Educational

Acute Coronary Syndromes

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by

Saim Khalid
in

Introduction

Acute Coronary Syndromes (ACS) represent a spectrum of clinical conditions caused by acute myocardial ischemia due to an abrupt reduction or complete cessation of coronary blood flow. The umbrella term ACS encompasses unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). These conditions remain leading causes of morbidity and mortality worldwide, making their timely recognition and management a cornerstone of modern cardiology.

Understanding ACS requires exploring its pathophysiological basis, clinical presentation, diagnostic tools, and early treatment strategies. This article will cover each of these aspects systematically.

Pathophysiology of ACS

The underlying mechanism of ACS is usually related to atherosclerotic plaque disruption within a coronary artery, followed by thrombosis and occlusion. Let’s break this down into stages:

1. Atherosclerotic Plaque Development

  • Atherosclerosis begins with endothelial injury due to risk factors such as hypertension, smoking, diabetes, and dyslipidemia.
  • Low-density lipoprotein (LDL) particles infiltrate the intima and undergo oxidation.
  • Inflammatory cells (monocytes, T-lymphocytes) migrate into the arterial wall, forming fatty streaks.
  • Over time, smooth muscle cells proliferate, and a fibrous cap develops around the lipid core.

2. Plaque Instability and Rupture

  • Some plaques are stable with thick fibrous caps, while others are vulnerable, having thin caps and large lipid cores.
  • When a vulnerable plaque ruptures or erodes, it exposes subendothelial collagen and lipid material, triggering platelet adhesion, activation, and aggregation.

3. Thrombus Formation

  • Activated platelets release thromboxane A2, serotonin, and ADP, promoting further aggregation.
  • The coagulation cascade is activated, generating thrombin and fibrin deposition.
  • The thrombus may be:
    • Partially occlusive → leading to unstable angina or NSTEMI.
    • Completely occlusive → resulting in STEMI.

4. Myocardial Ischemia and Necrosis

  • Ischemia occurs when myocardial oxygen demand exceeds supply.
  • The degree of ischemia depends on:
    • Size of the occluded artery.
    • Duration of occlusion.
    • Presence of collateral circulation.
  • If ischemia persists, irreversible myocardial necrosis (infarction) develops, with cell death beginning within 20–30 minutes.

Clinical Differentiation: Unstable Angina, NSTEMI, and STEMI

Although they share common pathophysiology, ACS entities differ in the extent of ischemia, necrosis, and ECG manifestations.

1. Unstable Angina (UA)

  • Defined as ischemic chest pain without myocardial necrosis (no troponin rise).
  • Symptoms:
    • Occurs at rest or with minimal exertion.
    • Increasing frequency, severity, or duration of angina.
    • Pain lasting >10 minutes, not fully relieved by rest/nitroglycerin.
  • ECG: May show ST depression or T-wave inversion but no persistent changes.
  • Biomarkers: Troponins are normal.

2. Non-ST Elevation Myocardial Infarction (NSTEMI)

  • Pathophysiology: Partial occlusion of a coronary artery with myocardial necrosis.
  • Symptoms: Similar to UA but more prolonged or severe.
  • ECG: ST depression, T-wave inversion, or nonspecific changes; no persistent ST elevation.
  • Biomarkers: Elevated troponins/CK-MB, confirming myocardial damage.

3. ST Elevation Myocardial Infarction (STEMI)

  • Pathophysiology: Complete coronary occlusion, resulting in transmural infarction.
  • Symptoms: Severe, crushing chest pain often radiating to arm, jaw, or back; associated with diaphoresis, nausea, syncope.
  • ECG:
    • ST-segment elevation in contiguous leads.
    • Development of pathological Q waves later.
  • Biomarkers: Markedly elevated troponins and CK-MB.

ECG and Biomarker Correlation

Electrocardiography (ECG) and cardiac biomarkers are essential for distinguishing among ACS types.

ECG Changes in ACS

  • Unstable Angina:
    • Normal ECG or transient ST depression/T-wave inversion.
  • NSTEMI:
    • ST depression (≥0.5 mm) or dynamic T-wave inversion.
    • No persistent ST elevation.
  • STEMI:
    • ST-segment elevation in ≥2 contiguous leads (≥1 mm in limb leads, ≥2 mm in chest leads).
    • Reciprocal ST depression in opposite leads.
    • Later development of Q waves and T-wave inversion.

Biomarkers

  • Troponins (I and T): Most sensitive and specific markers of myocardial injury; rise within 3–6 hours, peak at 12–24 hours, remain elevated for 7–14 days.
  • CK-MB: Useful for detecting reinfarction; rises within 3–6 hours, peaks at 24 hours, normalizes in 48–72 hours.
  • Myoglobin: Rises early but nonspecific.

Key Differentiation Based on Biomarkers:

  • UA → Normal troponins.
  • NSTEMI → Elevated troponins without ST elevation.
  • STEMI → Elevated troponins with ST elevation.

Early Management Strategies in ACS

Prompt management of ACS is crucial for reducing myocardial damage and improving survival.

1. Initial Assessment (ABCDE Approach)

  • Airway, Breathing, Circulation → ensure stability.
  • Obtain IV access, oxygen (if hypoxic), cardiac monitoring, and ECG within 10 minutes.
  • Detailed history (risk factors, symptom onset, prior CAD).

2. Immediate Pharmacological Therapy (MONA + B)

  • M – Morphine: For persistent chest pain and anxiety (use cautiously).
  • O – Oxygen: Only if SpO₂ < 90%.
  • N – Nitroglycerin: Sublingual for chest pain (unless contraindicated, e.g., hypotension, RV infarction, PDE-5 inhibitors).
  • A – Aspirin: 162–325 mg, chewed immediately; cornerstone therapy.
  • B – Beta-blockers: Reduce myocardial oxygen demand (unless contraindicated in bradycardia, hypotension, or severe asthma).

3. Antiplatelet and Anticoagulant Therapy

  • Dual Antiplatelet Therapy (DAPT):
    • Aspirin + P2Y12 inhibitor (clopidogrel, prasugrel, ticagrelor).
  • Anticoagulants:
    • Unfractionated heparin, low-molecular-weight heparin (enoxaparin), or bivalirudin to prevent thrombus extension.

4. Reperfusion Therapy

  • STEMI:
    • Primary Percutaneous Coronary Intervention (PCI): Gold standard, ideally within 90 minutes of first medical contact.
    • Fibrinolysis: If PCI not available within 120 minutes; agents include alteplase, tenecteplase.
  • NSTEMI/UA:
    • No fibrinolysis.
    • Early invasive strategy (PCI within 24–72 hours) for high-risk patients.

5. Adjunctive Therapies

  • Statins: High-intensity statins (e.g., atorvastatin 80 mg) initiated early.
  • ACE inhibitors/ARBs: Started within 24 hours, especially in LV dysfunction.
  • Aldosterone antagonists: For patients with heart failure and low EF.

Prognosis and Risk Stratification

Risk stratification guides management intensity:

  • TIMI Score and GRACE Score help predict mortality and ischemic complications.
  • High-risk features: advanced age, diabetes, prior MI, persistent chest pain, heart failure, hypotension, dynamic ECG changes, elevated biomarkers.

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