Stable Angina Pectoris

Definition

• Males constitute ~70% of all patients; women tend to present at a later age (>60 years) and with more atypical symptoms.

Pathophysiology

• Heart rate
• Systolic wall tension (preload + afterload)
• Myocardial contractility

Clinical Features

Symptoms

• Character: Heaviness, pressure, squeezing, smothering, or choking - rarely described as sharp pain
• Location: Central, substernal; patient typically places a clenched fist over the sternum (Levine's sign)
• Radiation: To either shoulder, ulnar aspect of forearm/hand, jaw, teeth, neck, back, interscapular region, or epigastrium. Notably, does not radiate to the trapezius muscles (that pattern suggests pericarditis)
• Duration: Typically 2-5 minutes
• Trigger: Exertion (exercise, hurrying, sexual activity), emotional stress, cold exposure, heavy meals
• Relief: Rest and/or sublingual nitroglycerin within 1-5 minutes

If angina does not respond to rest + sublingual nitroglycerin, the diagnosis should be reconsidered or unstable angina/ACS suspected.

Atypical Presentations

Comparison with Other Angina Types

Canadian Cardiovascular Society (CCS) Classification

Investigations

Electrocardiography

• Resting ECG may be normal in ~50% of patients
• Exercise stress ECG: ST-segment depression (horizontal or downsloping ≥1 mm) is the classic ischemic finding
• ST depression does not localize the site of ischemia; ST elevation during stress does

Imaging

• Echocardiography: Assess LV function, wall motion abnormalities, rule out valvular disease
• Stress echocardiography / Nuclear myocardial perfusion imaging: For risk stratification and assessing extent of ischemia
• Coronary CT angiography (CCTA): Excellent negative predictive value; identifies obstructive CAD non-invasively
• Coronary artery calcium (CAC) score: Adjunctive tool; should not be the sole basis for therapeutic decisions
• Invasive coronary angiography: Gold standard; defines anatomy and guides revascularization decisions

Risk Stratification Markers

• Extent of CAD and LV function are the most important prognostic determinants
• Worse prognosis: advanced age (>75 years), hypertension, dyslipidemia, diabetes, obesity, peripheral/cerebrovascular disease, prior MI
• Additional markers: elevated CRP, extensive coronary calcification on EBCT, increased carotid intimal thickness

Management

1. Explanation and reassurance
2. Identification and treatment of aggravating conditions
3. Adaptation of activity
4. Risk factor reduction
5. Drug therapy
6. Consideration of revascularization

1. Risk Factor Modification

• Smoking cessation (reduces carboxyhemoglobin, improves oxygen delivery)
• Control of hypertension, dyslipidemia, diabetes, obesity
• Treat thyrotoxicosis, anemia, LVH - these increase oxygen demand or reduce supply

2. Pharmacotherapy

Nitrates

• Mechanism: Systemic venodilation → reduce LV end-diastolic volume/pressure → reduce wall tension and O2 demand; also dilate epicardial coronary arteries and collaterals (via NO release → guanylyl cyclase → cGMP → smooth muscle relaxation)
• Sublingual NTG (0.3-0.6 mg): For acute episodes; up to 3 doses, 5 min apart
• Long-acting nitrates: Isosorbide dinitrate (10-40 mg orally 2-3x/day), Isosorbide 5-mononitrate (30-240 mg SR once daily)
• Important: A 10-12 hour nitrate-free interval is required daily to prevent tolerance

Beta-Blockers (First-line)

• Mechanism: Reduce heart rate and contractility → decrease myocardial O2 demand; also increase diastolic perfusion time by slowing heart rate
• Cardioselective agents (β1): Atenolol (50-200 mg/d), Bisoprolol, Metoprolol
• Non-selective: Propranolol, Nadolol, Carvedilol
• Target resting HR: 55-60 bpm
• Contraindications: Severe bronchospasm, significant bradycardia, advanced AV block (without pacemaker), decompensated heart failure

Calcium Channel Blockers (CCBs)

• Mechanism: Reduce myocardial O2 demand by vasodilation (reducing afterload) and/or slowing heart rate
• Dihydropyridines (Amlodipine, Nifedipine): Primarily vasodilatory; minimal chronotropic effect; used especially in vasospastic angina
• Non-dihydropyridines (Verapamil, Diltiazem): Both vasodilatory and rate-limiting; useful when beta-blockers are contraindicated
• Caution: Combining non-DHP CCBs with beta-blockers can cause profound bradycardia

Antiplatelet Therapy

• Aspirin (75-100 mg/day): Reduces risk of MI and death; mainstay in all patients with IHD without contraindication

Statins (HMG-CoA reductase inhibitors)

• Reduce LDL-cholesterol; stabilize plaques; reduce cardiovascular events
• High-intensity statin therapy indicated for all patients with established IHD

ACE Inhibitors / ARBs

• Indicated in patients with concomitant LV dysfunction, hypertension, or diabetes
• Reduce cardiovascular mortality in IHD

Ranolazine

• Late sodium current inhibitor; reduces intracellular Ca2+ overload; anti-ischemic without affecting HR or BP
• Useful as add-on therapy when beta-blockers/CCBs are insufficient or not tolerated

3. Revascularization

Percutaneous Coronary Intervention (PCI)

• Effective for symptom relief in patients with significant obstructive CAD
• A 2026 meta-analysis (PMID: 41130952) comparing PCI vs. optimal medical therapy in stable angina suggests similar outcomes for mortality/MI; PCI may provide superior angina relief but does not consistently improve survival over optimal medical therapy
• Drug-eluting stents are preferred over bare-metal stents

Coronary Artery Bypass Grafting (CABG)

• Preferred when:
  • Left main stenosis >50%
  • Triple-vessel disease
  • Double-vessel disease with proximal LAD involvement
  • Reduced LV function
  • Strongly abnormal exercise test
  • Diabetes with multi-vessel disease
• CABG provides more consistent and durable angina relief than PCI in complex anatomy

Prognosis

• Prognosis is determined primarily by LV function and extent of CAD
• The more myocardium at risk, the worse the outlook
• Annual mortality in medically managed stable angina: ~1-3%, varying widely by risk profile
• Patients with left main or three-vessel disease have substantially improved survival with CABG vs. medical therapy alone

Key Points Summary

• Harrison's Principles of Internal Medicine, 22nd Ed. (2025), Chapter 284 - Stable Ischemic Heart Disease
• Goldman-Cecil Medicine, International Edition - Chapter on CABG Indications
• Lippincott Illustrated Reviews: Pharmacology - Chapter 12 (Antianginal Drugs)
• PMID: 41130952 - Medical Management vs. PCI in Stable Angina (Meta-analysis, 2026)