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USMLE Step 1Cardiovascular physiologyEP 14 of 16

Unstable angina vs NSTEMI vs STEMI: from plaque to ACS

Acute coronary syndrome starts with a clot on a disrupted plaque. How much of the artery that clot blocks decides whether you see unstable angina, NSTEMI or STEMI.

  • 4:50 video
  • 3 min read
  • 3 sources
  • Published 10 Nov 2026
Video lesson · 4:50 · Watch on YouTubeSeries: Pressure–Volume Loops & Cardiac Physiology · @medservatory
Chapters (11)
By the end of this lesson

Explain how atherosclerotic plaque rupture or erosion and thrombus formation produce unstable angina, NSTEMI and STEMI, with the size and duration of the clot sorting the syndrome.

The short version

  1. Acute coronary syndrome is supply collapsing at rest because a clot suddenly forms inside a coronary artery.
  2. A thin fibrous cap over a large lipid core is the dangerous plaque, and it does not need to be tight.
  3. Rupture gives a red, fibrin-rich clot; erosion, with an intact cap, gives a white, platelet-rich clot.
  4. Clot size and duration sort the syndrome: unstable angina has normal troponin, NSTEMI has raised troponin without ST elevation, STEMI adds ST elevation.
  5. Rupture is the usual cause of STEMI, erosion is more often found in NSTEMI, and one normal early troponin is not enough to rule out an infarction.

A chest pain puzzle: what changed in the last hour?

A 52-year-old man has crushing chest pain that has lasted 40 minutes. His ECG shows 3 mm of ST elevation in leads V2 to V4. His coronary arteries were silent until now. So what changed?

This lesson explains unstable angina vs NSTEMI vs STEMI. Oxygen supply is coronary flow, and a stable plaque only causes ischaemia when demand rises. Acute coronary syndrome (ACS) is different: supply collapses at rest, because a clot suddenly forms inside the artery.[3]

Inside a plaque: lipid core and fibrous cap

An atherosclerotic plaque has two parts: a soft lipid core, and a fibrous cap over it.[1]

A plaque with a thin cap and a big lipid core is the dangerous, or vulnerable, kind. It does not need to be tight to cause trouble, which is why the artery can be quiet one day and blocked the next.[1][2]

Plaque rupture vs plaque erosion: two routes to a clot

Both routes end the same way: a disrupted surface, platelets, thrombin, and a clot in the lumen. They differ in what happens to the cap.[1]

Two ways a plaque makes a coronary clot
Plaque rupturePlaque erosion
CapThin cap weakened and tornCap stays intact
What is exposedLipid core meets bloodEndothelium lost; platelets stick to the bare plaque
ClotRed, rich in fibrinWhite, rich in platelets
Typical linkUsual cause of STEMIMore often found in NSTEMI; about 4 in 10 ACS culprit lesions in imaging (OCT) studies

In rupture, enzymes weaken the thin cap and it tears, exposing the lipid core to blood. In erosion the cap does not tear: the endothelium is lost and platelets adhere to the exposed plaque.[1][2]

Step two: the size of the clot sorts the syndrome

Once a clot has formed, the degree and duration of the blockage decide what the patient has. The three syndromes sit on one spectrum.[1][3]

  1. A small or flickering clot: unstable anginaFlow is cut for a while, then restored. The muscle is ischaemic, but troponin stays normal. This is ischaemia without myocardial injury.[1][3]
  2. A bigger clot that partly blocks the lumen, or blocks it briefly: NSTEMICells now die, mostly in the subendocardium, the inner layer of the wall and the furthest from the coronary arteries. Troponin leaks into blood, but the ECG shows no ST elevation.[3]
  3. A clot that usually blocks the artery completely: STEMIMuscle dies across the whole thickness of the wall, so the infarct is transmural. The ECG shows ST elevation and troponin rises too. STEMI needs the artery opened urgently.[1][3]
Clot size, troponin and ECG
SyndromeClotTroponinST elevation
Unstable anginaSmall or flickeringNormalNo
NSTEMIPartly blocks, or blocks brieflyRaisedNo
STEMIUsually blocks the artery completelyRaisedYes

Troponin is the line between unstable angina and infarction. ST elevation is what separates STEMI from NSTEMI. This ladder is the usual pattern; exceptions exist, for example a total occlusion with collateral flow can give an NSTEMI.[3]

Applying it to the opening case

The 52-year-old man
  1. Crushing chest pain for 40 minutes, with arteries that were silent until now: a clot has suddenly cut supply.
  2. 3 mm of ST elevation in leads V2 to V4: the ECG shows ST elevation.
  3. ST elevation points to a clot that fully blocks the artery, with transmural muscle death: STEMI.
  4. STEMI needs the artery opened urgently.

The same logic works in reverse. The ECG and the troponin give a clue to how big the clot is, even though you cannot see it. It is a tendency, not a measurement.[3]

Who causes what, and why troponin timing matters

Rupture is the usual cause of STEMI, while erosion turns up more often in NSTEMI. This is a tendency, not a rule.[1][2]

Practice question

Original · USMLE style
Your turnQB-MS-S1-CARD-020-01

A 61-year-old woman with type 2 diabetes mellitus and hypertension has had chest pressure at rest for 25 minutes. She is pale and diaphoretic. Her electrocardiogram shows 1.5 mm of ST-segment depression in leads V4 to V6 and no ST-segment elevation. Serum troponin I is 3.2 ng/mL (reference range: less than 0.04 ng/mL).

Which of the following best explains these findings?
Pick one option. Your answers stay on this device.

Common questions

What is the difference between unstable angina, NSTEMI and STEMI?

All three start with a clot on a disrupted plaque, and clot size sorts them. Unstable angina has ischaemia with normal troponin, NSTEMI has raised troponin without ST elevation, and STEMI has raised troponin with ST elevation.[1][3]

What is the difference between plaque rupture and plaque erosion?

In rupture a thin fibrous cap tears and exposes the lipid core, giving a red, fibrin-rich clot. In erosion the cap stays intact, the endothelium is lost, and platelets form a white, platelet-rich clot.[1][2]

Does a plaque have to be tight to cause a heart attack?

No. A plaque with a thin cap and a big lipid core is the dangerous kind, and it does not need to narrow the artery much.[1][2]

Why is one normal troponin not enough?

A single early troponin can still be normal in the first hours after onset, so an early normal value does not exclude myocardial injury. Serial measurements are needed.[3]

Which plaque event is more linked to STEMI?

Rupture is the usual cause of STEMI, and erosion is found more often in NSTEMI.[1][2]

Transcript

Read the full narration, by chapter625 words

0:00A chest pain puzzle: 3 mm of ST elevation

A 52-year-old man has crushing chest pain that has lasted 40 minutes. His ECG shows three millimetres of ST elevation in leads V two to V four. Yesterday his coronary arteries were silent. So what changed in the last hour? Today: explain how a plaque rupture or erosion makes a clot, and how the size of that clot sorts unstable angina, NSTEMI and STEMI.

0:27Last time: supply, demand and a clot at rest

Last time: oxygen supply is coronary flow, and a stable plaque only bites when demand rises. Acute coronary syndrome is different: supply collapses at rest, because a clot suddenly forms inside the artery.

0:43Inside a plaque: lipid core and fibrous cap

An atherosclerotic plaque has two parts: a soft lipid core, and a fibrous cap over it. A plaque with a thin cap and a big lipid core is the dangerous kind, and it does not need to be tight.

0:56Rupture vs erosion: two routes to a clot

Route one: plaque rupture. Enzymes weaken the thin cap and it tears, exposing the lipid core to blood. The clot is red, rich in fibrin. Route two: plaque erosion. Here the cap does not tear. The endothelium is lost, platelets stick to the bare plaque, and the clot is white, rich in platelets. About four in 10 events in imaging studies. Either way: a disrupted surface, platelets, thrombin, and a clot in the lumen.

1:30Clot size 1: unstable angina

Step two is the size of the clot. First, a small or flickering clot. Flow is cut for a while, then restored. The muscle is ischaemic, but troponin stays normal. That is unstable angina: ischaemia without myocardial injury.

1:47Clot size 2: NSTEMI

Next, a bigger clot that partly blocks the lumen, or blocks it briefly. Now cells die, mostly in the inner layer of the wall, the subendocardium, which is the furthest from the coronary arteries. Troponin leaks into blood, but the ECG shows no ST elevation. That is NSTEMI: injury with raised troponin, and no ST elevation.

2:13Clot size 3: STEMI

Last, a clot that fully blocks the artery. Muscle dies across the whole thickness of the wall, so the infarct is transmural. The ECG shows ST elevation, and troponin rises too. That is STEMI, and it needs the artery opened urgently.

2:33Who causes what, and why troponin timing matters

Rupture is the usual cause of STEMI; erosion turns up more in NSTEMI. And troponin can take hours to rise, so one normal value early is not enough.

2:45Practice question

Your turn. A 61-year-old woman with diabetes and hypertension has had chest pressure at rest for 25 minutes. The ECG shows 1.5 millimetres of ST depression in leads V four to V six, with no ST elevation. Troponin I is 3.2 nanograms per millilitre; the reference is below 0.04. Which of the following best explains her findings? A, a fixed coronary narrowing with a rise in demand and no thrombus. B, a partially occlusive thrombus on a disrupted plaque. C, coronary vasospasm without thrombus. D, a complete thrombotic occlusion with transmural infarction. E, an embolus from a left atrial thrombus. Pause here and decide.

3:40Answer: wrong options first, then the right one

A is out: nothing here raises her demand, and she is at rest. A fixed narrowing with demand gives effort angina. C is out: vasospasm classically gives brief ST elevation that eases, and plaque disease fits her risk factors far better. D is out: a complete occlusion with transmural infarction would give ST elevation. E is out: an embolus is possible, but nothing here points to atrial fibrillation or a source. B is correct: rest pain, raised troponin and no ST elevation make an NSTEMI, from a clot that only partly blocks the artery.

4:23Recap and next lesson

Rupture or erosion starts the clot, and rupture is the classic cause of STEMI. The size of the clot sorts the syndrome: unstable angina has normal troponin, NSTEMI has raised troponin, and STEMI adds ST elevation. And troponin is the line between unstable angina and infarction. Next: the drugs that rebalance supply and demand.

Sources

Numbers in the text, e.g. [1], point here
  1. Pathophysiology of Acute Coronary Syndromes. Life (Basel) 2023. pmc.ncbi.nlm.nih.gov/articles/PMC10381786/
  2. Riascos-Bernal. Pathogenesis of plaque erosion. Trends Cardiovasc Med 2025. pmc.ncbi.nlm.nih.gov/articles/PMC12506922/
  3. Advances in the Diagnosis and Management of Acute Coronary Syndromes. pmc.ncbi.nlm.nih.gov/articles/PMC13334565/

The practice question is original and its patient is synthetic. Every fact is checked against the sources above in independent accuracy reviews. Always follow your local guidelines and your own laboratory’s ranges.

Image credits. All art is drawn in code (original): artery cross-sections, clots, heart-wall diagrams, ECG strips, troponin slips and all handwriting. No licensed illustrations or 3D models are used. The ECG strips are schematic teaching drawings, not patient recordings. Thumbnail plate: Servier Medical Art (smart.servier.com), "Myocardial infarction, anteroseptal infarct", licensed under CC BY 4.0, recoloured and resized. Previous: EP 13 · Myocardial oxygen supply and demand · Next: EP 15 · Anti-ischaemic drugs

Corrections. None so far. Spotted an error? Email info@medservatory.com with the lesson code MS-S1-CARD-020.

For exam study only, not medical advice. Read the medical disclaimer.

In this series

Playlist on YouTube
← Previous · EP 13Myocardial oxygen supply and demand: why tachycardia causes ischaemia
  1. EP 01Pressure-volume loop explained: four phases, four valve events5:00
  2. EP 02Preload on the pressure-volume loop: EDV, stroke volume and the EDPVR5:04
  3. EP 03Afterload on the pressure-volume loop4:49
  4. EP 04Contractility on the pressure-volume loop: the ESPVR explained5:17
  5. EP 05Wiggers diagram explained: the cardiac cycle step by step5:30
  6. EP 06The Frank-Starling curve: preload, inotropy and heart failure4:44
  7. EP 07Aortic stenosis vs mitral regurgitation on the pressure-volume loop5:41
  8. EP 08Fick principle: how to calculate cardiac output5:07
  9. EP 09HFrEF vs HFpEF on the pressure-volume loop5:33
  10. EP 10Poiseuille's law and vascular resistance: why arterioles matter5:15
  11. EP 11Venous return and cardiac function curves: where they cross5:11
  12. EP 12The baroreceptor reflex: from stretch to vagal and sympathetic output5:17
  13. EP 13Myocardial oxygen supply and demand: why tachycardia causes ischaemia4:50
  14. EP 14Unstable angina vs NSTEMI vs STEMI: from plaque to ACS4:50
  15. EP 15Antianginal drugs: nitrates, beta blockers, calcium channel blockers4:56
  16. EP 16Complications of myocardial infarction, by timeline4:59