Unstable angina
Last reviewed: May 2026
Outline
Unstable angina (UA) is defined by transient myocardial ischemia from atherosclerotic plaque disruption with partial coronary thrombosis, in the absence of significant myonecrosis (i.e., troponin-negative). [1-2] It exists on the acute coronary syndrome (ACS) continuum and can rapidly progress to NSTEMI or STEMI. [1] The following figure illustrates the ACS spectrum from unstable angina through STEMI:
1. History
- Three principal presentations: [4]
- Rest angina: chest pain at rest, usually >20 minutes
- New-onset angina: <2 months, at least CCS Class III severity
- Crescendo angina: previously stable angina increasing in frequency, duration, or lower threshold
- Character: retrosternal pressure, heaviness, tightness, squeezing; may radiate to arms, neck, jaw [5]
- Associated symptoms: diaphoresis, dyspnea (most common anginal equivalent), nausea, lightheadedness, presyncope [5-6]
- Pain that is pleuritic, positional, or reproducible with palpation is lower risk for ACS, but does not exclude it [7]
- Relief with nitroglycerin is not diagnostic and should not be used as a diagnostic criterion [6]
- Atypical presentations more common in women, elderly, diabetics, and patients with renal insufficiency — may present with isolated dyspnea, epigastric pain, or fatigue [5]
2. Alarm Features
- Prolonged rest pain >20 minutes or accelerating symptoms over 48 hours [8]
- Hemodynamic instability: hypotension, tachycardia, bradycardia [8-9]
- Signs of heart failure: pulmonary edema, new S3, rales [8]
- New or worsening mitral regurgitation murmur [8]
- Syncope or presyncope
- Dynamic ECG changes (ST depression, transient ST elevation) [1]
- Sustained ventricular tachycardia [8]
- Any of these features classify the patient as high risk for short-term death or nonfatal MI [8][10]
3. Medications
Acute Treatment:
- Aspirin 162–325 mg loading, then 81 mg daily [11]
- P2Y₁₂ inhibitor: ticagrelor (180 mg load → 90 mg BID) or clopidogrel (300–600 mg load → 75 mg daily) [11-12]
- Anticoagulation: unfractionated heparin (60 U/kg bolus, 12 U/kg/hr), enoxaparin, fondaparinux, or bivalirudin [13-14]
- Nitroglycerin SL 0.4 mg q5min × 3 for ongoing ischemic pain; IV drip if refractory [10]
- Beta-blocker (metoprolol, atenolol) — reduces heart rate and myocardial oxygen demand [10][14]
- High-intensity statin (atorvastatin 80 mg or rosuvastatin 40 mg) — initiate early [11]
Contraindicated/Cautions:
- Nitroglycerin contraindicated with hypotension (SBP <90), RV infarction, or PDE-5 inhibitor use within 24–48 hours
- Avoid beta-blockers in acute decompensated HF, cardiogenic shock, severe bradycardia, or active bronchospasm
- NSAIDs (except aspirin) should be discontinued — increase cardiovascular risk
- Fibrinolytics are contraindicated in NSTE-ACS [15]
4. Diet
- Mediterranean-style diet is recommended for secondary prevention: emphasizes vegetables, fruits, legumes, nuts, whole grains, lean protein, and healthy fats (olive oil, fish) [16]
- Limit saturated fat to <6% of total calories; avoid trans fats entirely [16]
- Sodium restriction <2,300 mg/day (optimally <1,500 mg/day) [16]
- Limit refined carbohydrates and sugar-sweetened beverages [16]
- Nonprescription supplements (omega-3, vitamins C/D/E, beta-carotene) are not recommended for CVD event reduction [16]
- Adequate hydration; avoid excessive caffeine and alcohol acutely
5. Review of Systems
- Cardiovascular: palpitations, syncope, orthopnea, PND, lower extremity edema
- Pulmonary: dyspnea (most common anginal equivalent), pleuritic pain (suggests alternative diagnosis)
- GI: nausea, vomiting, epigastric pain (may be anginal equivalent or suggest alternative diagnosis such as GERD, peptic ulcer)
- Neurologic: lightheadedness, presyncope, altered mental status (suggests hemodynamic compromise)
- Vascular: claudication, prior stroke/TIA (suggests diffuse atherosclerotic disease, higher CAD likelihood) [5]
- Psychiatric: anxiety, panic symptoms (common mimic)
6. Collateral History and Family History
- Family history of premature CAD: first-degree relative with CVD <55 years (male) or <65 years (female) [11]
- Prior cardiac testing results, prior catheterization/stenting/CABG
- Medication compliance (especially antiplatelet agents, statins)
- Substance use: cocaine and amphetamine use can cause coronary vasospasm and ACS
- Functional status and baseline exercise tolerance
- Social support and ability to follow up
7. Risk Factors
- Major: age ≥65, male sex, hypertension, diabetes mellitus, hyperlipidemia, current smoking, obesity (BMI >30), family history of premature CAD [11]
- Atherosclerotic disease: prior MI, PCI/CABG, CVA/TIA, peripheral arterial disease [5]
- Chronic kidney disease and renal insufficiency [5]
- Cocaine/stimulant use
- Sedentary lifestyle
- Metabolic syndrome
8. Differential Diagnosis
Cannot-miss life-threatening diagnoses: [5][17]
- NSTEMI/STEMI — distinguished by troponin elevation and/or ST elevation
- Aortic dissection — tearing pain radiating to back, pulse differential, widened mediastinum
- Pulmonary embolism — pleuritic pain, dyspnea, tachycardia, risk factors for VTE
- Tension pneumothorax — acute dyspnea, unilateral absent breath sounds
- Esophageal rupture (Boerhaave) — post-emesis, subcutaneous emphysema
Other cardiovascular: [5]
- Pericarditis/myocarditis — positional pain, friction rub, diffuse ST elevation
- Takotsubo cardiomyopathy — emotional/physical stress trigger, apical ballooning
- MINOCA — MI with nonobstructive coronary arteries [9]
Non-cardiac mimics: [5]
- GERD, esophageal spasm, peptic ulcer disease
- Costochondritis, musculoskeletal chest wall pain
- Biliary disease, pancreatitis
- Panic disorder, anxiety
9. Past Medical History
- Prior ACS events, PCI, CABG, or known CAD
- Prior stress test results (positive, negative, equivocal)
- Known coronary artery calcium score or prior CT imaging
- Heart failure, valvular disease, arrhythmias
- Diabetes, CKD, peripheral vascular disease
- Bleeding history (impacts anticoagulation/antiplatelet decisions)
- Prior GI bleeding (impacts DAPT risk-benefit)
10. Physical Exam
Vital signs:
- Blood pressure in both arms (if dissection suspected) [15]
- Heart rate, respiratory rate, SpO₂, temperature
Cardiovascular:
- New S3 or S4 gallop — suggests LV dysfunction [8-9]
- New or worsening systolic murmur — acute MR or VSD [9]
- JVD, peripheral edema — signs of heart failure
- Peripheral pulses and bruits — assess for PAD (higher CAD likelihood) [15]
Pulmonary:
- Rales/crackles — pulmonary edema from ischemia-driven LV failure [8]
- Unequal breath sounds — consider pneumothorax
Other:
- Diaphoresis, cool/clammy extremities — signs of cardiogenic shock [9]
- Chest wall tenderness — suggests musculoskeletal cause but does not exclude ACS
- Pericardial friction rub — suggests pericarditis [15]
11. Lab Studies
- Cardiac troponin (hs-cTnI or hs-cTnT): the key differentiator — normal in UA, elevated in NSTEMI [1][9][18]
- Serial measurement at presentation and 1–3 hours later (hs-cTn) or 3–6 hours (conventional) [2][5]
- Two normal hs-cTn values within 1–3 hours have NPV ~99% for MI [2]
- CBC: assess for anemia (precipitant of demand ischemia)
- BMP/CMP: renal function (impacts anticoagulation dosing), electrolytes
- Coagulation studies: PT/INR, aPTT (baseline before anticoagulation)
- Lipid panel: baseline for statin initiation
- BNP/NT-proBNP: may be considered for risk stratification [5]
- D-dimer: if PE is in the differential
- HbA1c: screen for undiagnosed diabetes
12. Imaging
- Chest X-ray: first-line; assess for pulmonary edema, widened mediastinum, pneumothorax, pneumonia [19]
- Echocardiography: assess LV function, wall motion abnormalities, valvular pathology; urgent if hemodynamic instability [1][5]
- CT coronary angiography (CCTA): can stratify risk in low-to-intermediate risk patients with nondiagnostic ECG and negative troponins; normal CCTA effectively rules out obstructive CAD [2]
- Invasive coronary angiography: gold standard; indicated for high-risk patients or those with positive noninvasive testing [6][9]
- Stress testing (exercise or pharmacologic with imaging): for low-to-intermediate risk patients before or within 72 hours of discharge [15][20]
13. Special Tests
Risk Stratification Scores:
- HEART Score (above): scores 0–3 = low risk (MACE <2%), 4–6 = intermediate, 7–10 = high risk; validated for ED disposition decisions [19][22]
- TIMI Risk Score: 7 variables (age ≥65, ≥3 CAD risk factors, known CAD, ASA use, ≥2 anginal episodes in 24h, ST deviation, elevated biomarkers); score 0–7 [8][22]
- GRACE Score: predicts in-hospital and 6-month mortality; score >140 = high risk warranting catheterization within 24 hours [9][22]
- EDACS: combined with serial troponin and nonischemic ECG, identifies low-risk patients (30-day MACE <1%) [19]
- Killip Classification: stratifies by degree of heart failure (Class I–IV); strongly predicts mortality [9]
Point-of-care:
- JACC[1]
14. ECG
ECG should be obtained within 10 minutes of arrival. [5][19] Key findings in UA:
- ST-segment depression ≥0.5 mm in ≥2 contiguous leads (horizontal or downsloping) [1]
- Transient ST-segment elevation — resolves with symptom relief; suggests severe ischemia [1][8]
- T-wave inversion >1 mm in ≥2 contiguous leads with prominent R wave [1]
- Wellens syndrome: biphasic or deeply inverted T waves in V2–V3 — indicates critical proximal LAD stenosis [19]
- De Winter's sign: upsloping ST depression with tall symmetric T waves in precordial leads — proximal LAD occlusion [19]
- Normal ECG does not exclude ACS — occurs in 1–6% of confirmed ACS [5]
- If initial ECG is nondiagnostic, repeat at 15–30 minute intervals during the first hour [5]
- Consider posterior leads (V7–V9) if isolated ST depression in V1–V3 [5][19]
- New or presumed new LBBB requires clinical correlation; not a STEMI equivalent in isolation [1]
15. Assessment
Unstable angina represents transient myocardial ischemia without myonecrosis, defined by ischemic symptoms with normal serial troponins. [1] It is the least severe end of the ACS spectrum but carries significant risk of progression to MI. [9] With the advent of high-sensitivity troponin assays, many patients previously classified as UA are now reclassified as NSTEMI, making "true" UA increasingly uncommon. [9]
Severity stratification is based on clinical features, ECG findings, troponin trends, and validated risk scores (HEART, TIMI, GRACE). [5][10] Patients can be classified as:
- High risk: ongoing pain, dynamic ECG changes, hemodynamic instability, high HEART/TIMI/GRACE scores → early invasive strategy [6][9]
- Intermediate risk: resolved symptoms, nondiagnostic ECG, negative troponins but concerning history → observation and further testing [19]
- Low risk: resolved symptoms, normal ECG, negative serial troponins, low HEART score (≤3) → candidate for early discharge [19]
Complications to consider: progression to NSTEMI/STEMI, arrhythmias, acute heart failure, cardiogenic shock, mechanical complications (if MI develops). [1]
16. Treatment Plan
The following algorithm from the 2014 AHA/ACC guidelines outlines the management approach for NSTE-ACS:
Initial Stabilization:
- Continuous cardiac monitoring, IV access, supplemental O₂ if SpO₂ <90% [11]
- Aspirin 162–325 mg chewed immediately [11]
- Sublingual nitroglycerin 0.4 mg q5min × 3 for ongoing pain; IV NTG if refractory [10]
Anti-ischemic Therapy:
- Beta-blocker (oral metoprolol 25–50 mg or IV if hypertensive/tachycardic without contraindications) [10][14]
- Non-dihydropyridine CCB (diltiazem, verapamil) if beta-blocker contraindicated [14]
Antithrombotic Therapy:
- Dual antiplatelet therapy: aspirin + P2Y₁₂ inhibitor [11][13]
- Parenteral anticoagulation: UFH, enoxaparin, fondaparinux, or bivalirudin [13]
- P2Y₁₂ inhibitor pretreatment is no longer routinely recommended before catheterization in planned early invasive strategy [9]
Invasive vs. Ischemia-Guided Strategy:
- Early invasive (angiography within 24h): preferred for high-risk patients (GRACE >140, dynamic ECG changes, elevated troponin, hemodynamic instability) [5][9]
- Ischemia-guided (conservative): appropriate for low-risk patients who stabilize with medical therapy; noninvasive testing to guide need for catheterization [5]
Long-term Medications at Discharge:
- Aspirin indefinitely + P2Y₁₂ inhibitor for ≥12 months (DAPT) [11]
- High-intensity statin [11]
- Beta-blocker [14]
- ACE inhibitor/ARB (especially if LVEF <40%, HTN, DM, or CKD) [14]
- SGLT2 inhibitor consideration post-MI [11]
- Cardiac rehabilitation referral [23]
17. Disposition
Admit (inpatient or CCU): [5]
- Recurrent ischemic symptoms despite initial treatment
- Dynamic ECG changes or positive troponin (reclassified as NSTEMI)
- Hemodynamic instability, arrhythmias, or signs of heart failure
- High-risk features on clinical assessment or risk scores
- Need for early invasive strategy
Observation unit: [19]
Discharge from ED: [15][19]
- Low-risk patients: pain-free, normal/unchanged ECG, negative serial troponins (at least 2 values over 1–3h with hs-cTn), low HEART score (≤3) or EDACS (<16)
- Prescribe aspirin, sublingual NTG, and consider beta-blocker pending outpatient stress testing [15]
- Arrange outpatient stress test or CCTA within 72 hours [15]
Cardiology consultation triggers: [19]
18. Follow Up / Return Precautions
Follow-up timing:
- Low-risk patients discharged from ED: PCP or cardiology follow-up within 72 hours; stress testing within 72 hours if not done predischarge [15][20]
- Intermediate-risk patients: follow-up within 7 days, preferably with established cardiologist [19]
- Post-catheterization/revascularization: cardiology follow-up within 2–4 weeks; cardiac rehabilitation referral [19]
Return precautions — instruct patients to call 911 or return immediately for:
- Recurrence of chest pain, pressure, or tightness — especially at rest or lasting >5 minutes
- New or worsening shortness of breath
- Lightheadedness, syncope, or near-syncope
- Palpitations or sensation of rapid/irregular heartbeat
- Nitroglycerin not relieving symptoms after 1 dose (call 911)
Patient counseling:
- Take aspirin daily as prescribed; do not stop without physician guidance
- Keep sublingual NTG accessible; replace every 6 months
- Smoking cessation is the single most impactful lifestyle modification [23-24]
- Cardiac rehabilitation improves outcomes and reduces mortality [23]
- Expected recovery: with appropriate treatment and risk factor modification, prognosis is favorable; however, ongoing adherence to DAPT, statins, and lifestyle changes is essential for long-term event reduction [1]
References
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