2.2 Acute coronary syndrome

Aetiology and pathogenesis of Acute coronary syndrome

• Types of ACS

  • STEMI

  • NSTEMI

  • Unstable angina (UA)

• Primary cause: Obstruction of coronary artery by thrombus from atherosclerotic plaque

• Types of plaque complications:

  • Plaque Rupture (~60-75%):

    • Involves a vulnerable plaque with a large necrotic core and a thin fibrous cap

    • Fibrous cap is weakened by inflammation

    • When the cap ruptures, the thrombogenic core is exposed to blood, leading to platelet activation and thrombus formation

  • Plaque erosion (~25-40%)

    • Fibrous cap remains intact and thick, but endothelial lining is absent.

    • Underlying plaque lacks necrotic core and contains more smooth muscle cells and proteoglycan matrix, with fewer inflammatory cells

    • The loss of endothelium allows blood to interact with subendothelial components, triggering neutrophil recruitment and the formation of a neutrophil-rich thrombus.

• Vulnerable plaque:

  • Features: Thin cap (<65μm), large lipid pool, active macrophages.

  • Leads to Thin Cap Fibroatheroma (TCFA), major precursor of ACS.

• Other causes: SCAD, coronary spasm, microvascular dysfunction, MINOCA.

Clinical features of acute coronary syndrome

1. Common symptoms:

   • Chest pain: Substernal pressure/tightness, may radiate to jaw/left arm

   • Associated symptoms: Dyspnoea, diaphoresis, nausea, vomiting, palpitations

   • Atypical presentations: Especially in elderly, diabetics, women — may present with dyspnoea alone, nausea, or palpitations

2. ECG findings:

   • STEMI:

     • Complete coronary occlusion

     • ST elevation (J-point): Localises MI based on lead changes

     • Criteria: ≥ 1mm in all leads (except V2-V3); V2-V3: ≥ 2 mm (men≥40), ≥2.5 mm (men <40), ≥1.5 mm (women).

   • NSTEMI

     • Partial occlusion

     • ST depression and/or T wave inversions (subendocardial infarct)

3. Troponin:

   • Troponin I/T: Highly specific/sensitive for myocardial injury

   • Interpretation: Must consider context; other causes include myocarditis, PE, stroke, sepsis

   • Use hs-Troponin assay: >99th percentile = abnormal; dynamic change confirms MI

Differential diagnoses for central chest pain

• Life-threatening:

  • ACS

  • Aortic Dissection – sharp/ripping chest and back pain.

  • Pulmonary Embolism – dyspnoea, pleuritic pain, cough.

  • Tension Pneumothorax – sudden pleuritic pain + dyspnoea.

  • Esophageal Rupture – after vomiting/straining.

  • Takotsubo Cardiomyopathy – stress-related, MI mimic.

• Non-life-threatening:

  • Cardiac:

    • Stable Angina

    • Pericarditis/Myocarditis (pleuritic pain, relieved by leaning forward)

    • Aortic Stenosis (exertional pain, syncope)

  • Pulmonary:

    • Pneumonia, pneumothorax, malignancy, asthma/COPD, pleuritis

  • Gastrointestinal:

    • GERD, peptic ulcer, oesophagitis, motility disorders

Mechanisms of key cardiovascular symptoms

Shortness of Breath (Cardiac Origin)

1. Left ventricular dysfunction occurs (e.g. due to heart failure or acute MI).

2. Blood backs up into the left atrium, increasing left atrial pressure.

3. This pressure transmits to the pulmonary veins and capillaries.

4. Hydrostatic pressure rises in pulmonary circulation.

5. Fluid leaks into interstitial and alveolar spaces (pulmonary oedema).

6. Gas exchange is impaired → lungs become stiff → breathing effort increases.

7. Patient experiences dyspnoea (shortness of breath).

Chest Discomfort (Myocardial Ischaemia)

1. Reduced blood flow due to coronary artery narrowing or blockage.

2. Oxygen supply to cardiac muscle becomes insufficient.

3. Anaerobic metabolism begins; by-products like lactate, H+, adenosine accumulate.

4. These irritants stimulate nociceptive (pain) receptors in the myocardium.

5. Pain signals are transmitted via sympathetic nerves to spinal segments T1–T5.

6. The brain interprets this as chest discomfort or pain, sometimes radiating.

Claudication (Calf Pain)

1. During walking/exercise, leg muscles demand more oxygen.

2. Atherosclerosis in femoral or iliac arteries limits blood flow.

3. Oxygen delivery is insufficient → anaerobic metabolism begins.

4. Lactic acid and other metabolites build up in calf muscles.

5. These stimulate local pain receptors, causing cramping or aching pain.

6. Pain resolves with rest as oxygen demand decreases and perfusion improves.

Referred Pain

1. Heart pain signals travel through visceral afferents to spinal cord (T1–T5).

2. These spinal segments also receive input from somatic regions (e.g., left arm, neck, jaw).

3. The brain has difficulty localizing visceral pain precisely.

4. It misinterprets the pain as originating from the somatic areas.

5. This results in pain felt in non-cardiac sites, called referred pain.