How ACS is tested on Step 1
Questions give chest pain with ECG and troponin results and ask which syndrome or artery, the mechanism of a drug, or a complication days later.
Stable angina comes with exertion and fixed stenosis (usually ≥ 70%) and resolves with rest. Unstable angina is new, worsening, or at rest — it signals a disrupted plaque and belongs to ACS.
Pathophysiology
Vulnerable plaques have a large lipid core, a thin fibrous cap, and many macrophages releasing matrix metalloproteinases.
ECG and biomarkers
ST elevation in contiguous leads localizes the infarct and the culprit artery.
| Territory | Leads | Usual artery |
|---|---|---|
| Anteroseptal | V1–V2 | LAD (septal branches) |
| Anterior | V3–V4 | LAD |
| Lateral | I, aVL, V5–V6 | Left circumflex (or diagonal of LAD) |
| Inferior | II, III, aVF | RCA (most) or circumflex |
| Posterior | ST depression V1–V3 (tall R waves) | Posterior descending artery |
Inferior MI can cause bradycardia and AV block because the RCA usually supplies the SA and AV nodes; RV involvement causes hypotension that worsens with nitrates.
| Marker | Rises | Peaks | Returns to normal | Note |
|---|---|---|---|---|
| Troponin I/T | 3–6 h | 24–48 h | 7–10 days | Most specific; reinfarction shown by a new rise (> 20%) on serial values |
| CK-MB | 4–6 h | ~24 h | 2–3 days | Classic board answer for reinfarction (clears in 2–3 days) |
Normal troponin with rest chest pain and ischemic ECG changes points to unstable angina.
Treatment and drug mechanisms
Therapy restores flow, prevents new thrombus, and reduces myocardial oxygen demand.
| Drug | Mechanism | Benefit |
|---|---|---|
| Aspirin | Irreversible COX-1 inhibition → ↓ TXA₂ | ↓ Mortality |
| Clopidogrel, ticagrelor, prasugrel | Block P2Y12 ADP receptor | With aspirin = dual antiplatelet therapy |
| Heparin | Activates antithrombin | Stops thrombus growth |
| β blockers | ↓ HR and contractility → ↓ O₂ demand | ↓ Mortality, arrhythmias (avoid in shock, cocaine) |
| High-intensity statin | ↓ LDL, plaque stabilization | ↓ Recurrent events |
| ACE inhibitor | Limits remodeling | ↓ Mortality, especially with low EF |
| Nitroglycerin | Venodilation → ↓ preload | Pain relief only; avoid in RV infarct, PDE-5 inhibitor use |
| PCI or fibrinolysis | Reopens the artery | STEMI reperfusion |
Time is muscle: door-to-balloon time under 90 minutes for STEMI.
Clinical application
Read the ECG and the patient together.
A 61-year-old has crushing chest pain with ST elevation in II, III, and aVF and in right-sided lead V4R. Blood pressure falls from 112/70 to 78/50 after sublingual nitroglycerin; lungs are clear and JVP is elevated. What explains the hypotension and how should it be treated?
- Inferior ST elevation points to the RCA, which also supplies the right ventricle.
- ST elevation in V4R confirms right ventricular infarction.
- The infarcted RV depends on preload; nitroglycerin venodilates and drops RV filling.
- Clear lungs with high JVP fit right-sided failure.
Answer. Right ventricular infarction made worse by preload reduction. Give IV fluids, avoid nitrates and diuretics, and proceed to emergent PCI of the RCA.