Study Notes: Acute Coronary Syndrome (ACS)

Definition

• Acute Coronary Syndrome (ACS) is a spectrum of conditions caused by a thrombus formation within the coronary arteries, usually following the rupture of an atherosclerotic plaque.

• It includes:

  • Unstable Angina (UA)

  • Non-ST Elevation Myocardial Infarction (NSTEMI)

  • ST Elevation Myocardial Infarction (STEMI)

Anatomy and Blood Supply

• The heart receives blood via the coronary arteries, which originate from the aorta near the aortic valve.

• During diastole, backflow of blood from the aorta perfuses the coronary arteries.

Main Coronary Arteries:

1. Left Coronary Artery (LCA)

   • Left Anterior Descending (LAD): Supplies left ventricle, interventricular septum, and part of right ventricle.

   • Left Marginal Artery: Supplies the left ventricle.

   • Circumflex Artery: Supplies left atrium and part of left ventricle.

2. Right Coronary Artery (RCA)

   • Supplies right atrium, SA and AV nodes, and right ventricle.

Pathophysiology

• Atherosclerosis: Gradual buildup of fatty plaques containing lipids, cell debris, and inflammatory cells.

• These plaques form a fibrous cap over a thrombogenic core.

• Over years, plaques narrow the lumen, causing stable angina (ischemia during exertion).

• In ACS, plaques rupture, exposing thrombogenic material → clot formation → sudden reduction in blood flow → ischemia and necrosis.

Types of ACS

Type	Mechanism	ECG Changes	Myocardial Damage
Unstable Angina	Partial occlusion; ischemia without necrosis	ST depression / T-wave inversion possible	No cell death
NSTEMI	Partial occlusion; subendocardial necrosis	ST depression, T-wave inversion	Partial wall necrosis
STEMI	Complete occlusion; transmural necrosis	ST elevation	Full-thickness necrosis

Risk Factors

Modifiable:

• Smoking

• Hypertension

• Diabetes mellitus

• Hyperlipidemia

• Obesity

• Cocaine or stimulant use

Non-Modifiable:

• Increasing age

• Male sex

• Family history of CAD

• Ethnicity

Clinical Presentation

• Typical Symptoms:

  • Chest pain or pressure (heavy, dull)

  • Radiation to jaw, arm, or shoulder

  • Occurs at rest

• Atypical Symptoms:

  • Epigastric pain or indigestion

  • Lightheadedness, nausea, diaphoresis (sweating)

  • Palpitations, dyspnea (shortness of breath)

  • May present without chest pain (especially in women, elderly, or diabetics)

Diagnosis

1. ECG Findings

• STEMI:

  • ST elevation in ≥2 contiguous leads

  • Elevation ≥1 mm (except V2–V3: 1.5 mm in women, 2 mm in men)

  • May show pathologic Q waves (large infarctions)

• NSTEMI / Unstable Angina:

  • ST depression or T-wave inversion

  • No Q waves typically

• Localization:

  Leads	Region	Artery
  V1–V4	Anterior	LAD
  I, aVL, V5–V6	Lateral	Circumflex / LAD
  II, III, aVF	Inferior	RCA / Circumflex
  V7–V9	Posterior	RCA / Circumflex

2. Cardiac Biomarkers

• Troponin I or T → released from necrotic myocytes

  • Rises: 2–4 hours after onset

  • Peaks: 12–48 hours

  • Remains elevated: 4–15 days

  • Above 99th percentile = diagnostic of infarction

3. Imaging

• Coronary Angiography – definitive test, identifies occlusion for PCI.

• Chest X-ray – may show pulmonary edema, cardiomegaly, or alternate diagnosis.

• Echocardiogram – detects complications (e.g., valve damage, tamponade).

Management

Initial (Emergency) Management: “MONA”

Drug	Purpose
M – Morphine	Pain relief, reduces anxiety & preload
O – Oxygen	Maintain SpO₂ > 94%
N – Nitrates	Vasodilation (sublingual or IV GTN)
A – Aspirin	Antiplatelet effect (chewed immediately)

Additional:

• Antiemetic (e.g., metoclopramide) for nausea.

Definitive Management

STEMI:

• Reperfusion therapy within 12 hours of symptom onset:

  • Primary PCI (within 90 minutes of contact)

  • If unavailable → Fibrinolysis (e.g., alteplase, tenecteplase, reteplase)

NSTEMI / Unstable Angina:

• Antiplatelet therapy: Aspirin + P2Y12 inhibitor (ticagrelor, clopidogrel)

• Anticoagulation: Heparin (unfractionated IV or LMWH SC)

• High-risk patients may undergo early PCI.

Secondary Prevention

1. Antiplatelets: Continue dual therapy (Aspirin + P2Y12 inhibitor)

2. Statins: Lower LDL, stabilize plaques

3. ACE inhibitors / ARBs: Prevent remodeling, control BP

4. Beta-blockers: Reduce oxygen demand, improve survival post-MI

5. Lifestyle modifications: Stop smoking, diet, exercise, weight control

Key Points Summary

• ACS = Unstable Angina + NSTEMI + STEMI

• Caused by plaque rupture → thrombosis → ischemia → necrosis

• ST elevation = complete occlusion (STEMI)

• Troponin = marker of myocardial injury

• PCI = gold standard for reperfusion

• MONA + secondary prevention are cornerstone therapies