Acute Coronary Syndrome (ACS): Study Notes

Acute Coronary Syndrome (ACS): Study Notes

Definition

• ACS = spectrum of conditions caused by thrombus formation after rupture of an atherosclerotic plaque in coronary arteries.

• Includes:

  • Unstable angina (UA)

  • Non-ST elevation MI (NSTEMI)

  • ST elevation MI (STEMI)

Coronary Artery Anatomy

• Coronary arteries branch from aorta near the aortic valve.

• Perfusion occurs mainly during diastole (backflow fills coronaries).

• Left coronary artery (LCA):

  • LAD: LV, interventricular septum, some RV.

  • Circumflex: LA + part of LV.

  • Left marginal: LV.

• Right coronary artery (RCA): RA, SA & AV nodes, RV.

Pathophysiology

• Atherosclerosis: fatty plaques with fibrous cap (lipids, debris, inflammatory cells).

• Stable angina = gradual narrowing → ischemia on exertion.

• ACS = plaque rupture → thrombogenic material exposed → clot formation → sudden ischemia.

• Outcomes:

  • UA = ischemia, no necrosis.

  • NSTEMI = partial necrosis (subendocardial).

  • STEMI = transmural necrosis, complete occlusion.

Risk Factors

• Modifiable: smoking, HTN, diabetes, hyperlipidemia, obesity, cocaine/drugs.

• Non-modifiable: age, male sex, family history, ethnicity.

Clinical Presentation

• Typical symptoms: chest pain/pressure (heavy, dull), radiates to jaw/arm/shoulder; may occur at rest.

• Other symptoms: indigestion-like pain, back/epigastric pain, nausea, vomiting, diaphoresis, palpitations, dyspnea, lightheadedness.

• Atypical presentations: more common in women, elderly, diabetics → often no chest pain.

Diagnosis

ECG

• STEMI: ST elevation (≥1 mm in ≥2 contiguous leads; exceptions in V2–V3: 1.5 mm women, 2 mm men).

  • New LBBB also diagnostic.

  • Q waves may form later in large infarcts.

  • Lead correlations:

    • V1–V4 → anterior (LAD).

    • I, aVL, V5–V6 → lateral (LCx, LAD).

    • II, III, aVF → inferior (RCA/LCx).

    • V7–V9 → posterior (LCx/RCA).

• NSTEMI/UA: ST depression, T-wave inversions.

  • NSTEMI = necrosis (positive troponins).

  • UA = no necrosis (negative troponins).

• Note: reciprocal changes in opposite leads; Scarbosa criteria in LBBB/paced rhythm.

Labs

• Cardiac troponins (I/T): gold standard.

  • Rise ~2 hrs post-onset, peak 12–48 hrs, remain ↑ 4–15 days.

Imaging

• Coronary angiography: definitive, guides PCI.

• CXR: may show pulmonary edema, cardiomegaly, or alternate causes.

• Echo: assess LV function, valve disruption, tamponade (not always acutely).

Management

Initial Measures (MONA mnemonic)

• Morphine (analgesia).

• Oxygen (if SpO₂ <94%, except COPD patients with lower targets).

• Nitrates (e.g., GTN sublingual/IV).

• Aspirin (antiplatelet).

• ± antiemetics (metoclopramide).

Definitive Therapy

• STEMI:

  • Primary PCI (within 90 min of contact) = gold standard.

  • If PCI unavailable → fibrinolysis (tPA: alteplase, tenecteplase, reteplase).

• High-risk NSTEMI/UA: early angiography ± PCI.

Pharmacologic Therapy

• Dual antiplatelet therapy (DAPT): aspirin + P2Y12 inhibitor (clopidogrel, ticagrelor).

• Anticoagulation: UFH (IV) or LMWH (SC).

• Statins: high-intensity → lipid lowering + plaque stabilization.

• ACE inhibitors/ARBs: start early unless contraindicated.

• β-blockers: especially in LV systolic dysfunction (avoid in acute HF, bradycardia, hypotension).

Secondary Prevention

• Lifestyle: stop smoking, diet, exercise, weight control.

• Medications: continue aspirin, statin, ACEi/ARB, β-blocker, P2Y12 (up to 12 months).

Key summary:
ACS is caused by plaque rupture + thrombus → ischemia ± necrosis.
Diagnosis = ECG + troponins.
STEMI = urgent reperfusion (PCI or fibrinolysis).
NSTEMI/UA = antiplatelets + anticoagulation + risk-based PCI.