Acute Coronary Syndrome: STEMI vs NSTEMI vs UA Diagnosis & Treatment

Creator: Progress Note
Published: 2026-07-22
Keywords: acute coronary syndrome STEMI NSTEMI, STEMI treatment door-to-balloon, NSTEMI management, ACS troponin diagnosis, unstable angina vs NSTEMI, dual antiplatelet therapy ACS

The 60-second version

STEMI: ST elevation ≥2 contiguous leads or new LBBB → primary PCI ≤90 min (door-to-balloon)
NSTEMI vs UA: both have ST depression/T-wave changes; NSTEMI has troponin elevation, UA does not
Dual antiplatelet (aspirin + P2Y12) + anticoagulation + early invasive strategy for high-risk NSTEMI
Killip IV (cardiogenic shock) = 81% in-hospital mortality — emergent PCI + IABP/Impella
Mechanical complications days 3–5: free wall rupture (tamponade), papillary muscle rupture (acute MR), VSD — all require emergent surgery

STEMI vs NSTEMI vs Unstable Angina

ACS is caused by plaque rupture with superimposed thrombus. **STEMI**: complete occlusion → ST elevation in ≥2 contiguous leads (≥1 mm limb leads; ≥2 mm precordial; ≥2.5 mm V2–V3 in men <40), new LBBB, or posterior MI (tall R in V1-2, ST depression V1-2, ST elevation in V7-9). Troponin rises >4h, peaks 24h, normalizes 7–10 days. **NSTEMI**: partial occlusion → ST depression, T-wave inversion, or normal ECG with troponin elevation. Same spectrum: NSTEMI (troponin positive) vs unstable angina (troponin negative). UA: rest angina, new-onset (<2 months) severe angina, or crescendo angina. TIMI risk score for NSTEMI/UA: 7 variables (age ≥65, ≥3 CAD risk factors, known CAD, ASA use in past 7 days, severe anginal events, ST deviation ≥0.5 mm, elevated troponin) → score 0-7, predicts 14-day MACE.

Reperfusion and Acute Management

**STEMI**: primary PCI is preferred (door-to-balloon ≤90 min for PCI-capable center, ≤120 min for transfer). Fibrinolysis (tPA, tenecteplase) if PCI not available within 120 min (door-to-needle ≤30 min) — absolute contraindications: prior ICH, ischemic stroke <3 months, aortic dissection, active bleeding. Post-lysis: PCI at 3–24h (pharmacoinvasive strategy). **NSTEMI/UA**: anticoagulation (heparin UFH or LMWH/fondaparinux) + dual antiplatelet (aspirin + P2Y12 inhibitor). Invasive strategy (PCI within 24–48h) for: elevated troponin, ST changes, TIMI score ≥3, hemodynamic instability, recurrent ischemia. Conservative strategy for low-risk UA. **Medications**: aspirin 325 mg loading → 81 mg daily; P2Y12 inhibitors (ticagrelor or prasugrel preferred over clopidogrel for STEMI/high-risk NSTEMI); anticoagulation (UFH, bivalirudin, enoxaparin); beta-blockers (start within 24h if no HF, low output, heart block, or reactive airways); high-intensity statin; ACE inhibitor/ARB (EF <40%, HTN, DM, CKD); nitrates (symptom relief, not mortality benefit).

Complications and Killip Classification

**Killip classification** (in-hospital mortality predictor): Class I (no HF signs, 6% mortality), Class II (S3 or bibasilar rales <50% lung fields, 17%), Class III (acute pulmonary edema, 38%), Class IV (cardiogenic shock — BP <90 + end-organ hypoperfusion, 81%). **Mechanical complications** (days 3–5, peak after fibrinolysis): Free wall rupture → cardiac tamponade (sudden hemodynamic collapse, pericardial effusion on echo) → emergent surgery. Papillary muscle rupture → acute severe MR (new harsh holosystolic murmur, acute pulmonary edema) → emergent valve surgery or IABP bridge. VSD → new harsh holosystolic murmur with step-up in O2 saturation from RA to RV on right heart cath → emergent surgical repair. **Dressler's syndrome** (weeks to months): pericarditis post-MI — pleuritic chest pain, friction rub, fever, elevated ESR; treat with NSAIDs + colchicine. **Right ventricular MI** (inferior STEMI + RV involvement): hypotension + JVD + clear lungs; treat with IV fluids (preload-dependent), avoid nitrates and diuretics.

Test yourself

Quick check — 3 questions

1. A 58-year-old man presents with 2 hours of crushing chest pain. ECG shows ST elevations in V1–V4. He arrives at a PCI-capable hospital. What is the most important time target?

2. A patient with inferior STEMI develops hypotension, JVD, and clear lung fields after PCI. What is the most appropriate next step?

3. A 65-year-old man is admitted for NSTEMI with troponin elevation and ST depressions in V4–V6. He is hemodynamically stable. What is the appropriate antiplatelet strategy?

Frequently asked questions

When should fibrinolysis be used instead of primary PCI for STEMI?

Fibrinolysis is appropriate when PCI-capable lab is not available within 120 minutes of first medical contact. Door-to-needle time for fibrinolysis should be ≤30 minutes. Absolute contraindications: prior ICH at any time, known structural cerebrovascular lesion, ischemic stroke within 3 months, suspected aortic dissection, significant closed-head trauma within 3 months, active internal bleeding. After fibrinolysis, pharmacoinvasive strategy (PCI at 3–24h) is recommended.

Why is right ventricular MI treated differently from left ventricular MI?

RV MI (complicating inferior STEMI) causes RV failure with reduced preload delivery to the LV. The RV becomes preload-dependent — it needs adequate filling to generate cardiac output. Nitrates and diuretics reduce preload and can cause profound hypotension. Treatment: IV fluid boluses to maintain preload, early revascularization (PCI of RCA), and avoidance of preload-reducing drugs. The classic triad is hypotension + JVD + clear lungs.

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