidaemia - FHx of premature coronary artery disease
- Family history of premature coronary artery disease
- Presence of other cardiovascular diseases
- Established coronary artery disease (e.g. previous MI, coronary revascularisation)
Other risk factors: [Ref]
- CKDChronic kidney disease
- Chronic inflammatory conditions (e.g. rheumatoid arthritis, SLE)
- Premature menopause
- Pregnancy-related complications (e.g. pre-eclampsia, gestational diabetes)
Complications
Complications of MI can be organised by the time frame after the event: [Ref1, Ref2]
| Timeframe | Complication | Presentation |
|---|---|---|
| Early (0-24 hours) | Arrhythmia | Common life-threatening arrhythmias:
|
| Acute heart failure / cardiogenic shock | ||
| Intermediate (0-1 week) | Papillary muscle rupture | Presents as acute mitral regurgitation
|
| Ventricular septal rupture | Presents as left-to-right shunting:
|
|
| Ventricular free wall rupture | Presents as cardiac tamponade (Beck’s triad):
|
|
| Late (>1-2 weeks) | Congestive heart failure | Causes HFrEFHeart failure with reduced ejection fraction |
| Left ventricular aneurysm | Presents as:
|
|
| Dressler syndrome | Autoimmune pericarditis:
Typical pericarditis ECG features – widespread concave ST elevation + PR depression |
|
Diagnosis
Clinical Features
Chest pain / discomfort is the main presenting feature of ACS, it can be mapped to the SOCRATES framework: [Ref]
- Site: central or retrosternal (typically non-specific)
- Onset: sudden onset, usually at rest
- Character: heavy / crushing / tightness
- Radiation: classically to the left arm, neck, jaw
- Associated symptoms: dyspnoea, nausea, vomiting, diaphoresis
- Timing: often lasts >15 min and does not resolve spontaneously
- Exacerbating factors: often precipitated by exertion or emotional stress but may occur at rest (ACS symptoms is characteristically not relieved by rest and nitrate)
- Severity: can be severe
Typical ACS features:
- Chest pain / discomfort lasting >15 min
- Chest pain associated with dyspnoea, nausea, vomiting, and diaphoresis (particularly a combination of these)
- Chest pain associated with haemodynamic instability
- Abrupt deterioration in previously stable angina, with recurrent chest pain occurring frequently and with little or no exertion
Atypical features of ACS include epigastric pain or the absence of chest pain with accompanying N&V, dyspnoea, and diaphoresis. They are usually seen in:
- Inferior MI (esp. if epigastric pain)
- Female
- Diabetes (due to autonomic neuropathy)
Reproducible chest pain on palpation makes ACS less likely, it is more suggestive of musculoskeletal causes of chest pain.
Other clues of musculoskeletal chest pain:
- Pain on movement
- Pain in a very specific location (cardiac chest pain is typically non-specific)
Referral and Initial Assessment
Referral Criteria
This mainly applies to those who present to a non-hospital setting (e.g. GP, health centre)
There are 2 main referral scenarios:
| Scenario | Recommended action |
|---|---|
|
Emergency referral to hospital (usually via ambulance) |
|
Urgent same-day referral to hospital |
Initial Assessment
Apart from a detailed clinical history and examination, perform ALL the following in suspected ACS cases:
- 12-lead ECG – most immediate test to perform (followed by serial ECGs)
- High-sensitivity cardiac troponin T/I (followed by serial samples)
- Other tests (non-ACS specific, but are routinely performed in patients with chest pain)
- Chest X-ray – to rule out chest pathology and ACS complications
- Routine bloods (including FBC, LFT, renal function, blood glucose)
Diagnostic Criteria
Diagnostic criteria of ACS: [Ref]
| ACS spectrum | Diagnostic criteria |
|---|---|
| STEMI |
|
| NSTEMI | |
| Unstable angina |
|
Troponin Interpretation
Rise and/or fall of cardiac troponin is indicative of myocardial infarction (STEMI and NSTEMI) (but not unstable angina, as there is no necrosis) [Ref]
- Troponin is a marker of myocardial injury, not specific to MI
- Necrosis in STEMI and NSTEMI causes a dynamic release of troponin, thus the rise and/or fall pattern
- A persistently raised troponin level is NOT indicative of ACS
Choice of cardiac biomarkers in re-infarction (myocardial infarction occurring within 28 days from the initial event) (NB if it occurs >28 days, it is termed a recurrent infarction)
- Creatine kinase-MB was historically used to diagnose re-infarction due to its shorter half life (compared to troponin), which allows the detection a new rise after the initial peak
- However latest guidelines recommend cardiac troponin as the preferred biomarker in re-infarction [Ref1][Ref2]
- If a re-infarction is suspected, a cardiac troponin measurement should be obtained immediately, followed by a second sample at 3-6 hours after
- Re-infarction can be diagnosed if there is a ≥20% increase in the second ≥20% increase in the second cTn value, provided this value also exceeds the 99th percentile upper reference limit (provided this value also exceeds the 99th percentile upper reference limit)
Important non-ACS causes of elevated troponin: [Ref]
| Category | Important causes |
|---|---|
| Cardiovascular causes |
|
| Non-cardiac causes |
|
ECG Interpretation
STEMI
Dynamic ECG changes seen in STEMI: [Ref]
- ST elevation in ≥2 contiguous leadsContiguous leads refer to leads of the same anatomical region (i.e. group of leads in the table below)
- Reciprocal ST depression in opposite territory – presence strengthens diagnosis of STEMI as opposed to other causes of ST elevation
- Hyperacute T waves, T wave inversion, pathological Q wave
Dynamic changes in ECG (and troponin levels) are characteristic of ACS.
ECG changes over time in STEMI:
- Hyperacute T wavesTall broad-based T waves *Not same as the sharp and narrow tall tented T waves in hyperkalaemia
- ST elevation
- T wave inversion
- Q wave (pathological) formation – may persist indefinitely
ECG changes in various myocardial territories: [Ref]
| Territory | Coronary artery involved | Leads with ST elevation | Leads with reciprocal ST depression | Other notes |
|---|---|---|---|---|
| Anterior | LADLeft anterior descending | V1-V4 | Inferior leads (II, III, aVF) | Poor R wave progression is common |
| Lateral | LCxLeft circumflex | V5-V6, I, aVL | Often occurs with anterior MI (anterolateral MI) | |
| Inferior | RCARight coronary artery | II, III, aVF | Lateral leads (I, aVL +/- V5-V6) | AV block is common in inferior MI |
| Posterior | PDAPosterior descending artery | V7-V9 | Anterior leads (V1-V4) | Often occurs with inferior MI, always consider using posterior leads (V7-V9) in inferior MI to exclude posterior MI |
Other important causes of ST elevation:
| Cause | Features |
|---|---|
| Pericarditis | Widespread ‘global’ changes (not specific to myocardial territory):
No reciprocal ST depression, apart from in V1 and aVR Clinical features are important in distinguishing from STEMI:
|
| Myocarditis | Non-specific ECG changes, often widespread:
Clinical features are important in distinguishing from STEMI:
Note that myocarditis commonly causes an elevated cardiac troponin |
| Left bundle branch block | ECG changes:
|
| Brugada syndrome | ECG changes seen in V1-V3
|
| Prinzmetal (vasospastic) angina | Transient ST elevation during angina episodes
Classically caused by cocaine induced coronary vasospasm |
| Early repolarisation | Seen in young, healthy adults
|
NSTEMI and Unstable Angina
Main changes include: [Ref]
- Normal ECG
- ST depression (horizontal / down-sloping)
- T wave inversion
Management
Immediate Management
Once ACS is suspected based on clinical suspicionTreatment for acute coronary syndrome (ACS) should be initiated immediately upon clinical suspicion, without waiting for confirmatory diagnostic biomarker (e.g., troponin) results., the following should be started ASAP (often given at pre-hospital):
- Aspirin 300mg
- Pain relief
- GTN (sublingual /buccal) – should be avoided in suspected right ventricular infarction (e.g. inferior MI)
- IV morphine (esp. if MI is suspected)
- Oxygen therapy (only if SpO2 <94%, or <88% in those who are at risk of type 2 respiratory failure)
MONA is a common acronym
- M – Morphine
- O – Oxygen
- N – Nitrate
- A – Aspirin 300mg
Definitive Management
There are 2 management pathways – depending on whether it is STEMI or non-STEMI (i.e. NSTEMI and unstable angina):
- STEMI pathway – 2 options
- Reperfusion therapy (PCIPercutaneous coronary intervention / fibrinolysis)
- Medical management
- NSTEMI / unstable angina pathway – 2 options (depending on risk stratification)
- PCIPercutaneous coronary intervention
- Medical management
The STEMI criteria as per ESC guidelines:
New ST elevation at J point in ≥2 contiguous leadsLeads that correspond to a specific myocardial / coronary territory: - Anterior = V1,2,3,4 - Lateral = I, avL, V5,6 - Inferior = II, III, aVF:
- ST elevation in V2-V3
- Men <40 y/o: ≥2.5mm
- Men ≥40 y/o: ≥2.0mm
- Women of any age: ≥1.5mm
- AND/OR
- Other leads: ≥1mm in the absence of LVHLeft ventricular hypertrophy / LBBBLeft bundle branch block
STEMI Management Algorithm
Initial management: aspirin 300mg (if not already given as part of immediate management)
Definitive management depends on eligibility for reperfusion therapy, which is determined by time from symptom onset – cut-off is 12 hours.
Symptom Onset <12 hours → Reperfusion Therapy
There are 2 options for reperfusion therapy:
- Angiography +/- percutaneous coronary intervention (PCI)
- Fibrinolysis (medical)
The choice is determined by whether there is access to PCI within 120 min (2 hours).
NICE guidelines also made the following recommendations regarding PCI:
- Offer if symptoms onset <12 hours with acute STEMI + cardiogenic shock
- Consider if onset >12 hours with evidence of MI
- Consider if onset >12 hours but develops cardiogenic shock
Access Within 120 min → Angiography +/- PCI
Recommendations regarding angiography +/- PCI:
- Drug-eluting stent preferred over bare metal stent, if stenting indicated
- Radial access is preferred over femoral access
Adjuvant drug therapy:
- Dual antiplatelet therapy
- 1st line: aspirin + prasugrel
- If patient already takes oral anticoagulant: aspirin + clopidogrel
- Anti-thrombin therapy during PCI
- Radical access: UFHUnfractionated heparin (also known as just heparin) + bailout GpIIb/IIIa inhibitorThis means that there is no intention of using GpIIb/IIIa inhibitor routinely during PCI. It is only considered when the clinical or angiographic features (such as worsening or persistent thrombus burden) have changed during the procedure, such that there may be benefit to give it.
- Femoral access: bivalirudin + bailout GpIIb/IIIa inhibitorThis means that there is no intention of using GpIIb/IIIa inhibitor routinely during PCI. It is only considered when the clinical or angiographic features (such as worsening or persistent thrombus burden) have changed during the procedure, such that there may be benefit to give it.
Choice of drug is often not that straightforward. Influenced by local guidelines and local availability.
NICE also recommend offering ticagrelor or clopidogrel as an alternative in people aged 75 and over, considering whether the risk of bleeding with prasugrel outweighs its benefit.
No Access Within 120 min → Fibrinolysis
Offer all the following:
- Fibrinolytic agent: tissue plasminogen activator (e.g. alteplase, streptokinase)
- Anti-thrombin
- Dual antiplatelet therapy
- 1st line: aspirin + ticagrelor
- High bleeding risk: aspirin + clopidogrel OR aspirin monotherapy
Then, offer ECG 60-90 minutes after:
- If ST elevation still present on ECG → immediate angiography +/- PCI if indicated
- Do not repeat fibrinolytic therapy
Symptom Onset >12 hours → Medical Management
Dual antiplatelet therapy
- 1st line: aspirin + ticagrelor
- High bleeding risk: aspirin + clopidogrel OR aspirin monotherapy
Tests Before Discharge
Offer echocardiogram to assess left ventricular function in all patients who had a STEMI.
NSTEMI / Unstable Angina Management Algorithm
Initial management (both):
- Aspirin 300mg (if not already given as part of immediate management)
- Antithrombin therapy
- 1st line: fondaparinux
- If high bleeding riskExamples outlined by NICE: - Advancing age - Bleeding complications - Renal impairment - Low body weight / renal impairment (creatinine >265 mmol/L) / immediate angiography planned: UFHUnfractionated heparin (also known as heparin)
Definitive management depends on risk stratification with GRACE score (predicts 6-month mortality).
If the patient is clinically unstable → offer immediate PCI without taking GRACE score into account.
GRACE >3.0% (intermediate / high / highest)
Offer all of the following:
- Angiography +/- PCI within 72 hours
- UFHUnfractionated heparin (also known as heparin), even if fondaparinux has been given
- Dual antiplatelet therapy
- 1st line: aspirin + prasugrel / ticagrelor
- Already taking oral anticoagulant: aspirin + clopidogrel
Recommendations regarding angiography +/- PCI:
- Drug-eluting stent, if stenting indicated
- Radial access, preferred over femoral access
GRACE ≤3.0% (low / lowest)
Medical management with dual antiplatelet therapy:
- 1st line: aspirin + ticagrelor
- High bleeding risk: aspirin + clopidogrel OR aspirin monotherapy
Only consider angiography +/- PCI if ischaemia testing is positive
Tests Before Discharge
- Offer echocardiogram to assess left ventricular function
- In all NSTEMI cases
- Consider in unstable angina
- Consider ischaemia testing in those who have been medically managed without coronary angiography
Choice of Dual Antiplatelet Therapy in ACS
The choice of DAPT in ACS is confusing; therefore this section serves to summarise the recommendations.
However, it is extremely unlikely that the UKMLA to question on ticagrelor vs prasugrel vs clopidogrel. It should be sufficient to learn that DAPT (aspirin + another P2Y12 inhibitor) is given in ACS.
| Scenarior | Choice of DAPT |
|---|---|
| PCI is not intended (applies for STEMI, NSTEMI, unstable angina) |
|
| PCI is intended for STEMI |
|
| PCI is intended for NSTEMI / unstable angina |
|
The above recommendations are based on outcomes in various trials. Key points to be aware of, regarding the choice of P2Y12 inhibitors:
- Clopidogrel has the lowest bleeding risk (but moderate efficacy at reducing thrombotic events)
- Prasugrel and ticagrelor have greater efficacy at reducing thrombotic events, but at the cost of a higher bleeding risk
- Prasugrel is by far the most potent agent
ACS Secondary Prevention Guidelines
Conservative Management
- Cardiac rehabilitation programIncludes: - Physical activity adapted to individual's capacity - Health education including their work driving, flying and sexual activity - Stress Management - Lifestyle advice
- Lifestyle advice
- Mediterranean-style diet
- Regular physical activityAdvise physical activity of at least 20-30 minutes or to increase duration and intensity gradually up to that point.
- Smoking cessation
- Advice on alcohol consumption<14 units of alcohol per week, spread evenly over 3 or more days
- Weight management
- Sexual activity can be resumed 4 weeks after
NICE guideline recommendations regarding various supplements:
| Omega-3 fatty acid | Do not recommend
|
| Beta-carotene | Advise against |
| Vitamin E/C/B9 (folic acid) | Do not recommend |
Pharmacological Management
Offer ALL the following to ALL patients:
- Dual antiplatelet therapy
- Aspirin lifelong (if aspirin not appropriate → clopidogrel)
- 2nd antiplatelet agent for up to 12 months
- High-intensity statin (e.g. atorvastatin 80mg) life-long
- ACE inhibitor for life-long – start once hemodynamically stable
- Beta blocker for 12 months if normal LVEF – start once hemodynamically stable
Add-on if there are heart failure features and ↓ LVEFLeft ventricular ejection fraction
- Aldosterone antagonist (e.g. spironolactone) – initiate within 3-14 days of MI, preferably after starting ACE inhibitor
References
NICE Visual Summary – STEMI Management
NICE Visual Summary – NSTEMI and Unstable Angina
NICE Visual Summary – Secondary Prevention
