Rapid Review·Cardiovascular
Select any text to highlight it or add a note.
PATHOLOGY
T1Must knowCoronary Artery Disease & Angina
p306
Videos
1 to play here
Play 1 here
Focus on
Three anginas separated by what provokes them, and the acute coronary syndrome spectrum.
Key takeaways
What ischemia does to the myocyte
The clock
within 60 seconds of ischemia the cardiomyocyte stops contracting; after 30 minutes the loss is irreversible. Restore flow before 30 minutes and contractility returns over hours to days.Why the cell swells
ischemia means ATP deficiency, so the Na+/K+ ATPase and the sarcoplasmic reticulum Ca2+ ATPase stall, Na+ and Ca2+ accumulate inside the cell, and water follows them into the cell and its mitochondria.Angina
chest pain from ischemic myocardium, caused by coronary narrowing or spasm, with no necrosis. That last clause is what keeps troponin negative.The three anginas
Stable angina
usually from atherosclerosis with 70% or greater occlusion. Exertional chest pain in a classic distribution, relieved by rest or nitroglycerin. ECG may show ST depression.Unstable angina
thrombosis causing incomplete occlusion. Rising frequency or intensity of exertional pain, or any chest pain at rest. No biomarker elevation, which is the only thing separating it from NSTEMI.Vasospastic angina (formerly Prinzmetal or variant)
occurs at rest, often at night, from coronary artery spasm with transient ST elevation or depression and a structurally normal coronary tree. The spasm comes from endothelial dysfunction (too little nitric oxide) plus sympathetic overactivity.- Tobacco smoking is a major risk factor. Other triggers: cocaine, amphetamines, alcohol, triptans.
- Treat with calcium channel blockers, nitrates, and smoking cessation. Beta-blockers can worsen it, by leaving alpha-mediated vasoconstriction unopposed.
| Feature | Stable | Unstable | Vasospastic (Prinzmetal) |
|---|---|---|---|
| Trigger | Exertion | Minimal exertion or rest | Rest, often at night |
| Mechanism | Fixed atherosclerosis, 70% or more | Thrombosis, incomplete occlusion | Coronary spasm |
| Relieved by | Rest or nitroglycerin | Not reliably | Calcium channel blockers |
| Troponin | Normal | Normal | Normal |
| Treatment | Antianginals | ACS protocol | CCBs, nitrates, smoking cessation |
| Risk factors | Atherosclerosis risk factors | Same | Smoking; cocaine, amphetamines, alcohol, triptans |
The acute coronary syndrome spectrum
Myocardial infarction
most often an acute coronary syndrome: rupture of a coronary atherosclerotic plaque with acute thrombosis.- It can also arise from prolonged supply-demand mismatch without plaque rupture, as when a patient with stable angina develops sustained tachycardia and hypotension from pneumonia and the troponin rises anyway.
Which plaque kills
a slow-growing stable plaque produces gradual ischemia, and the myocardium has time to grow collaterals, so necrosis is less likely. An unstable plaque (active inflammation, lipid-rich core, thin fibrous cap) ruptures abruptly, before any collaterals exist.| Feature | Stable angina | Unstable angina | NSTEMI | STEMI |
|---|---|---|---|---|
| Pain | On exertion | Mild exertion or at rest | At rest | At rest |
| Troponin | Not elevated | Not elevated | Elevated | Elevated |
| Infarction | None | None | Subendocardial | Transmural |
| ECG | Possible ST depression or T-wave inversion | Possible ST depression or T-wave inversion | ST depression, T-wave inversion | ST elevation, pathologic Q waves |
| Feature | Unstable angina | NSTEMI |
|---|---|---|
| Presentation | Identical | Identical |
| ECG | Can be identical | Can be identical |
| Troponin | Negative | POSITIVE |
Is it even the heart?
| Source | How it behaves |
|---|---|
| Coronary artery disease | Substernal, brought on by exertion, relieved by rest or nitroglycerin |
| Pulmonary or pleuritic (pleurisy, pneumonia, pericarditis, pulmonary embolism) | Sharp, stabbing, worse on inspiration; pericarditis is worse lying flat |
| Aortic (dissection, intramural hematoma) | Abrupt and maximal at onset, severe "tearing", may radiate to the back; hypertension or an inherited aortopathy |
| Esophageal | Substernal, may refer to the neck, with regurgitation; provoked by lying down, nonexertional, relieved by antacids |
| Chest wall (costochondritis) | Persistent, worse with movement or position change, often after repetitive activity |
A smoker has chest pain at 3 a.m. with transient ST elevation, and the angiogram is clean. Diagnosis, and which common antianginal must you avoid?
Vasospastic angina. Avoid beta-blockers: with beta receptors blocked, alpha-mediated vasoconstriction runs unopposed and the spasm worsens. Use calcium channel blockers and nitrates.
How it's tested
Unstable angina and NSTEMI present identically and can look identical on ECG, so the troponin is the only thing that separates them, which is why serial measurements are required rather than a single draw. Vasospastic angina is the one that happens at rest in a smoker with transient ST changes and structurally normal coronaries, and the management trap is that beta-blockers can worsen it by leaving alpha-mediated vasoconstriction unopposed.
Go deeper
First Aid 2026 — CV/Pathology (p.306) · B&B — Ischemic heart disease · Mehlman — HY Cardio (stable vs unstable vs Prinzmetal)
Flashcards for this page
Card 1 of 5 · try-out only, nothing is saved
(...)
(...)
You just read one page of 944
The rest of Step 1, written exactly like this.
Rapid Review is the reading layer of a full Step 1 platform: a schedule fitted to your exam date, flashcards for every page, and a mentor a message away.
Every Step 1 system
Written the same way: what to know, how it’s tested, where to go deeper.
A plan built to your exam date
Tell us when you sit, and the schedule fits the whole library and your question bank to it.
Flashcards for every page
Ready-made spaced-repetition decks linked to each topic, so nothing you read gets forgotten.
