What is the difference between stable and unstable angina?

Stable angina is predictable chest discomfort triggered by exertion or emotional stress and relieved within minutes by rest or sublingual nitroglycerin; it comes from a fixed coronary narrowing, usually 70% or more of the diameter. Unstable angina is an acute coronary syndrome: chest pain at rest (usually over 20 minutes), new-onset severe angina, or angina that is becoming more frequent, longer or easier to provoke. It comes from a disrupted plaque with a partial clot, and troponin stays below the 99th-percentile cutoff used to diagnose myocardial infarction.

How do you tell unstable angina from NSTEMI?

Only by troponin. Both cause rest or crescendo chest pain and can show ST depression or T-wave inversion on the ECG. In unstable angina, troponin stays below the 99th-percentile upper reference limit, meaning ischemia without myocardial necrosis. In NSTEMI, troponin goes above that cutoff, with a rise or fall on serial testing. Because troponin lags behind the injury, it is measured serially: at presentation and 1 to 2 hours later with a high-sensitivity assay, or at 0 and 3 to 6 hours with a conventional assay.

Is unstable angina a heart attack?

Not by definition, because there is no myocardial necrosis and troponin stays below the infarction cutoff, but it is an acute coronary syndrome and a medical emergency. The same unstable plaque and clot that cause unstable angina can progress to NSTEMI or STEMI. Patients are admitted and treated on the acute coronary syndrome pathway, with antiplatelet drugs, anticoagulation, a high-intensity statin and, for intermediate- or high-risk patients, coronary angiography during the admission.

What ECG changes are seen in stable and unstable angina?

In stable angina the resting ECG is often normal, and ST-segment depression appears during ischemia, for example on an exercise stress test. In unstable angina, transient ST depression or T-wave inversion may appear during pain and resolve afterward; transient ST elevation can also occur. Persistent ST elevation of at least 1 mm in two contiguous leads means STEMI. A normal ECG does not exclude coronary ischemia, so the ECG is repeated with recurrent symptoms.

How is unstable angina treated under the 2025 ACC/AHA guideline?

Unstable angina is managed as a non-ST-elevation acute coronary syndrome. Patients get chewed aspirin plus a P2Y12 inhibitor, with ticagrelor or prasugrel preferred over clopidogrel if they undergo PCI; parenteral anticoagulation such as heparin or enoxaparin; a high-intensity statin; nitroglycerin for ongoing pain; and an oral beta-blocker if there is no contraindication. Intermediate- and high-risk patients have coronary angiography during the admission. Fibrinolytic drugs are not used, because they help only STEMI.

Does relief with nitroglycerin prove chest pain is angina?

No. Nitroglycerin relaxes smooth muscle in general, so it can also relieve esophageal spasm and biliary pain, and the Merck Manual advises that its effect, or lack of effect, should not be used for diagnosis. Look instead at the trigger and pattern (exertion, rest pain, crescendo), the ECG during symptoms, and serial troponins. Esophageal spasm typically causes chest pain together with difficulty swallowing both solids and liquids.

Stable vs Unstable Angina vs NSTEMI: Troponin & ECG Clues

Stable angina is predictable chest pressure that comes on with exertion or emotional stress and fades within minutes with rest or sublingual nitroglycerin, because a fixed atherosclerotic stenosis (usually narrowing the diameter by 70% or more) cannot raise flow when demand rises. Unstable angina is an acute coronary syndrome (ACS): angina at rest (usually lasting more than 20 minutes), new-onset severe angina, or a crescendo pattern, caused by a disrupted plaque with a nonocclusive thrombus, while troponin stays below the 99th-percentile upper reference limit. The only thing that separates unstable angina from NSTEMI is troponin: a value above that limit, with a rise or fall on serial testing, means myocardial necrosis. Stable angina is worked up as an outpatient; unstable angina goes on the ACS pathway of the 2025 ACC/AHA guideline: aspirin plus a P2Y12 inhibitor, parenteral anticoagulation, a high-intensity statin and, for intermediate- or high-risk patients, coronary angiography during the admission.

The Q-bank question

A 61-year-old man with hypertension, type 2 diabetes and a 30-pack-year smoking history has had chest pressure for 2 years that always starts after two flights of stairs and stops within 3 minutes of rest. Over the past 10 days, the pressure starts after walking one block, lasts longer, and has woken him from sleep twice. This morning he had 25 minutes of substernal pressure while sitting still; he is now pain-free. Blood pressure is 146/88 mm Hg and pulse 84/min; the examination is normal. During a brief recurrence in the emergency department, the ECG shows 1.5-mm horizontal ST depression in V4-V6 that resolves when the pain stops. High-sensitivity troponin on arrival and 2 hours later is below the 99th-percentile upper reference limit both times.

Which of the following is the most likely diagnosis?

A. Stable angina B. Unstable angina C. Non-ST-elevation myocardial infarction (NSTEMI) D. ST-elevation myocardial infarction (STEMI) E. Vasospastic (Prinzmetal) angina F. Acute pericarditis G. Distal (diffuse) esophageal spasm

Answer: B. Unstable angina. Three features turn this into an ACS: a crescendo pattern (lower threshold, longer episodes), pain at night and at rest, and a rest episode longer than 20 minutes. The ECG shows transient ST depression (subendocardial ischemia), and serial high-sensitivity troponins stay below the 99th percentile, so there is no evidence of necrosis. Ischemia without infarction, in an unstable pattern, is unstable angina.

Why every other answer is wrong

A. Stable angina. Correct for the first 2 years: same trigger, same threshold, relief within minutes. But angina that becomes distinctly more frequent, more severe, longer or lower in threshold is unstable angina by definition. Walking one block is now his trigger (Canadian Cardiovascular Society class 3), so the change in pattern is the whole question.
C. NSTEMI. Same plaque biology, the same symptoms and often the same ECG (ST depression or T-wave inversion). The difference is troponin above the 99th percentile. That is why troponin is measured serially: at presentation and 1-2 hours later with a high-sensitivity assay, or at 0 and 3-6 hours with a conventional assay. One normal early value does not exclude MI, because troponin lags behind the injury. More on assays in troponin and CK-MB.
D. STEMI. Needs ST elevation of at least 1 mm in 2 or more contiguous leads (higher cut-offs in V2-V3) that is not quickly reversed by nitroglycerin, usually from an occlusive thrombus. This ECG shows depression, not elevation. STEMI goes to emergency reperfusion; see STEMI vs NSTEMI management.
E. Vasospastic angina. Also causes rest pain, typically at night or in the early morning, but the ECG during an attack classically shows transient ST elevation from epicardial coronary spasm, and attacks are only rarely brought on by exertion. A 2-year exertional history that is now accelerating is atherosclerotic, not spastic. Full breakdown: Prinzmetal angina.
F. Acute pericarditis. Sharp pain worse with breathing, coughing or swallowing and eased by sitting up and leaning forward, a friction rub, and diffuse concave ST elevation with PR depression, without reciprocal ST depression (except in aVR and V1). Pressure-like exertional pain with localized ST depression is ischemia.
G. Esophageal spasm. The classic look-alike, because nitroglycerin also relaxes smooth muscle in the esophagus: Merck warns that relief, or no relief, with nitroglycerin should not be used for diagnosis. Spasm gives substernal pain with dysphagia for solids and liquids, which very hot or cold drinks can aggravate, and ischemia must be excluded first. Exertional triggers plus ischemic ST changes point to the heart.

Stable angina vs unstable angina vs NSTEMI vs STEMI

	Stable angina	Unstable angina	NSTEMI	STEMI
Pattern	Predictable: exertion, emotion, cold, exertion after a meal	Rest pain (usually over 20 min), new-onset severe, or crescendo	Like unstable angina	Usually severe and persistent
Relief	Within minutes with rest; SL nitroglycerin works in 1.5-3 min	Less predictable; may need repeated or IV nitroglycerin	Like unstable angina	Persistent pain; ST elevation not quickly reversed by nitroglycerin
Lesion	Fixed stenosis, usually 70% or more	Plaque disruption with a nonocclusive thrombus	Plaque disruption with thrombus, plus necrosis	Usually an occlusive thrombus
Troponin	Normal	Below the 99th percentile	Above the 99th percentile	Above the 99th percentile
ECG	Often normal at rest; ST depression during ischemia	Transient ST depression or T-wave inversion (sometimes transient ST elevation)	ST depression, T-wave inversion or nonspecific	ST elevation of 1 mm or more in 2+ contiguous leads
Classic exam label	Demand ischemia	Ischemia without infarction	Subendocardial infarct	Transmural infarct
Where it is managed	Outpatient	Admit: ACS pathway	Admit: ACS pathway	Emergency reperfusion

Pathophysiology: why the same plaque gives different stories

Stable angina is demand ischemia. A fixed stenosis cannot raise flow when heart rate, blood pressure and contractility rise. Merck notes that angina does not usually develop when the diameter reduction is under 70% unless spasm or thrombosis is added. Rest lowers demand, so the episode ends; cold weather and exertion after a meal make it worse. For why diastole and the subendocardium matter, see coronary autoregulation.
Unstable angina is supply ischemia. A vulnerable plaque ruptures or erodes, platelets aggregate, and a nonocclusive thrombus narrows the lumen further, so ischemia now happens at rest, with no change in demand. That is why the pain no longer tracks exertion.
NSTEMI and STEMI are the same process gone further: enough ischemia to kill myocytes (troponin rises), and in STEMI usually a complete occlusion with ST elevation.

Diagnosis: what to order and when

ECG within 10 minutes of first medical contact, repeated with any recurrent pain. A normal ECG between episodes does not exclude coronary ischemia.
Serial troponin: high-sensitivity assay at presentation and 1-2 hours later (conventional assay: 0 and 3-6 hours). NSTEMI needs a value above the 99th percentile with a rise or fall.
Risk scores: GRACE and TIMI. Merck classes a GRACE score over 140 as high risk; refractory angina, heart failure, cardiogenic shock, or hemodynamic or electrical instability is very high risk and goes to angiography within 2 hours.
Suspected stable angina (pain-free, stable pattern): exercise ECG if the resting ECG is normal and the patient can exercise; stress imaging (echocardiography, SPECT or PET perfusion, cardiac MRI) when the resting ECG is abnormal or more accuracy is needed; pharmacologic stress (eg, dobutamine or dipyridamole) when the patient cannot exercise. Coronary CT angiography is the anatomic alternative, and invasive angiography is the gold standard when revascularization is being considered.

Management: outpatient optimization vs the 2025 ACS pathway

	Stable angina	Unstable angina / NSTE-ACS
Antiplatelet	Low-dose aspirin	Aspirin 162-325 mg chewed, then 81 mg daily, plus a P2Y12 inhibitor
Anticoagulant	None	Unfractionated heparin, enoxaparin, fondaparinux or bivalirudin
Lipids	Statin, intensified with ezetimibe or a PCSK9 inhibitor as needed	High-intensity statin for all, with the option of starting ezetimibe at the same time
Anti-ischemic	SL nitroglycerin for attacks; beta-blocker for most; calcium channel blocker or long-acting nitrate as alternatives or add-ons; ranolazine for refractory symptoms	Nitroglycerin for ongoing pain; oral beta-blocker within 24 hours if stable and no contraindication
Angiography	When revascularization is considered: angina despite medicines, or suspected high-risk anatomy (eg, left main)	Invasive approach during the admission for intermediate- or high-risk patients
Fibrinolytics	Not used	Not used: they help STEMI only and worsen outcomes in unstable angina and NSTEMI

Key 2025 ACC/AHA ACS recommendations worth knowing by name:

Ticagrelor or prasugrel is recommended in preference to clopidogrel in ACS patients undergoing PCI. Prasugrel is contraindicated after a prior stroke or TIA.
DAPT for at least 12 months is the default for ACS patients who are not at high bleeding risk. In patients who have tolerated DAPT with ticagrelor, switching to ticagrelor monotherapy 1 month or more after PCI is also recommended, to reduce bleeding.
High-intensity statin for every ACS patient. Adding a nonstatin agent is recommended if LDL-C stays at 70 mg/dL or more on a maximally tolerated statin, and is reasonable if it is 55 to under 70 mg/dL.
Timing of angiography in NSTE-ACS (Merck's summary): within 2 hours if very high risk, within 24 hours if high risk, before discharge (within 72 hours) if intermediate risk; if low risk, noninvasive testing first (stress test or coronary CT angiography), then angiography only if indicated.

Nitrates are avoided with a systolic blood pressure under 90 mm Hg, right ventricular infarction or recent phosphodiesterase-5 inhibitor use (eg, sildenafil, tadalafil). Morphine is used sparingly because it can blunt the effect of oral P2Y12 inhibitors.

How USMLE tests it

One phrase flips the diagnosis. "Now with less exertion," "woke him from sleep," "25 minutes at rest" or "new in the past 2 weeks" turns stable angina into unstable angina, and the next step becomes admission, not a routine stress test.
Unstable angina vs NSTEMI is a troponin question. Same symptoms, same ECG, different biomarker. Expect serial troponins in the stem.
ST depression vs ST elevation. ST depression points to subendocardial ischemia (stable angina during exercise, unstable angina, NSTEMI); ST elevation points to STEMI, vasospasm or pericarditis, and the distribution and the history tell you which (see how to read an ECG).
Nitroglycerin relief proves nothing. Esophageal and biliary smooth muscle relax too.
Atypical presentations. Merck notes that women often have epigastric symptoms, palpitations or pain away from the sternum, and older adults may present with dyspnea, syncope, falls or delirium.
Fibrinolysis is a STEMI-only answer. Picking it for unstable angina or NSTEMI is always wrong.

Key takeaways

Stable angina: predictable, exertional, relieved by rest or nitroglycerin within minutes, troponin normal, fixed stenosis.
Unstable angina: rest pain over about 20 minutes, new-onset severe angina or a crescendo pattern; troponin below the 99th percentile; plaque disruption with a nonocclusive thrombus.
NSTEMI = unstable angina plus a troponin above the 99th percentile; measure troponin serially (0 and 1-2 hours with a high-sensitivity assay).
ECG within 10 minutes; transient ST depression or T-wave inversion is typical of unstable angina and NSTEMI.
2025 ACC/AHA ACS pathway: aspirin plus a P2Y12 inhibitor (ticagrelor or prasugrel preferred for PCI), parenteral anticoagulation, high-intensity statin, invasive strategy for intermediate- or high-risk patients, no fibrinolytics.
Stable angina: aspirin, statin, SL nitroglycerin, beta-blocker for most, and stress testing to confirm.