UNSTABLE ANGINA

✓ Medically ReviewedDISEASEID: MDBT0152🚨 TRIAGE: EMERGENCYICD-10: I20.0

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Definition

CLINICAL DEFINITION

Unstable angina is a clinical syndrome within the spectrum of non-ST-elevation acute coronary syndromes (NSTE-ACS) characterised by myocardial ischaemia at rest or with minimal exertion, without evidence of myocardial necrosis (i.e., cardiac biomarkers remain within the normal reference range). It typically presents as new-onset severe angina, angina at rest lasting >20 minutes, or a crescendo pattern of previously stable angina.

IN PLAIN ENGLISH

Unstable angina is a serious heart condition where the heart muscle suddenly does not get enough blood flow and oxygen, causing severe chest pain that can happen even when you are resting. It is a medical emergency that warns of a possible impending heart attack.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Unstable angina is NOT a myocardial infarction (heart attack), as there is no detectable myocardial necrosis or elevation in cardiac biomarkers (troponin). It is also NOT stable angina, which is predictable chest pain that occurs with a consistent level of exertion and is relieved by rest or nitrates.

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Word Breakdown

un-

=not, opposite of

angin-

=choking or strangling (from Greek 'agkhonē')

Literal Meaning: Not stable choking or strangling pain

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Abbreviations

UA=Unstable Angina — a type of acute coronary syndrome

ACS=Acute Coronary Syndrome — the broader category including UA, NSTEMI, and STEMI

NSTE-ACS=Non-ST-Elevation Acute Coronary Syndrome — encompasses UA and NSTEMI

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Synonyms & Variants

Crescendo Angina›Angina at Rest›New-Onset Severe Angina›Pre-infarction Angina›

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Category-Specific Context

As a Disease within the acute coronary syndrome spectrum, unstable angina represents a critical threshold of myocardial ischaemia caused by acute plaque disruption and partial or intermittent thrombotic occlusion. It is classified alongside non-ST-elevation myocardial infarction (NSTEMI) under NSTE-ACS, distinguished solely by the absence of biomarker evidence of myocardial necrosis.

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Clinical Context & Usage

CLINICAL SETTINGS

Emergency DepartmentCardiology WardChest Pain UnitIntensive Care UnitGeneral Medicine Ward

USAGE & DOCUMENTATION NOTES

In clinical documentation, unstable angina is often abbreviated as UA and grouped under NSTE-ACS. It is frequently documented based on clinical history (rest pain, crescendo pattern) and negative serial troponins. Clinicians often use risk stratification tools like the GRACE or TIMI scores in the notes to guide decisions regarding early invasive versus conservative management.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

The pathophysiology of unstable angina involves the rupture or erosion of an atherosclerotic plaque in a coronary artery, leading to platelet aggregation and the formation of a non-occlusive or transiently occlusive thrombus. This results in a sudden reduction in coronary blood flow and myocardial oxygen supply. Unlike stable angina, where ischaemia is driven by a fixed stenosis during increased demand, unstable angina is driven by an acute supply-side failure. The transient nature of the thrombus or the presence of collateral circulation prevents prolonged ischaemia sufficient to cause irreversible myocardial necrosis, hence cardiac biomarkers remain normal. Vasospasm and microvascular dysfunction may also contribute to the ischaemic burden.

PRIMARY CAUSES

Atherosclerotic plaque rupture or erosion

Exposure of subendothelial collagen and lipid core triggers platelet activation and thrombus formation, causing acute partial or intermittent coronary artery occlusion.

Coronary artery vasospasm (Prinzmetal's angina)

Hyperreactivity of coronary vascular smooth muscle leads to severe transient focal spasm, reducing myocardial blood flow independently of fixed atherosclerotic disease.

Severe anaemia or hypoxaemia

Profoundly reduced oxygen-carrying capacity or arterial oxygen tension exacerbates supply-demand mismatch in the presence of underlying coronary stenosis.

Tachyarrhythmias

Rapid heart rates significantly shorten diastolic filling time (when coronary perfusion occurs) and increase myocardial oxygen demand, precipitating ischaemia.

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Drug-Induced Causes

💊 Sympathomimetics (e.g., cocaine, amphetamines, ephedrine) ↗

Mechanism: Induce severe coronary vasospasm and increase myocardial oxygen demand through alpha- and beta-adrenergic stimulation.

→ Discontinue the offending agent; manage with benzodiazepines and vasodilators (e.g., nitrates, calcium channel blockers). Beta-blockers are generally avoided in acute cocaine toxicity due to the risk of unopposed alpha-adrenergic stimulation.

💊 Triptans (e.g., sumatriptan) ↗

Mechanism: Serotonin 1B/1D receptor agonists can cause coronary artery vasoconstriction.

→ Discontinue use; contraindicated in patients with known ischaemic heart disease or Prinzmetal's angina.

💊 Ergot alkaloids (e.g., ergotamine) ↗

Mechanism: Potent vasoconstrictors that can precipitate coronary spasm.

→ Stop medication; administer coronary vasodilators if ischaemia occurs.

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Epidemiology

Prevalence:The incidence of unstable angina has been declining in many high-income countries due to improved primary prevention and the reclassification of many UA cases as NSTEMI with the advent of high-sensitivity troponin assays. Historically, UA accounted for a significant proportion of acute coronary syndrome admissions, but contemporary registries show NSTEMI now predominates among NSTE-ACS presentations.

Age Group:Primarily affects older adults, with the incidence rising sharply after age 45 in men and age 55 in women. However, it can occur in younger individuals with significant risk factors such as familial hypercholesterolaemia, heavy smoking, or cocaine use.

Sex Predilection:Male

Geographic Distribution:Prevalence and incidence vary globally, heavily influenced by the regional prevalence of atherosclerotic risk factors (smoking, hypertension, diabetes, obesity). Higher rates are observed in regions undergoing rapid epidemiological transition and urbanisation, while age-standardised rates have fallen in many Western countries.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 EMERGENCY

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

Chest pain with dynamic ST-segment depression or transient ST-elevation — raises high suspicion for severe proximal or left main coronary artery disease requiring urgent coronary angiography.
Recurrent or refractory chest pain despite maximal medical therapy — indicates ongoing ischaemia and high risk of imminent myocardial infarction, mandating an early invasive strategy.

URGENT EVALUATION TRIGGERS

Chest pain lasting >20 minutes at rest.
New-onset angina that markedly limits ordinary physical activity (e.g., CCS Class III).
Crescendo pattern of previously stable angina (increasing in frequency, duration, or occurring at a lower threshold of exertion).
Angina accompanied by new or worsening heart failure symptoms, haemodynamic instability, or life-threatening arrhythmias.

Contraindications & Precautions

CONTRAINDICATIONS

Fibrinolytic (thrombolytic) therapy — absolutely contraindicated in NSTE-ACS (including unstable angina) as it provides no benefit and increases the risk of bleeding and intracranial haemorrhage.
Phosphodiesterase-5 inhibitors (e.g.
sildenafil) — contraindicated in patients taking nitrates due to the risk of profound
refractory hypotension.
Non-dihydropyridine calcium channel blockers (e.g.
verapamil
diltiazem) — generally avoided or used with extreme caution in patients with severe left ventricular systolic dysfunction or decompensated heart failure.

SPECIAL PRECAUTIONS

Beta-blockers must be used cautiously or avoided in patients with signs of acute heart failure
low cardiac output state
or high-degree atrioventricular block.
Dual antiplatelet therapy (DAPT) increases bleeding risk; assess patient-specific bleeding risk (e.g.
PRECISE-DAPT score) and consider gastroprotection (PPI) in high-risk individuals.
Anticoagulants (e.g.
enoxaparin
fondaparinux
unfractionated heparin) require dose adjustment or careful monitoring in patients with severe renal impairment.

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Myocardial Infarction (NSTEMI or STEMI) — progression of the thrombotic occlusion leading to myocardial necrosis.
Life-threatening arrhythmias (e.g.
ventricular tachycardia
ventricular fibrillation) — triggered by acute ischaemia altering myocardial electrical stability.
Cardiogenic shock — severe
extensive ischaemia leading to acute pump failure
though less common in UA than in large infarctions.
Heart failure — acute ischaemic dysfunction of the left ventricle causing pulmonary oedema.

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Stable Angina

Both involve myocardial ischaemia, but stable angina is predictable, exertion-related, and relieved by rest, whereas unstable angina is unpredictable, occurs at rest, and represents an acute emergency.

Non-ST-Elevation Myocardial Infarction (NSTEMI)

Both present identically on ECG and clinically as NSTE-ACS; they are distinguished only by the presence (NSTEMI) or absence (UA) of elevated cardiac biomarkers indicating necrosis.

Prinzmetal's Angina

Both can present with rest pain, but Prinzmetal's is caused by focal coronary vasospasm often with transient ST-elevation, rather than atherosclerotic plaque rupture.

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Acute Pericarditis

Key Distinguishing Feature: Pleuritic chest pain that improves on leaning forward; ECG shows diffuse concave ST-elevation and PR depression, unlike the ST-depression or T-wave inversion of UA.

Aortic Dissection

Key Distinguishing Feature: Sudden onset, severe 'tearing' chest pain radiating to the back; may present with pulse deficits or a new aortic regurgitation murmur. Requires immediate CT angiography.

Pulmonary Embolism

Key Distinguishing Feature: Pleuritic chest pain, dyspnoea, tachycardia, and hypoxia; ECG may show S1Q3T3 pattern or right heart strain, and D-dimer/CTPA are diagnostic.

Gastro-oesophageal Reflux Disease (GORD) / Oesophageal Spasm

Key Distinguishing Feature: Burning retrosternal pain related to meals or recumbency, often relieved by antacids; lacks exertional trigger and ischaemic ECG changes.

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Clinical Pearls

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The introduction of high-sensitivity troponin assays has significantly reduced the clinical diagnosis of unstable angina, as many patients who previously would have been diagnosed with UA now show minor biomarker elevations and are classified as having an NSTEMI.

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Fibrinolytic therapy is strictly contraindicated in unstable angina and NSTEMI. Unlike STEMI, where immediate reperfusion of a completely occluded artery is required, NSTE-ACS involves partial or intermittent occlusion, and thrombolytics increase bleeding risk without improving outcomes.

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Risk stratification using tools like the GRACE score is essential upon presentation. It estimates the 6-month mortality risk and helps guide the decision between an early invasive strategy (angiography within 24 hours) versus a conservative or delayed invasive approach.

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A normal initial ECG and negative first troponin do not rule out unstable angina or evolving NSTEMI. Serial ECGs and repeat troponin testing at appropriate intervals (e.g., 0 and 1-hour or 0 and 3-hour algorithms) are mandatory for patients with ongoing or recurrent symptoms.

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Example Usage & SOAP

CLINICAL SENTENCE

"A 62-year-old male with a history of hypertension and smoking presented to the Emergency Department with a 2-hour history of crushing central chest pain radiating to the left arm that occurred at rest, with an initial ECG showing lateral ST-depression and negative high-sensitivity troponin, consistent with unstable angina."

IN A SOAP NOTE

S: 58-year-old female reports sudden onset of heavy, squeezing substernal chest pain starting 45 minutes ago while watching television. Pain radiates to the jaw and is associated with diaphoresis and nausea. She reports similar but milder episodes over the past week when walking up stairs. O: BP 155/90 mmHg, HR 92 bpm, RR 18, SpO2 98% on room air. Diaphoretic and anxious. Lungs clear to auscultation. CV: regular rate and rhythm, no murmurs, JVP not elevated. ECG: 1 mm horizontal ST-depression in leads V4-V6. Initial hs-cTnI is 12 ng/L (normal <14 ng/L). A: Unstable angina (NSTE-ACS). TIMI score 4, GRACE score 135 (intermediate-high risk). P: Administered aspirin 300 mg PO, ticagrelor 180 mg PO, and sublingual nitroglycerin with partial relief. Started on intravenous unfractionated heparin infusion. Cardiology consulted for early invasive strategy (coronary angiography within 24 hours). Admitted to Chest Pain Unit for serial troponins and continuous telemetry.

DIFFERENTIAL DIAGNOSIS CONTEXT

Differential for acute chest pain at rest: (1) Acute Coronary Syndrome (Unstable Angina/NSTEMI/STEMI) — evaluate with serial ECGs and high-sensitivity troponins; (2) Aortic Dissection — assess for pulse deficits, widened mediastinum on CXR, and confirm with CT aortogram if high clinical suspicion; (3) Pulmonary Embolism — assess for tachycardia, hypoxia, right heart strain on ECG, and evaluate with D-dimer or CTPA; (4) Acute Pericarditis — look for pleuritic pain, positional relief, and diffuse ST-elevation on ECG; (5) Gastrointestinal causes (e.g., severe GORD, oesophageal spasm, peptic ulcer perforation) — consider if cardiac and pulmonary causes are excluded and pain relates to meals or recumbency.

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Classifications & Scoring

GRADING SYSTEM

Canadian Cardiovascular Society (CCS) Grading of Angina Pectoris

Classifies the severity of angina based on physical activity limitations. Class I: Ordinary physical activity does not cause angina. Class II: Slight limitation of ordinary activity. Class III: Marked limitation of ordinary physical activity. Class IV: Inability to carry on any physical activity without discomfort or symptoms at rest. Note: Unstable angina is often categorised separately or as Class III/IV with recent worsening.

View Reference ↗

SCORING TOOL

TIMI Risk Score for UA/NSTEMI

Estimates the 14-day risk of death, new/recurrent MI, or severe recurrent ischaemia requiring urgent revascularisation. Incorporates 7 variables: age >=65, >=3 CAD risk factors, known CAD (stenosis >=50%), ASA use in past 7 days, severe angina (>=2 episodes in 24h), ST changes >=0.5mm, and positive cardiac marker.

Clinical Calculator ↗

SCORING TOOL

GRACE Risk Score

Predicts in-hospital and 6-month mortality or combined mortality/MI in patients with ACS. Variables include age, heart rate, systolic BP, Killip class, cardiac arrest at admission, ST-segment deviation, elevated cardiac enzymes, and serum creatinine.

Clinical Calculator ↗

SCORING TOOL

HEART Score

Used in the emergency department to stratify the risk of major adverse cardiac events (MACE) within 6 weeks for patients with undifferentiated chest pain. Components: History, ECG, Age, Risk factors, and initial Troponin.

Clinical Calculator ↗

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Prognosis

SHORT-TERM OUTCOME

With appropriate medical therapy and risk stratification, the short-term risk of death or myocardial infarction is significantly reduced. However, patients with high-risk features (e.g., dynamic ST-T changes, elevated GRACE score) remain at elevated risk for adverse events within the first 30 days.

LONG-TERM PROGNOSIS

Long-term prognosis depends heavily on the extent of underlying coronary artery disease, left ventricular function, and adherence to secondary prevention (antiplatelets, statins, risk factor modification). Patients with multi-vessel disease or reduced ejection fraction have higher long-term mortality and morbidity.

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References & Coding

ICD-10 DIAGNOSTIC CODE

I20.0

LITERATURE CITATIONS & GUIDELINES

[1]Collet JP et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2021;42(14):1289-1367.

[2]Amsterdam EA et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. J Am Coll Cardiol. 2014;64(24):e139-e228.

[3]Thygesen K et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018;72(18):2231-2264.

MEDICAL DISCLAIMER — This content is intended for educational purposes and qualified healthcare professionals only. Always refer to current clinical diagnostic criteria, institutional protocols, and official guidelines. Medobo is not responsible for clinical decisions made based on this content.

UNSTABLE ANGINA

Definition

Word Breakdown

Abbreviations

Synonyms & Variants

Category-Specific Context

Clinical Context & Usage

Primary Causes & Pathophysiology

Drug-Induced Causes

Epidemiology

Red Flags & Triage ★

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

URGENT EVALUATION TRIGGERS

Contraindications & Precautions

CONTRAINDICATIONS

SPECIAL PRECAUTIONS

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Confused With (LASA & DDx) ★

Clinical Pearls

Example Usage & SOAP

Classifications & Scoring

Canadian Cardiovascular Society (CCS) Grading of Angina Pectoris

TIMI Risk Score for UA/NSTEMI

GRACE Risk Score

HEART Score

Prognosis

SHORT-TERM OUTCOME

LONG-TERM PROGNOSIS

Related Terms

References & Coding