Acute Coronary Syndrome (ACS)

Acute coronary syndrome most commonly occurs when an atherosclerotic plaque within a coronary artery ruptures, leading to thrombus formation and vessel occlusion. In high-flow arteries such as the coronaries, thrombi are predominantly platelet-rich. For this reason, antiplatelet drugs—including aspirin, clopidogrel, and ticagrelor—form the cornerstone of treatment.

ACS is divided into three clinical entities:

• Unstable angina
• ST-elevation myocardial infarction (STEMI)
• Non–ST-elevation myocardial infarction (NSTEMI)

Coronary Artery Anatomy

Two main coronary arteries arise from the base of the aorta:

• Right coronary artery (RCA)
• Left coronary artery (LCA)

Right Coronary Artery (RCA)

The RCA courses along the right side and inferior surface of the heart and supplies blood to:

• Right atrium
• Right ventricle
• Inferior portion of the left ventricle
• Posterior interventricular septum

Left Coronary Artery (LCA)

The left coronary artery divides into two major branches:

• Circumflex artery
• Left anterior descending (LAD) artery

Circumflex Artery

This vessel wraps around the left side and posterior aspect of the heart and supplies:

• Left atrium
• Posterior region of the left ventricle

Left Anterior Descending (LAD) Artery

The LAD runs down the anterior interventricular groove and supplies:

• Anterior wall of the left ventricle
• Anterior interventricular septum

Clinical Presentation

ACS classically presents with central, crushing or constricting chest pain.

Associated symptoms commonly include:

• Radiation of pain to the arms or jaw
• Nausea and vomiting
• Profuse sweating and clamminess
• A sense of impending doom
• Breathlessness
• Palpitations

Symptoms typically persist for more than 15 minutes, even at rest.

A silent myocardial infarction occurs when typical chest pain is absent. This presentation is particularly common in patients with diabetes.

ECG Changes in ACS

STEMI

• ST-segment elevation
• New-onset left bundle branch block

NSTEMI

• ST-segment depression
• T-wave inversion

Pathological Q waves indicate a deep, full-thickness (transmural) infarction and usually develop 6 hours or more after symptom onset.

Coronary Artery Territories on ECG

Troponin

Troponin is a protein found in both cardiac and skeletal muscle. The specific troponin subtype, reference range, and diagnostic thresholds vary between laboratories, so local guidance should always be followed.

Elevated troponin levels reflect myocardial ischaemia, as the protein is released from injured cardiac muscle.

Troponin measurement is essential for diagnosing NSTEMI, but it is not required to diagnose STEMI, which is identified based on clinical features and ECG findings.

Serial troponin testing may be required (e.g. at presentation and 3 hours later). A significantly raised or rising troponin level in the context of suspected ACS confirms an NSTEMI.

Troponin elevation is not specific to ACS. Other causes include:

• Chronic kidney disease
• Sepsis
• Myocarditis
• Aortic dissection
• Pulmonary embolism

Additional Investigations

Further investigations for suspected or confirmed ACS include:

• Baseline blood tests (FBC, U&E, LFTs, lipids, glucose)
• Chest X-ray to assess for pulmonary oedema or alternative diagnoses
• Echocardiography (once stable) to evaluate cardiac function, particularly left ventricular performance

Classification of ACS

All patients presenting with suspected cardiac chest pain should undergo ECG and troponin testing. The combination of these results determines the diagnosis.

STEMI

Diagnosed when the ECG demonstrates:

• ST elevation, or
• New left bundle branch block

NSTEMI

Diagnosed when troponin is elevated with either:

• A normal ECG, or
• ECG changes such as ST depression or T-wave inversion

Unstable Angina

Diagnosed when symptoms suggest ACS but troponin levels are normal, with either:

• A normal ECG, or
• ECG changes such as ST depression or T-wave inversion

If both ECG and troponin are normal in a patient with chest pain, the diagnosis may be unstable angina or a non-cardiac cause (e.g. musculoskeletal pain).

Initial Management

This section is based on NICE guidance for chest pain (2016) and ACS (2020) and is intended for exam preparation. Local protocols and senior input should always guide real-world management.

Initial treatment can be recalled using the “CPAIN” mnemonic:

• C – Call an ambulance
• P – Perform an ECG
• A – Aspirin 300 mg
• I – Intravenous morphine if needed (with an antiemetic such as metoclopramide)
• N – Nitrate (GTN)

If the patient is pain-free but experienced symptoms within the previous 72 hours, same-day hospital assessment is required—typically via ambulatory care. Emergency admission is necessary if ECG abnormalities or complications (e.g. heart failure) are present.

Management of STEMI

Patients presenting within 12 hours of symptom onset should be urgently discussed with a cardiac centre for:

• Primary PCI (if available within 2 hours), or
• Thrombolysis (if PCI cannot be delivered within 2 hours)

The cardiac team will advise on pre-procedural medications, such as aspirin and prasugrel.

Percutaneous Coronary Intervention (PCI)

A catheter is inserted via the radial artery (preferred) or femoral artery and advanced to the coronary arteries under fluoroscopic guidance. Contrast dye identifies the occluded vessel.

Treatment options include:

• Balloon angioplasty
• Thrombus aspiration
• Stent insertion to maintain vessel patency

Thrombolysis

Thrombolytic therapy uses fibrinolytic drugs to dissolve clots by breaking down fibrin. This carries a significant bleeding risk.

Examples include:

• Streptokinase
• Alteplase
• Tenecteplase

Management of NSTEMI

NSTEMI treatment can be remembered using the “BATMAN” mnemonic:

• B – Base angiography decisions on the GRACE score
• A – Aspirin 300 mg stat
• T – Ticagrelor 180 mg stat (clopidogrel if high bleeding risk; prasugrel if proceeding to angiography)
• M – Morphine titrated for pain control
• A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography planned)
• N – Nitrate (GTN)

Oxygen should only be given if oxygen saturation falls below 95% (unless COPD is present).

Angiography in NSTEMI

Haemodynamically unstable patients should undergo immediate angiography, similar to STEMI management.

The GRACE score estimates 6-month mortality risk:

• ≤ 3% → low risk
• 3% → moderate to high risk

Patients at moderate or high risk should undergo early angiography with PCI, ideally within 72 hours.

Ongoing Management

Following acute treatment, patients require:

• Echocardiography (once stable) to assess left ventricular function
• Cardiac rehabilitation
• Long-term secondary prevention

Secondary Prevention Medication

Secondary prevention therapy can be recalled using the “6 As”:

• Aspirin 75 mg daily indefinitely
• Another antiplatelet (e.g. clopidogrel or ticagrelor) for 12 months
• Atorvastatin 80 mg daily
• ACE inhibitor (e.g. ramipril), titrated to tolerance
• Atenolol or another beta blocker (commonly bisoprolol)
• Aldosterone antagonist for patients with heart failure (e.g. eplerenone up to 50 mg daily)

Dual antiplatelet duration depends on the type of stent used during PCI.

Renal function and potassium levels must be closely monitored in patients taking ACE inhibitors and aldosterone antagonists. A 2016 MHRA safety alert highlighted the risk of fatal hyperkalaemia when combining spironolactone or eplerenone with ACE inhibitors or ARBs.

Complications of Myocardial Infarction

Complications can be remembered using the “DREAD” mnemonic:

• D – Death
• R – Rupture of septum or papillary muscles
• E – oEdema (heart failure)
• A – Arrhythmias and aneurysm
• D – Dressler’s syndrome

Dressler’s Syndrome

Dressler’s syndrome, also known as post–myocardial infarction syndrome, typically occurs 2–3 weeks after an MI. It results from an autoimmune inflammatory response affecting the pericardium.

Although now less common due to improved ACS management, it presents with:

• Pleuritic chest pain
• Low-grade fever
• Pericardial friction rub

Complications may include pericardial effusion and, rarely, cardiac tamponade.

Diagnosis is supported by:

• ECG changes (widespread ST elevation and T-wave inversion)
• Echocardiographic evidence of pericardial effusion
• Raised inflammatory markers (CRP and ESR)

Treatment includes NSAIDs (e.g. aspirin or ibuprofen), with corticosteroids (e.g. prednisolone) reserved for severe cases. Pericardiocentesis may be required for significant effusions.

Types of Myocardial Infarction

Understanding MI subtypes is useful for exams, though these terms are less commonly used clinically.

• Type 1: Acute coronary event (classic MI)
• Type 2: Oxygen supply–demand mismatch (e.g. anaemia, tachycardia, hypotension)
• Type 3: Sudden cardiac death suggestive of MI
• Type 4: MI related to cardiac procedures (PCI, stenting, CABG)

These can be remembered using the “ACDC” mnemonic:

• A – ACS-type MI
• C – Can’t cope MI
• D – Dead by MI
• C – Caused by us MI

Last updated January 2026