Stable Angina

Angina pectoris is chest and/or adjacent-area discomfort caused by myocardial ischemia — an inadequate blood/oxygen supply to the heart muscle relative to demand — most commonly due to obstructive coronary artery disease (CAD), the build-up of atherosclerotic plaque in the coronary arteries.^[1] Stable angina refers to anginal discomfort occurring in a predictable pattern, typically brought on by physical exertion or emotional stress and relieved by rest or nitroglycerin within a few minutes. It is the classic presentation of what current guidelines term chronic coronary syndrome — a broader spectrum that also includes stabilized CAD after a prior acute coronary syndrome (ACS) or revascularization, heart failure/left ventricular dysfunction due to obstructive CAD, microvascular or vasospastic angina, and clinically silent CAD found incidentally or on screening.^[2] This chapter assumes CAD is the underlying cause of angina; other conditions that can produce or worsen myocardial ischemia — tachyarrhythmia, severe or uncontrolled hypertension, severe aortic stenosis, hypertrophic cardiomyopathy, anemia, and functional problems of the coronary tree such as spasm or microvascular dysfunction — must be considered during assessment, both to direct appropriate treatment and to avoid a treatment that could cause harm in an alternative diagnosis (long-acting nitrate therapy, for example, can harm a patient whose angina is actually due to hypertrophic cardiomyopathy).

Typical presentation

Chest discomfort — classically described as squeezing, pressure, heaviness, or tightness rather than sharp pain — that is substernal or in an adjacent area, precipitated by physical exertion or emotional stress, and relieved within about 10 minutes by rest or sublingual nitroglycerin. The pattern is predictable from episode to episode: a similar trigger threshold, a similar character, and reliable relief with rest/nitroglycerin.

Atypical and anginal-equivalent presentation

Women, older adults, and patients with diabetes more often present atypically — dyspnea, fatigue, or epigastric discomfort on exertion without classic chest pain (an "anginal equivalent"). A high index of suspicion in these groups avoids a missed or delayed diagnosis.

Distinguishing stable from unstable presentations

The single most important discrimination on presentation is whether the pattern is still stable — predictable, exertional, reliably relieved by rest/nitroglycerin — or has become unstable: angina now occurring at rest, a new crescendo pattern (more frequent, more severe, more prolonged, or provoked by progressively less exertion than the patient's baseline), or angina no longer relieved by the usual dose of nitroglycerin. Any of these changes should raise suspicion for an acute coronary syndrome rather than a stable-angina exacerbation, and the patient should be managed with an ACS-appropriate urgent-assessment pathway (immediate ECG and troponin) rather than continued outpatient stable-angina management — see the comparison table at the top of Assessment & Diagnosis below.

• Smoking (current or significant past exposure).
• Diabetes mellitus.
• Dyslipidemia.
• Hypertension.
• Obesity.
• Sedentary lifestyle / lack of regular exercise.
• Unhealthy alcohol use.
• Chronic psychosocial stress.
• Family history of premature CAD (first-degree relative with MI before age 55 if male, before age 65 if female).
• Known CAD, prior MI, or prior coronary revascularization (PCI or CABG).
• Chronic kidney disease.
• Increasing age; male sex carries a higher baseline pretest probability at a given age, though the gap narrows with age (see Assessment & Diagnosis).

Differentiating stable angina from an evolving acute coronary syndrome

When the presentation matches the right-hand column, manage the patient using an acute-coronary-syndrome pathway rather than continuing stable-angina management.

History

A thorough history focused on age, sex, and the character of the discomfort (location, quality, precipitating and relieving factors) is the most important tool for estimating the likelihood that obstructive CAD explains the symptoms. Three questions establish the type of chest pain: is it substernal; is it precipitated by exertion; is it relieved within about 10 minutes of rest (or nitroglycerin)? A "yes" to all 3 is typical angina; "yes" to 2 is atypical angina; "yes" to 1 or none is nonanginal chest pain.^[3]

These figures are the pretest probability that a patient with this symptom pattern, age, and sex has obstructive CAD on angiography — use them to decide how aggressively to pursue further testing, not as a standalone diagnosis.^[3] Also identify modifiable CAD risk factors during the history (see Risk Factors).

Physical examination

• Assess for tachycardia and hypertension.
• Look for evidence of atherosclerotic disease elsewhere (e.g., arterial bruits).
• Assess for valvular heart disease, particularly aortic stenosis.
• Assess for decompensated heart failure.

Laboratory testing

• CBC (evaluates for anemia as a contributor to or mimic of angina).
• Serum creatinine and electrolytes.
• Fasting glucose and lipid profile.
• Hemoglobin A1c.

Noninvasive cardiovascular testing

• Resting 12-lead ECG in every patient.
• Echocardiogram when important valvular disease, LV systolic dysfunction, or a cardiomyopathy is suspected.
• Physiologic ("stress") testing — exercise or pharmacologic stress (adenosine, dipyridamole, or dobutamine) paired with ECG, echocardiography, or nuclear myocardial perfusion imaging — to support the diagnosis of obstructive CAD and to risk-stratify.
• Coronary CT angiography as an alternative anatomic testing strategy; it has a high negative predictive value and offers both diagnostic and prognostic information.

When testing is not indicated: further diagnostic testing for CAD is not needed in a patient with very low pretest probability and a clearly alternative explanation for symptoms, nor in a patient who already has an established indication for coronary angiography (e.g., high-risk clinical presentation) regardless of a noninvasive test result.

Severity classification and risk stratification

Record the CCS class at diagnosis and at follow-up — it is the standard way to communicate angina severity and to track whether therapy is working.^[4]

Duke Treadmill Score

The Duke Treadmill Score is a validated prognostic tool calculated from a standard exercise ECG stress test: Score = exercise time (minutes) − (5 × maximal ST-segment deviation in mm) − (4 × angina index), where the angina index is 0 (no angina during the test), 1 (non-limiting angina), or 2 (angina that forces the test to stop). A score of +5 or higher indicates low risk, −10 to +4 indicates moderate risk, and −11 or lower indicates high risk warranting consideration of angiography.

Unlike the TIMI risk score used in acute coronary syndromes, the Duke Treadmill Score is not a simple point-sum — exercise time and ST deviation are continuous inputs combined with different weighting coefficients into a formula, the same reason the GRACE score does not get a checkbox-style interactive calculator on this platform. Use this table to understand and interpret a treadmill report, but calculate the actual score using the treadmill software or a validated calculator rather than by hand.

Revascularization referral triggers

Refer for coronary angiography with a view to revascularization when angina remains limiting despite optimized medical therapy, or independent of symptom control when coronary anatomy is high-risk — left main stenosis greater than 50%, or three-vessel disease greater than 70% stenosis, particularly with a left ventricular ejection fraction under 50%. Revascularization in stable CAD without one of these high-risk features has not been shown to reduce death or MI compared with optimal medical therapy alone and should not be pursued as a default strategy purely to avoid escalating medical therapy.^[2]

• Improve quality of life by decreasing or preventing angina and improving exercise tolerance.
• Minimize the risk of cardiovascular death and nonfatal MI.
• Achieve LDL under 1.8 mmol/L (70 mg/dL), or at least a 50% reduction from baseline on statin therapy.
• Achieve guideline blood pressure targets appropriate to the patient's overall risk profile.
• Achieve individualized glycemic targets in patients with diabetes.
• Achieve smoking cessation.
• Treat every modifiable risk factor that promotes the development and progression of CAD.

• Regular aerobic exercise (walking, jogging, cycling, swimming) as tolerated by symptoms.
• A heart-healthy diet — vegetables, fruits, nuts, whole grains, and fish, avoiding processed foods high in trans fats.
• Smoking cessation — offer pharmacotherapy (nicotine replacement therapy, bupropion, or varenicline) to every patient who smokes; this is one of the highest-yield interventions available.
• Alcohol in moderation only.
• Stress-management techniques.
• Cardiac rehabilitation referral, particularly for higher-risk patients (e.g., those with concomitant heart failure).
• Nitrate-free interval: every patient on a long-acting nitrate (oral or transdermal) needs a scheduled 10-12 hour nitrate-free period every 24 hours to prevent pharmacologic tolerance — the antianginal effect of nitrates is lost with continuous around-the-clock exposure. Schedule the nitrate-free interval for a time when symptoms are least likely, usually overnight.^[8]
• Sublingual nitroglycerin technique counselling: advise the patient to sit down before taking a dose to reduce the risk of presyncope or syncope, and to expect headache as a common, usually self-limiting side effect. If discomfort persists 5 minutes after 1 dose, a second dose may be taken, and a third after another 5 minutes if needed; if discomfort persists despite 3 doses over about 15 minutes, the patient should seek emergency medical attention immediately rather than continuing to self-treat.
• Revascularization (percutaneous coronary intervention or coronary artery bypass graft surgery) improves quality of life in patients whose symptoms remain limiting despite optimized medical therapy, and improves longer-term prognosis in patients with high-risk coronary anatomy (see Assessment & Diagnosis for specific referral triggers).
• For patients who remain symptomatic despite optimized medical therapy and for whom revascularization is not possible, additional non-pharmacologic options (enhanced external counterpulsation, coronary sinus reduction) may be considered through specialist referral.
• Annual influenza vaccination, along with recommended COVID-19 and pneumococcal vaccination.
• Review and reinforce medication adherence at every encounter.

Pregnancy

Stable angina from established CAD is uncommon in patients of reproductive age but occurs, particularly with traditional risk factors present; spontaneous coronary artery dissection is an important alternative diagnosis to consider in this age group and needs its own specialist-directed evaluation. Manage with combined obstetric/cardiology input. Sublingual nitroglycerin, beta-blockers, and nondihydropyridine calcium channel blockers can be used with standard obstetric monitoring. ACE inhibitors, ARBs, and statins are contraindicated in pregnancy — hold these regardless of the non-pregnancy indication and discuss alternative strategies with obstetric cardiology. ASA at low dose (81 mg/day) is compatible with pregnancy.

Breastfeeding

Beta-blockers, nondihydropyridine and dihydropyridine calcium channel blockers, and low-dose ASA are generally considered compatible with breastfeeding. Statin data in lactation are limited; individualize the decision to continue or hold a statin with the patient and her care team given the strength of the underlying secondary-prevention indication.

Older adults

Beta-blockers and heart-rate-lowering calcium channel blockers are, in practice, usually titrated to a resting heart rate target of 50-60 bpm; use a lower starting dose in older or frailer patients, who are more sensitive to bradycardia and hypotension. Advise sitting when taking sublingual nitroglycerin given a higher presyncope/syncope risk with age. If a beta-blocker is desired in a patient with resting bradycardia, an agent with intrinsic sympathomimetic activity (acebutolol, pindolol) may be considered — see Drug Tables.

Renal impairment

Atenolol and nadolol are renally cleared and need dose reduction in significant renal impairment. ACE inhibitor/ARB initiation requires baseline and follow-up creatinine and potassium monitoring, with dose reduction or discontinuation if creatinine rises substantially or hyperkalemia develops. Ranolazine requires caution and closer monitoring in moderate renal impairment.

Hepatic impairment

Most beta-blockers and calcium channel blockers undergo hepatic metabolism — use a lower starting dose and titrate more cautiously in significant hepatic impairment. Ranolazine is contraindicated in clinically significant hepatic impairment.

Hypertrophic cardiomyopathy or severe aortic stenosis

Confirm angina is due to obstructive CAD before starting long-acting nitrate therapy — nitrates can worsen outflow tract obstruction in hypertrophic cardiomyopathy and can cause harmful hypotension in severe aortic stenosis. Refer for specialist assessment if either is suspected rather than proceeding with standard anti-anginal therapy.

Reassess anginal frequency, CCS functional class, and exercise tolerance at every follow-up visit — this is the primary marker of whether therapy is working. Titrate heart-rate-lowering agents (beta-blockers, diltiazem, verapamil) to a resting heart rate of 50-60 bpm, and titrate dihydropyridine calcium channel blockers and nitrates to maximum symptom relief with minimal adverse effects. Recheck a fasting lipid panel 6-8 weeks after starting or adjusting a statin to confirm the LDL target is met, then periodically thereafter. Recheck creatinine and potassium 1-2 weeks after starting or increasing an ACE inhibitor/ARB dose. Confirm the nitrate-free interval is actually being followed at every visit for a patient on a long-acting nitrate — this is a common, easily corrected source of apparent treatment failure. Reinforce smoking cessation, cardiac rehabilitation attendance, and medication adherence at every encounter. Any change in symptom pattern toward the "unstable" column of the comparison table above warrants immediate reassessment rather than waiting for the next scheduled visit.

1. Confirm adherence to the prescribed regimen and confirm correct sublingual nitroglycerin technique (sitting position, timing relative to activity).
2. Confirm the nitrate-free interval is actually being observed if the patient is on a long-acting nitrate — tolerance from a missed nitrate-free period is a common, easily corrected cause of apparent treatment failure.
3. Optimize the first-line agent to its maximally tolerated dose before adding a second drug.
4. Add second-line therapy (a long-acting nitrate with a proper nitrate-free interval, or a dihydropyridine calcium channel blocker if first-line therapy was a beta-blocker) if symptoms persist on optimized first-line monotherapy.
5. Add ranolazine if symptoms persist on optimized combination therapy, or if first-line agents are not tolerated.
6. Reassess for reversible contributors to refractory symptoms — anemia, thyrotoxicosis, uncontrolled hypertension, tachyarrhythmia, or uncontrolled comorbid conditions.
7. Refer for coronary angiography and revascularization work-up if angina remains limiting despite optimized medical therapy, or sooner if high-risk anatomy is already suspected.
8. Reconsider whether the pattern has actually shifted from stable to unstable — new-onset rest angina, crescendo pattern, or nitroglycerin-unresponsive symptoms require an ACS pathway, not further stable-angina dose escalation.

• Prescribing a long-acting nitrate without a scheduled nitrate-free interval — tolerance develops and the drug stops working.^[8]
• Starting a beta-blocker in suspected or documented vasospastic (Prinzmetal) angina — use a calcium channel blocker and/or nitrate instead.
• Stopping a beta-blocker abruptly after chronic high-dose therapy — this can precipitate rebound tachycardia and worsening ischemia; taper over 10-14 days.
• Missing the interaction between nitrates and PDE5 inhibitors (sildenafil, tadalafil, vardenafil) — the combination can cause severe, potentially fatal hypotension.
• Starting or continuing a nondihydropyridine calcium channel blocker (diltiazem, verapamil) in a patient with significant LV systolic dysfunction.
• Combining a nondihydropyridine calcium channel blocker with a beta-blocker without close monitoring for additive bradycardia and AV block.
• Using ivabradine for angina alone without a qualifying concomitant heart-failure indication — it is not independently approved for this in Canada, and trial data in angina patients without heart failure did not show a mortality/MI benefit.^[5]
• Withholding a statin because baseline LDL "looks fine" — every patient with stable CAD needs a high-intensity statin targeting LDL under 1.8 mmol/L or at least a 50% reduction, regardless of baseline value.
• Missing hypertrophic cardiomyopathy or severe aortic stenosis as an alternative cause of angina before starting nitrate therapy, which can worsen either condition.
• Treating a change toward an unstable symptom pattern (rest angina, crescendo pattern, nitroglycerin-unresponsive symptoms) as a routine stable-angina follow-up issue instead of an urgent ACS-pathway assessment.
• Using NSAIDs (especially COX-2 inhibitors) liberally in a patient with established CAD — if genuinely needed for quality of life, use the lowest effective dose for the shortest possible duration given increased vascular event risk.

How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Select any linked drug name to open its complete Pharmasist Drug Database page.

Nitrates

Effective for both preventing anginal episodes and treating acute attacks. Long-acting formulations require a scheduled 10-12 hour nitrate-free period every 24 hours to prevent pharmacologic tolerance.

Antianginal — Late sodium current inhibitor

Add-on therapy for anginal symptoms, or an option when beta-blockers, calcium channel blockers, and nitrates are not tolerated.

Antianginal — Sinus node (If) inhibitor

Reduces heart rate via a mechanism distinct from beta-blockers or calcium channel blockers. In Canada, this drug's Health Canada indication is for heart failure with reduced ejection fraction — use for angina is restricted to patients who also meet that heart-failure indication, not for angina alone.

Beta-blockers, non-selective

Not first-line if vasospastic angina is suspected. Taper over 10-14 days rather than stopping abruptly — abrupt withdrawal can precipitate rebound tachycardia and worsening ischemia. Contraindicated in asthma and in 2nd-/3rd-degree heart block without a pacemaker.

Beta-blockers, selective (beta1)

Preferred over non-selective agents when fewer non-cardiac effects are desired. Same tapering and heart-block cautions as non-selective agents.

Beta-blockers with intrinsic sympathomimetic activity

Considered specifically when a beta-blocker is desired in a patient with resting bradycardia — these agents lower resting heart rate less than agents without ISA.

Calcium channel blockers, dihydropyridine

Act primarily by arterial dilation; typically used as 2nd-line add-on to a beta-blocker. Amlodipine and nifedipine extended-release are Health Canada-approved for angina; felodipine has shown effectiveness in trials but does not carry a Health Canada angina indication and is not included here for that reason.

Calcium channel blockers, nondihydropyridine

1st-line antianginal option, and preferred over a beta-blocker when vasospastic angina is suspected. Avoid in significant LV systolic dysfunction; use with caution in AV nodal disease.

Antiplatelet agents

ASA is first-line for essentially all patients; clopidogrel is reserved for ASA contraindication/intolerance in the absence of a recent ACS or stent. Ticagrelor's role in stable CAD is specifically for high-risk post-MI secondary prevention, not routine use.

Dual-pathway antithrombotic therapy

An option in patients with stable CAD at elevated ischemic risk and acceptable bleeding risk, in addition to (not instead of) standard antiplatelet therapy — individualize given the trade-off between reduced ischemic events and increased bleeding.

Lipid-lowering therapy

High-intensity statin for every patient with stable CAD regardless of baseline LDL, targeting LDL under 1.8 mmol/L (70 mg/dL) or at least a 50% reduction from baseline.

ACE inhibitors / ARB

Indicated for stable CAD with a compelling indication (hypertension, diabetes, CKD, LV dysfunction), and reasonable to consider even without one given demonstrated benefit in broader high-risk populations.

Anti-inflammatory secondary prevention

Low-dose colchicine reduces the risk of MI, stroke, and the need for revascularization when added to standard secondary-prevention therapy in patients with established CAD; the 2024 ESC guideline upgraded this to a stronger recommendation on the basis of the LoDoCo2 trial.

Not available in Canada: nicorandil and trimetazidine are used for angina in some other countries but do not have Health Canada market authorization, so no Canadian dosing exists for either.

Evidence note: Drug inventory, dosing, adverse effects, and comments reflect standard Canadian practice, cross-checked against the current ESC and AHA/ACC chronic coronary disease guidelines.^[1][2]