Stable Angina

Part I: Diagnosis and Management of Stable Angina

1.1 Differentiating Stable vs. Unstable Angina: The Core Clinical Distinction

Stable angina

• Predictable chest discomfort due to myocardial ischemia from mismatch of oxygen supply/demand, usually from atherosclerotic coronary disease.
• Pain: heavy, dull or tight; builds over minutes; typically 5–10 minutes.
• Triggered by exertion or emotional stress; reliably relieved by rest or sublingual glyceryl trinitrate (GTN).

Unstable angina (an Acute Coronary Syndrome)

• Change in a previously predictable pattern: new onset, more severe/frequent, or occurring at rest/minimal exertion.
• Pain often >15 minutes and may not be fully relieved by rest or GTN.
• Suggests plaque disruption with non-occlusive thrombus and risk of myocardial infarction (MI).
• Requires urgent medical attention.

Important differentials to consider (non-exhaustive)

• Pulmonary embolism, aortic dissection, pericarditis (sharp, pleuritic, positional pain), gastro-oesophageal reflux, oesophageal spasm (may respond to GTN), musculoskeletal pain, anxiety.

Comparison table (high-yield)

1.2 Initial Workup of Exertional Chest Pain in General Practice

GP role: triage — distinguish stable, non-urgent presentations from life-threatening emergencies using history, examination, and identification of “red flags.”

Red flags warranting immediate ambulance/ED referral

• Chest pain lasting ≥10 minutes or new pain at rest.
• Chest pain with severe dyspnoea, syncope, or presyncope.
• Hemodynamic instability (HR >120 bpm, SBP <90 mmHg).
• Signs of heart failure or pulmonary oedema.
• New ECG changes: ST-elevation/depression, new LBBB, complete heart block.

Assessment in clinic (if no red flags)

• Thorough history: onset, duration, character, precipitating/relieving factors.
• Cardiovascular risk factors: HTN, diabetes, hyperlipidaemia, smoking, obesity, family history, age.
• Resting 12‑lead ECG: first-line, quick, low-cost. Note: a normal ECG does NOT exclude ACS.
• Baseline bloods: FBE, U\&E, LFTs, glucose, fasting lipids, HbA1c. High-sensitivity troponin is primarily a hospital test.
• If pattern is changed from previous stable angina (e.g., now at rest), treat as suspected ACS and refer urgently.

1.3 The Role of Diagnostic Testing

For low-to-intermediate risk symptomatic patients without red flags, use non-invasive testing to confirm CAD and guide management.

Exercise Stress Testing (EST)

• Indicated in intermediate pre-test probability and when the patient can exercise and baseline ECG is interpretable.
• Limits/contraindications: recent MI (within days), unstable angina, severe aortic stenosis, uncontrolled arrhythmia, inability to achieve adequate HR, baseline ECG abnormalities (LBBB, paced rhythm).

Stress Echocardiography

• Imaging-based assessment for wall motion abnormalities under stress.
• Useful when baseline ECG is non-diagnostic or abnormal (e.g., LBBB), or when biomarkers are negative after a low-risk ACS.

Coronary Artery Calcium (CAC) Score

• Non-contrast CT to quantify coronary calcium.
• Best reserved for asymptomatic, intermediate-risk individuals to refine primary prevention decisions (e.g., statin initiation).
• Not appropriate for symptomatic patients with exertional chest pain.

Common AMC pitfall: ordering CAC for symptomatic patients — inappropriate. Use functional testing (stress echo/EST) for symptomatic evaluation.

1.4 Chronic Medical Management and Secondary Prevention

Goals: symptom relief and reduction of future cardiovascular events/mortality.

Symptomatic (anti-ischaemic) pharmacotherapy

• First-line: Beta-blockers (reduce HR/BP) or calcium channel blockers (amlodipine, diltiazem) — choose based on comorbidities and contraindications.
• Second-line: Long-acting nitrates if monotherapy insufficient or not tolerated.
• Acute relief: Short-acting nitrates (sublingual GTN spray/tablets) for episodic use; advise patients to sit and stop activity before taking.

Secondary prevention (long-term)

• Antiplatelet: Low-dose aspirin (75–150 mg daily) for established CAD. Clopidogrel if aspirin allergy. Routine primary prevention with aspirin not generally recommended due to bleeding risk.
• Statin therapy: Indicated for all patients with CAD regardless of baseline cholesterol — plaque-stabilizing effect. Target LDL-C <1.4 mmol/L or ≥50% reduction.
• Renin–angiotensin inhibitors: ACE inhibitors or ARBs for patients with HTN, diabetes, or LV systolic dysfunction.

Lifestyle & cardiac rehabilitation

• Smoking cessation is the single most impactful intervention.
• Heart-healthy diet, regular moderate-intensity exercise (~30 minutes most days), weight management, glycaemic and BP control.
• Cardiac rehabilitation: structured programs for exercise, education, and risk-factor management — important especially for high-risk or underserved populations.

Part II: The Acute Event — Acute Coronary Syndrome (ACS)

2.1 ER Encounters: Triage and Initial Stabilisation

ACS includes unstable angina, NSTEMI, and STEMI. Early steps:

• 12‑lead ECG within 10 minutes of first clinical contact to identify STEMI/ACOMI.
• Serial ECGs if initial ECG is non-diagnostic but symptoms persist.
• Cardiac biomarkers (troponin): rise typically 2–4 hours after injury — a negative initial troponin does not exclude MI.
• ACOMI (Acute Coronary Occlusion Myocardial Infarction): newer terminology to capture occlusion patterns without classic ST-elevation (e.g., posterior MI) to ensure timely reperfusion.
• Older adults may present atypically (dyspnoea, syncope, confusion) — treat MI equivalents with high suspicion.

2.2 Reperfusion Therapy: A Time-Critical Decision

STEMI reperfusion options

• Primary PCI: preferred when achievable within guideline timeframes. First medical contact to balloon <60 minutes at PCI-capable hospital; transfer target <90 minutes if initially at non-PCI center.
• Fibrinolysis: indicated when timely PCI not available (e.g., remote/rural setting with transfer >90 minutes). After successful fibrinolysis, transfer to PCI-capable center within 6–24 hours.

NSTEMI/Unstable angina

• Not usually immediate revascularization unless hemodynamically unstable or high-risk features present.
• Medical stabilization: dual antiplatelet therapy (aspirin + P2Y12 inhibitor), anticoagulation (heparin/enoxaparin), nitrates, analgesia (morphine when needed).

2.3 Post-MI Care: A Continuum of Management

Complications timeline and key features

Notes

• Early: arrhythmias are leading cause of death in first 24 hours.
• Mechanical complications (e.g., papillary muscle rupture causing acute MR) are surgical emergencies.
• Dressler’s syndrome is autoimmune pericarditis weeks after MI; treat with high-dose aspirin/NSAIDs and avoid anticoagulants if significant effusion.

Part III: Nuances and Exam-Specific Knowledge

3.1 Managing Patients with Multiple Comorbidities

• Geriatric patients often present atypically (dyspnoea, syncope, confusion) — maintain high suspicion for ACS.
• Polypharmacy: risk of drug–drug interactions and adverse effects. Deprescribing may be appropriate when harms outweigh benefits or treatment goals change.
• Example: combination of digoxin and thiazide diuretic → risk of hypokalaemia causing digoxin toxicity.

3.2 Antiplatelet and Anticoagulation Management

Dual antiplatelet therapy (DAPT)

• After DES placement post-ACS: aspirin + P2Y12 inhibitor for at least 12 months typically. Consider shorter duration (3–6 months) if high bleeding risk — individualized decision in consultation with cardiology.

Perioperative anticoagulation (warfarin example)

• Stop warfarin 3–5 days pre-op to allow INR to fall.
• For high thromboembolic risk patients, bridge with short-acting heparin when INR sub-therapeutic; stop heparin 12–24 hours before surgery; resume post-op when bleeding risk acceptable.

3.3 Key AMC Exam Themes

• Atypical MI presentations (esp. elderly/comorbid).
• Time-based reperfusion decisions (fibrinolysis vs PCI).
• Drug interactions and adverse effects (CYP3A4 interactions, statin-induced myopathy).
• Safety-first principle: when in doubt, choose urgent admission/observation.
• Updated guideline knowledge (e.g., ACOMI terminology, LDL-C targets).