Chronic Stable Angina & Coronary Revascularization
Pills prevent the heart attack; revascularization treats symptoms and high-risk anatomy
Overview and pathophysiology
Demand ischemia. Chronic stable angina is the symptom of myocardial ischemia caused by a fixed atherosclerotic narrowing. A stenosis of about 70% or more in a major epicardial artery (50% or more in the left main) cannot increase flow enough when myocardial oxygen demand rises. Demand is set by heart rate, contractility, and wall stress (preload and afterload), so exertion, emotional stress, cold air, and large meals provoke symptoms. The subendocardium, farthest from the epicardial vessels and compressed during systole, becomes ischemic first, which is why exercise produces ST depression. Unlike an acute coronary syndrome, there is no plaque rupture or occlusive thrombus and troponin does not rise.
The central principle. In stable disease, medications and risk-factor control prevent myocardial infarction and death, while revascularization is reserved for symptoms that medical therapy cannot control and for anatomy in which surgery improves survival.
Presentation and evaluation
Typical angina has three features: substernal pressure, tightness, or heaviness lasting a few minutes; provocation by exertion or emotional stress; and relief within minutes by rest or sublingual nitroglycerin. Pain that is sharp, positional, pleuritic, reproducible by palpation, or lasting seconds is unlikely to be angina. Women, older adults, and people with diabetes more often report anginal equivalents such as exertional dyspnea or fatigue.
Severity is graded with the Canadian Cardiovascular Society classes: class I, angina only with strenuous or prolonged exertion; class II, slight limitation of ordinary activity; class III, marked limitation of ordinary activity; class IV, angina with any activity or at rest.
Angina that is new and severe (CCS class III or IV), occurs at rest (often lasting more than 20 minutes), or is crescendo in frequency or severity is unstable angina. It is managed as an acute coronary syndrome with admission and serial troponins, not with outpatient testing.
Initial evaluation. Obtain a resting ECG (often normal), lipid panel, A1c, and an echocardiogram to assess LV function, which guides later revascularization decisions. Ischemia is confirmed with an exercise ECG when the patient can exercise and the resting ECG is interpretable. A baseline ECG that cannot be read for ischemia (left bundle branch block, paced rhythm, pre-excitation, 1 mm or more of resting ST depression, digoxin effect, LVH with strain) calls for stress imaging with echocardiography or nuclear perfusion, and patients who cannot exercise receive pharmacologic stress. Coronary CT angiography is an anatomic alternative.
High-risk findings that lead directly to invasive coronary angiography include ST depression of 2 mm or more or at a low workload, a fall in systolic blood pressure with exercise, sustained ventricular arrhythmia, large or multiple perfusion defects, and a fall in EF with stress. Angina refractory to maximal medical therapy is the other common indication.
Guideline-directed medical therapy
Event-reducing therapy. Every patient receives low-dose aspirin (75–100 mg daily), with clopidogrel as the substitute for aspirin allergy, and a high-intensity statin (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) aiming for an LDL reduction of at least 50%. The 2026 ACC/AHA guideline sets an LDL goal below 70 mg/dL, and below 55 mg/dL for very high-risk ASCVD; if LDL stays above goal on a maximally tolerated statin, add ezetimibe or a PCSK9 inhibitor. An ACE inhibitor or ARB is added for hypertension, diabetes, chronic kidney disease, or an EF of 40% or less, and patients with type 2 diabetes benefit from an SGLT2 inhibitor or GLP-1 receptor agonist with proven cardiovascular benefit. Niacin and fibrates added to a statin do not reduce events.
Sublingual nitroglycerin. Every patient carries it: one dose at the onset of angina, and emergency services are called if pain has not improved 5 minutes after the first dose.
- β-Blockerfirst-line antianginal; titrate to a resting heart rate of about 55–60/min; a calcium channel blocker substitutes if β-blockers are contraindicated
- Add amlodipine or a long-acting nitrateif angina persists; a dihydropyridine is the CCB that combines safely with a β-blocker
- Add ranolazinewhen angina persists or blood pressure and heart rate limit further titration
- Angiography and revascularizationfor angina that still limits daily activity despite optimal therapy
| Drug | Mechanism | Key cautions |
|---|---|---|
| β-Blockers (metoprolol, atenolol, bisoprolol) | ↓ Heart rate and contractility; longer diastolic filling | Avoid in marked bradycardia, high-grade AV block, decompensated HF, vasospastic angina; lower mortality after MI and in HFrEF |
| Dihydropyridine CCB (amlodipine) | Arterial and coronary vasodilation; ↓ afterload | Peripheral edema, headache, flushing; avoid short-acting nifedipine (reflex tachycardia) |
| Non-dihydropyridine CCB (verapamil, diltiazem) | ↓ Heart rate and contractility plus vasodilation | Do not combine with a β-blocker (bradycardia, AV block); avoid in HFrEF |
| Nitrates (nitroglycerin, isosorbide mononitrate) | NO → ↑ cGMP → venodilation (↓ preload) and coronary dilation | Headache, hypotension, reflex tachycardia; tolerance without a 10–14 h nitrate-free interval |
| Ranolazine | Blocks the late inward Na⁺ current, reducing Ca²⁺ overload and diastolic wall tension | No effect on HR or BP; QT prolongation; CYP3A4 interactions (ketoconazole, clarithromycin, rifampin) |
Nitrates and PDE-5 inhibitors both raise cGMP, and together they can cause profound hypotension. No nitrate may be given within 24 hours of sildenafil or vardenafil or within 48 hours of tadalafil. Nitrates are also hazardous in severe aortic stenosis and hypertrophic obstructive cardiomyopathy, which depend on preload.
Revascularization
PCI versus medical therapy. In stable disease, adding PCI to optimal medical therapy improves angina and quality of life but does not reduce death or myocardial infarction, as shown by the COURAGE and ISCHEMIA trials. The sequence is therefore medical therapy first, with revascularization for refractory symptoms or high-risk anatomy.
When CABG is favored. CABG improves survival in significant left main disease (50% or more), in 3-vessel disease, and in 2-vessel disease involving the proximal LAD, particularly in patients with diabetes or reduced LV function. In diabetic patients with multivessel disease, the FREEDOM trial showed lower death and MI with CABG than with drug-eluting stents, with slightly more strokes. Complex anatomy, reflected in a high SYNTAX score, also favors surgery, and decisions are made by a heart team of cardiologists and surgeons.
Conduits. The left internal mammary (thoracic) artery grafted to the LAD remains more than 90% patent at 10 years and underpins the survival benefit of CABG. Saphenous vein grafts fare worse: only about half to 60% remain open at 10 years, failing early from thrombosis and later from intimal hyperplasia and accelerated atherosclerosis.
When PCI is reasonable. PCI with drug-eluting stents suits 1- or 2-vessel disease that spares the proximal LAD in patients with refractory angina, and patients whose surgical risk is prohibitive. Dual antiplatelet therapy (aspirin plus a P2Y12 inhibitor) follows every stent.
| Feature | CABG | PCI |
|---|---|---|
| Best anatomy | Left main; 3-vessel; 2-vessel with proximal LAD | 1–2 vessels sparing the proximal LAD |
| Patients who benefit most | Diabetes, reduced EF, complex anatomy (high SYNTAX score) | Refractory angina with simpler anatomy; high surgical risk |
| Survival benefit | Yes, in the indications above | No reduction in death or MI in stable disease |
| Main drawbacks | Sternotomy, stroke, longer recovery, vein graft failure | Restenosis, stent thrombosis, need for DAPT |
Special situations and secondary prevention
Microvascular angina. Some patients, more often women, have typical exertional angina and ischemia on stress testing but no obstructive epicardial stenosis at angiography. Coronary microvascular dysfunction, with reduced coronary flow reserve, is the usual explanation. It is not benign and carries increased cardiovascular risk. Treatment centers on risk-factor control, statins, ACE inhibitors, and antianginal therapy with β-blockers or calcium channel blockers. Vasospastic (Prinzmetal) angina differs: it occurs at rest, often at night or early morning, with transient ST elevation.
Cardiac rehabilitation. Supervised exercise training combined with education and risk-factor and psychosocial counseling is recommended for stable angina and after MI, PCI, or CABG. It improves exercise capacity and angina and lowers cardiovascular mortality and hospitalization, yet it remains underused.
Risk-factor targets. Complete smoking cessation, at least 150 minutes per week of moderate exercise, weight control, and an annual influenza vaccine complete secondary prevention alongside the drug therapy above.