Stable Angina

01Pathophysiology

Stable angina results from a fixed, flow-limiting atherosclerotic plaque in one or more coronary arteries. The plaque is typically stable with a thick fibrous cap and does not rupture. At rest, coronary blood flow distal to the stenosis is sufficient because compensatory arteriolar vasodilation maintains adequate perfusion. The problem arises during states of increased myocardial oxygen demand, such as physical exertion, emotional stress, cold exposure, or heavy meals.

The fundamental mechanism is a supply-demand mismatch. When the heart rate and contractility increase during exercise, the myocardium requires more oxygen. A stenosis of ≥70% prevents the coronary artery from increasing flow proportionally. The subendocardium is the most vulnerable zone because it is the last region to be perfused and the first to experience ischemic injury. This is why ischemia manifests as ST-segment depression on ECG rather than ST elevation, which would indicate transmural ischemia.

Ischemia triggers anaerobic metabolism in the myocardium, producing lactate and hydrogen ions. These metabolites stimulate cardiac afferent nerve fibers (traveling via sympathetic pathways to the C7-T4 dorsal root ganglia), producing the sensation of substernal chest pressure. This is also why the pain can radiate to the left arm, jaw, or shoulder, as visceral and somatic afferents converge at the same spinal cord levels (viscerosomatic convergence).

Critically, the plaque in stable angina is non-ruptured. There is no acute thrombus formation, which distinguishes it from acute coronary syndromes. This is why troponins remain negative and the pattern of symptoms is predictable and reproducible from episode to episode.

02Classification and Clinical Manifestation

The Canadian Cardiovascular Society (CCS) grading system classifies the functional severity of angina:

Important exam consideration: CCS Class IV can overlap with unstable angina when symptoms occur at rest. The distinguishing feature of stable angina is that the pattern has not changed in character, frequency, or duration over the preceding 2 months. Once the pattern accelerates or symptoms appear at rest in a new fashion, the diagnosis shifts to unstable angina.

Typical vs. Atypical Presentations

Typical angina meets all three criteria: (1) substernal quality, (2) provoked by exertion or stress, and (3) relieved by rest or nitroglycerin. Atypical angina meets only two of three. Non-cardiac chest pain meets zero or one.

03Diagnostic Workup

Step 1: Resting ECG. This is obtained in every patient presenting with chest pain. In stable angina, the resting ECG is often completely normal between episodes. During an episode of ischemia, you may see transient ST depression or T-wave inversions that resolve when the pain stops. If you see persistent ST elevation, pathological Q waves in a new distribution, or troponin elevation, you are no longer dealing with stable angina.

Step 2: Determine pre-test probability. Before ordering a stress test, assess the patient's likelihood of obstructive coronary artery disease based on age, sex, and symptom character. Stress testing is most useful in patients with intermediate pre-test probability (roughly 15% to 85%). In very low probability patients, a positive result is likely a false positive. In very high probability patients, you can proceed directly to coronary angiography because the stress test adds minimal information.

Step 3: Choose the right stress test. The decision tree is as follows:

• Can the patient exercise AND is the resting ECG interpretable? Use an exercise treadmill ECG (the standard exercise stress test). This is the cheapest and most accessible option.

• Can the patient exercise BUT the resting ECG is uninterpretable (e.g., left bundle branch block, left ventricular hypertrophy with repolarization changes, paced rhythm, digoxin use, pre-excitation, >1 mm baseline ST depression)? Use exercise stress with imaging (stress echocardiography or nuclear myocardial perfusion imaging).

• Cannot exercise? Use pharmacologic stress with imaging. Dobutamine is paired with echocardiography (simulates exercise by increasing contractility and heart rate). Vasodilators such as adenosine, dipyridamole, or regadenoson are paired with nuclear perfusion imaging (they dilate normal coronaries but not stenotic ones, creating a "coronary steal" effect that produces differential perfusion).

Step 4: Interpret results. A positive exercise stress test shows ≥1 mm of horizontal or downsloping ST-segment depression measured at the J-point. High-risk features on stress testing include: ST depression ≥2 mm, ST depression at low workload or persisting >5 minutes into recovery, drop in systolic blood pressure during exercise, or ventricular tachycardia during the test. These findings warrant coronary angiography.

Step 5: Coronary angiography. This is the gold standard for defining coronary anatomy. It is indicated when stress testing shows high-risk features, when non-invasive tests are inconclusive, or when the patient has refractory symptoms despite medical therapy. It also allows simultaneous therapeutic intervention with percutaneous coronary intervention (PCI).

04Management and Treatment

Acute Relief. Every patient with stable angina should carry sublingual nitroglycerin (0.4 mg tablets or spray). Instruct the patient to sit before using it (risk of orthostatic hypotension). If chest pain does not resolve after one dose, they should call emergency services. The classic teaching of "take 3 doses 5 minutes apart before calling for help" has been revised in many guidelines to emphasize earlier activation of emergency response. Critical contraindication: nitroglycerin must not be used within 24 hours of sildenafil or vardenafil, or within 48 hours of tadalafil (PDE-5 inhibitors). The combination causes severe, potentially fatal hypotension. This is one of the most tested drug interactions on any licensing exam.

Chronic Anti-Anginal Therapy. Beta-blockers are the first-line chronic therapy. They reduce myocardial oxygen demand by decreasing heart rate, contractility, and blood pressure. The target resting heart rate is 55 to 60 bpm. Beta-blockers also improve survival post-myocardial infarction, which is an added benefit in patients with known CAD. Contraindications include severe reactive airway disease (severe asthma), decompensated heart failure, symptomatic bradycardia, and second- or third-degree atrioventricular block.

If beta-blockers are contraindicated or insufficient alone, add or substitute a calcium channel blocker. Dihydropyridine CCBs (amlodipine, nifedipine) primarily cause vasodilation and are safe to combine with beta-blockers. Non-dihydropyridine CCBs (diltiazem, verapamil) also reduce heart rate and contractility; do not combine these with beta-blockers due to the risk of severe bradycardia, heart block, and cardiogenic shock.

Long-acting nitrates such as isosorbide mononitrate are effective anti-anginal agents but require a 10 to 14 hour nitrate-free interval each day (typically overnight) to prevent pharmacologic tolerance. Without this interval, the nitrate becomes progressively less effective.

Ranolazine is a late sodium current inhibitor used as add-on therapy when beta-blockers, CCBs, and nitrates are insufficient. It does not significantly affect heart rate or blood pressure. It prolongs the QT interval and should be avoided in patients already on other QT-prolonging drugs. It is also contraindicated with strong CYP3A inhibitors.

Secondary Prevention. All patients must receive aspirin (75 to 162 mg daily) and a high-intensity statin regardless of baseline LDL. Smoking cessation, blood pressure control, glucose management in diabetics, weight management, and regular exercise are foundational.

Revascularization. Medical therapy is the initial strategy for most patients with stable angina. Revascularization is considered when symptoms are refractory to optimal medical therapy, or when anatomy is high-risk. CABG is preferred over PCI for left main coronary artery disease, three-vessel disease (especially in patients with diabetes mellitus or reduced ejection fraction), and complex lesions. PCI is reasonable for focal one- or two-vessel disease causing symptoms despite medications.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on stable angina questions is by confusing it with unstable angina or NSTEMI. The vignette will describe a patient with chest pain, and the key to diagnosis lies in two features: (1) the pattern is predictable and reproducible with a consistent level of exertion, and (2) troponins are negative. If the question describes any change in pattern, new rest pain, or troponin elevation, you must shift your diagnosis.

A second frequent trap involves choosing the wrong stress test. Students often default to the exercise treadmill ECG for every patient. But if the vignette mentions a left bundle branch block, LVH on ECG, pacemaker, digoxin use, or a patient who is unable to exercise (wheelchair-bound, severe arthritis, peripheral vascular disease), you must select stress imaging or pharmacologic stress testing instead. A standard treadmill ECG will be uninterpretable in these patients, making it a wrong answer regardless of how "classic" the history sounds.

A third pitfall is the nitroglycerin and PDE-5 inhibitor interaction. A vignette may describe a patient with stable angina who presents with chest pain after taking sildenafil. The question will ask for the next step. The answer is not sublingual nitroglycerin. You must use alternative agents and support blood pressure. This is a heavily tested pharmacology point.

Finally, students sometimes rush to revascularization when the correct answer is optimal medical therapy first. Landmark trials have demonstrated that for most patients with stable angina and preserved ventricular function, medical therapy provides equivalent outcomes to PCI. Revascularization is reserved for refractory symptoms or high-risk coronary anatomy. The core competency being tested here is understanding the stepwise logic of management: risk factor modification and medical therapy come first, and revascularization is not the default.