Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Diagnose and risk-stratify NSTE-ACS, deliver antithrombotic care safely and match invasive timing to instability, ischaemic risk and bleeding risk.
NSTE-ACS is a working syndrome refined by serial ECG, high-sensitivity troponin and coronary assessment. Type 2 MI and non-ischaemic myocardial injury require different treatment despite similar biomarker elevation.
Risk assessment has two axes: ischaemic risk determines urgency and likely benefit from angiography; bleeding and comorbidity determine treatment harm. Both must be documented.
A low-risk result supports selective non-invasive testing and prevention assessment, but persistent or recurrent symptoms should prompt re-evaluation rather than premature discharge.
Rupture or erosion of a coronary plaque exposes thrombogenic material and produces a platelet-rich thrombus that may be subtotal, intermittent or occasionally completely occlusive. Smoking, diabetes, hypertension and dyslipidaemia increase the underlying atherosclerotic risk.
A plaque-associated thrombus can wax and wane or shed distal microemboli, causing rest or crescendo ischaemia without persistent ST elevation. Fixed coronary disease may increase vulnerability, but supply-demand imbalance without acute atherothrombosis is assessed separately as type 2 myocardial infarction when it causes acute ischaemia, or as myocardial injury when ischaemic evidence is absent.
Plaque disruption activates platelets and coagulation within a coronary artery. The resulting thrombus may cause subtotal, intermittent or complete occlusion; the absence of persistent ST elevation does not reliably predict the angiographic degree of obstruction.
Thrombotic obstruction, local vasoconstriction and distal microembolisation reduce perfusion. Oxygen delivery becomes inadequate for myocardial demand, particularly within the vulnerable subendocardial layers.
Ischaemic myocardium alters electrical repolarisation and contraction, producing pain, ST depression or T-wave change. The initial ECG can nevertheless remain normal or non-specific.
Sufficiently prolonged ischaemia kills cardiomyocytes and causes a rise or fall in circulating troponin, defining NSTEMI when clinical evidence of acute ischaemia is also present.
When coronary ischaemia causes new, rest or crescendo symptoms without detectable myocardial necrosis, the syndrome is unstable angina. Recurrent obstruction can still progress to infarction.
Refractory or recurrent rest pain, shock, acute heart failure, serious arrhythmia or dynamic widespread ST change requires immediate invasive assessment.
A rise or fall of troponin with at least one value above the 99th centile plus clinical, ECG, imaging or angiographic evidence of acute ischaemia.
New, crescendo or rest ischaemic symptoms without myocardial necrosis; high-sensitivity assays have reduced but not abolished this diagnosis.
New ST depression or transient ST elevation during pain materially raises risk even if the initial troponin is low.
Active bleeding, recent intracranial haemorrhage, severe thrombocytopenia or urgent surgical need changes antithrombotic strategy and requires senior input.
Persistent diagnostic ST elevation or another recognised acute occlusion pattern requires an emergency reperfusion pathway. The ECG pattern does not by itself prove complete arterial occlusion, and serial ECGs are important because findings can evolve.
Type 2 myocardial infarction requires acute ischaemia from a supply-demand imbalance unrelated to acute coronary atherothrombosis; a troponin rise without ischaemic evidence is myocardial injury, not infarction. Sepsis, anaemia, hypoxia or tachyarrhythmia may provide the alternative mechanism.
Myocarditis may reproduce pain, ECG changes and troponin elevation. Inflammatory or electrical features and a non-coronary injury pattern on cardiac magnetic resonance favour myocarditis.
Pulmonary embolism can cause chest pain, breathlessness and troponin release. Pleuritic symptoms, hypoxaemia, thromboembolic risk and right-heart strain distinguish it from primary coronary ischaemia.
Abrupt severe pain radiating to the back, pulse or blood-pressure asymmetry and neurological signs raise concern for dissection. Antithrombotic treatment may be harmful until this is addressed.
Anaemia, hypoxaemia, sepsis, tachyarrhythmia, pulmonary embolism and myocarditis can cause troponin elevation; seek ischaemic evidence and mechanism.
An unstable plaque or residual severe stenosis can thrombose again, extend myocardial necrosis or become completely occlusive. Recurrent rest pain and dynamic ECG change indicate continuing risk.
Ischaemic myocardium becomes electrically unstable and may develop bradyarrhythmia, ventricular tachycardia or fibrillation. Arrhythmia can abruptly reduce cardiac output before extensive necrosis is evident.
Loss of functioning myocardium and ischaemic stunning impair contraction and raise filling pressures. Acute pulmonary oedema, functional mitral regurgitation or cardiogenic shock may follow.
Coronary atherosclerosis persists beyond the acute episode. Without effective secondary prevention, patients remain at increased risk of recurrent infarction, heart failure, stroke and cardiovascular death.
Risk scores guide stable patients; refractory pain, shock, acute heart failure or malignant arrhythmia requires immediate angiography.
Fondaparinux alone does not provide adequate catheter protection during PCI; add systemic IV UFH in the catheter laboratory and adjust the procedural dose to glycoprotein IIb/IIIa use, activated clotting time and bleeding risk.
Loading before the angiogram in NSTE-ACS increases bleeding without a proven pre-PCI benefit.
A dynamic elevation still needs evidence of ischaemia and a mechanism before type 1 NSTEMI treatment is assumed.
High-sensitivity troponin has made it less common, not impossible.
Avoid mechanically adding full ACS DAPT to anticoagulation; select agent and duration from ischaemic and bleeding risk.
Calling any troponin rise NSTEMI without evidence of ischaemia.
Waiting for GRACE calculation in a haemodynamically unstable patient.
Giving fondaparinux alone during PCI without procedural UFH.
Loading prasugrel before coronary anatomy is defined in NSTE-ACS.
Discharging without stating the antiplatelet and anticoagulant combination and intended stop dates.
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A patient with suspected NSTEMI develops recurrent pain, pulmonary oedema and hypotension. What is the best invasive timing?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Active major bleeding or true hypersensitivity; assess gastroprotection and combined antithrombotic bleeding risk.
Contraindicated with active clinically significant bleeding, acute bacterial endocarditis or creatinine clearance below 20 ml/min. If serum creatinine is above 265 micromol/l, NICE advises considering UFH adjusted to clotting monitoring. At PCI after fondaparinux, add IV UFH: 70–100 units/kg without a glycoprotein IIb/IIIa inhibitor or 50–70 units/kg with one, adjusted to activated clotting time and bleeding risk.
Bleeding, previous intracranial haemorrhage, severe hepatic impairment, strong CYP3A interactions, dyspnoea and bradyarrhythmia; avoid routine combination with a necessary oral anticoagulant.
Do not give before anatomy is defined in NSTE-ACS. Contraindicated after stroke or TIA, in active bleeding and in severe hepatic impairment; heightened bleeding risk at low weight or older age.
Active bleeding, CYP2C19 interactions and variable response; choose loading dose from timing, age, PCI and anticoagulant plan.
Liver disease, myopathy, pregnancy and interacting medicines; monitor lipids and transaminases under NICE NG238.