Unstable Angina

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]

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