Cardiovascular

Acute Coronary Syndrome

Acute coronary syndrome (ACS) is acute myocardial ischaemia, usually from thrombosis on a disrupted coronary plaque, triaged by the first ECG into a reperfusion pathway or a troponin pathway.

In a nutshell

Acute coronary syndrome (ACS) is acute myocardial ischaemia from a culprit coronary lesion. Give aspirin 300 mg chewed immediately, then let the ECG decide: ST-elevation myocardial infarction (STEMI) goes straight to reperfusion, everything else to troponin and formal risk scoring.

Classic presentation

Prolonged central chest pressure at rest radiating to an arm or the jaw, with sweating, nausea and breathlessness, although ACS can present with none of these.

Key points

STEMI and non-ST-elevation ACS (NSTE-ACS) are presentation pathways, not proof of complete versus partial occlusion or transmural versus subendocardial infarction.
Left bundle branch block, right bundle branch block and ventricular pacing hide ST elevation. With highly suspicious symptoms, manage as STEMI whether or not the block is old.
Sgarbossa and modified Sgarbossa (Smith) criteria are the tools used to identify occlusion behind a left bundle branch block or a paced rhythm.
ST depression of 1 mm or more in six or more leads, with ST elevation in aVR or V1, suggests multivessel or left main disease.
Posterior occlusion shows as ST depression in V1 to V3 with tall R waves and upright T waves. Confirm with posterior leads V7 to V9.
Right ventricular infarction is preload dependent, so nitrates can drop the blood pressure sharply. Suspect it in inferior STEMI and record V3R and V4R.
Do not assess symptoms differently by sex or ethnicity, and do not dismiss breathlessness, syncope or epigastric discomfort when the context suggests ACS.
NICE's early rule-out strategies are a single sample at presentation using a threshold near the assay's limit of detection, or a second sample at 30 minutes to 3 hours.
After ACS without known diabetes, check HbA1c before discharge and fasting glucose no earlier than 4 days. Neither should delay discharge.
Aspirin after myocardial infarction (MI) is 75 mg once daily, continued indefinitely. The 300 mg is a single loading dose only.
Advise 20 to 30 minutes of activity a day to slight breathlessness, and that sexual activity is usually safe about 4 weeks after an uncomplicated MI.

First-line investigation

A 12-lead ECG within 10 minutes of first medical contact. A normal tracing does not exclude ACS, so repeat it during symptoms.

Management

The first ten minutes

ABCDE (airway, breathing, circulation, disability, exposure), IV access, rhythm and saturation monitoring, defibrillator to hand, 12-lead ECG within 10 minutes of first medical contact.^2,5
Aspirin 300 mg orally, chewed or dispersed. Oxygen only if saturation is below 94%: target 94% to 98%, or 88% to 92% if at risk of hypercapnic respiratory failure.^3,1,5,6
Glyceryl trinitrate (GTN) sublingual: 1 tablet (500 or 600 micrograms) or 1 to 2 sprays of 400 micrograms, repeat at 5 minutes, maximum 3 doses.⁷
Severe pain: morphine 5 to 10 mg by slow IV injection at 1 to 2 mg/minute, or 2.5 to 5 mg if frail or elderly.⁸
Abrupt severe chest or back pain, a pulse deficit or new aortic regurgitation: exclude aortic dissection before fibrinolysis or any antithrombotic escalation.^1,3

STEMI: reperfuse, and do not wait for troponin

STEMI is new ST elevation at the J point in two contiguous leads: 1 mm or more in every lead except V2 and V3.²
V2 to V3 threshold: 2.5 mm or more in men under 40, 2 mm or more in men 40 and over, 1.5 mm or more in women of any age.²
Within 12 hours of onset: primary percutaneous coronary intervention (PCI) if deliverable within 120 minutes of when fibrinolysis could have been given. Otherwise fibrinolysis.³
Primary PCI: prasugrel 60 mg then 10 mg daily (5 mg if under 60 kg or aged 75 and over) with aspirin. Already anticoagulated: clopidogrel instead.^3,9,10
Radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor. Femoral: consider bivalirudin. No routine glycoprotein IIb/IIIa inhibitor or fibrinolytic before the catheter laboratory.³
Fibrinolysis: tenecteplase IV over 10 seconds within 6 hours, 30 mg under 60 kg rising 5 mg per 10 kg band to 50 mg at 90 kg and above.^3,11
Alteplase alternative, accelerated myocardial infarction regimen: 15 mg IV bolus, then 0.75 mg/kg over 30 minutes, then 0.5 mg/kg over 60 minutes, maximum 100 mg.¹²
Give an antithrombin with the fibrinolytic. Repeat the ECG at 60 to 90 minutes: residual ST elevation means immediate angiography with follow-on PCI. Never repeat lysis.³
Not treated with PCI: ticagrelor 180 mg then 90 mg twice daily with aspirin, or clopidogrel 300 mg then 75 mg daily if bleeding risk is high.^3,13,10

Unstable angina and NSTEMI: anticoagulate, score, then choose

Aspirin 300 mg loading then 75 mg daily indefinitely. Fondaparinux 2.5 mg subcutaneously once daily unless bleeding risk is high or immediate angiography is planned.^3,6,14
Creatinine above 265 micromoles per litre: unfractionated heparin instead, 5000 units IV loading then 18 units/kg/hour, adjusted by clotting monitoring.^3,15
Give unfractionated heparin in the catheter laboratory to anyone having PCI, whether or not fondaparinux was given. In November 2020 this was off-label.³
GRACE (Global Registry of Acute Cardiac Events) predicts six-month mortality. Above 3.0%: consider angiography within 72 hours. At 3.0% or less: consider conservative management.³
Having angiography, no anticoagulation indication: prasugrel or ticagrelor with aspirin, prasugrel only once anatomy is defined and PCI intended. On an anticoagulant: clopidogrel.^3,9
PCI not indicated: ticagrelor with aspirin, or clopidogrel with aspirin, or aspirin alone, if bleeding risk is high.^3,13

What overrides the risk score

An unstable clinical condition means immediate coronary angiography, whatever the risk score says.³
Shock, refractory ischaemia, acute heart failure, malignant arrhythmia, arrest or a new murmur: immediate senior cardiology and critical-care review with emergency echocardiography.^3,2
Keep blood glucose below 11.0 mmol/litre while avoiding hypoglycaemia, first considering a dose-adjusted insulin infusion. Do not routinely use intensive insulin therapy.³

Five drugs before discharge

Aspirin 75 mg once daily indefinitely, and continue dual antiplatelet therapy (DAPT) for up to 12 months after an MI unless contraindicated.^3,6
Atorvastatin 80 mg once daily, started without delay. Target LDL-cholesterol 2.0 mmol/litre or below, or non-HDL cholesterol 2.6 mmol/litre or below.^16,17
Start an ACE inhibitor once stable and continue indefinitely. BNF schedules differ; with post-MI heart failure, ramipril starts at 2.5 mg twice daily after 48 hours.^3,18
Start a beta-blocker once stable. With heart failure and reduced LVEF, bisoprolol may start at 1.25 mg daily and titrate to 10 mg; otherwise review at 12 months.^3,19
Heart failure with reduced LVEF: add an aldosterone antagonist licensed post-MI within 3 to 14 days, after the ACE inhibitor. Halve or stop it for hyperkalaemia.³
Assess left ventricular function. Begin cardiac rehabilitation before discharge, with the first session within 10 days of discharge.³

Exam traps

A single raised troponin is not automatically NSTEMI. It may be chronic or non-ischaemic myocardial injury, and MI still requires evidence of acute ischaemia.
The 120 minutes is measured from when fibrinolysis could otherwise have been given, not from first medical contact.
Do not give dual antiplatelet therapy for undifferentiated chest pain before unstable angina or NSTEMI has been diagnosed.
Failed reperfusion after fibrinolysis is treated with immediate angiography, never with a second dose of fibrinolytic.
Do not use level of consciousness after cardiac arrest caused by suspected STEMI to decide eligibility for angiography.
Prasugrel is withheld until the coronary anatomy is defined and PCI is intended. Ticagrelor is not.
Troponin cut-offs are assay-specific and published for each assay. That is why hospitals differ, and it is not the same as checking local policy.
A young person with a low six-month mortality score can still be high risk and benefit from early angiography.
A posterior myocardial infarction is an occluded artery, so it earns primary PCI, not the NSTEMI pathway.

Illustrations

Plaque disruption and coronary thrombosisDiagram of an atherosclerotic plaque with cap disruption, platelet activation and thrombus in the coronary lumen. This is a common type 1 ACS mechanism, not a diagram that determines the presenting ECG label or proves the degree of occlusion.PassFinals · original

Schematic troponin rise and fallA teaching schematic of troponin concentration over time after myocardial injury. It is not an assay rule-out algorithm: high-sensitivity assays use validated, assay-specific thresholds and intervals, and symptom timing and acute change must be interpreted with evidence of ischaemia.PassFinals · original

Key sources

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.