2.6 Atherosclerosis beyond coronary arteries

Peripheral Arterial Disease (PAD)

• Definition: Atherosclerosis of the arteries supplying the extremities (commonly lower limbs) → impaired blood flow

• Forms:

  • Chronic limb ischaemia: develops over time; ranges from asymptomatic to critical limb ischaemia

  • Acute limb ischaemia: sudden drop in perfusion → limb threat

Signs and symptoms

• Asymptomatic: ABI <0.9 without symptoms

• Intermittent claudication:

  • Cramp/ache/tightness in muscles distal to stenosis (commonly calf)

  • Triggered by walking, uphill, rushing → relieved by rest

  • Claudication distance = severity marker

• Chronic limb-threatening ischaemia (CLTI):

  • Rest pain: >2 weeks, worse at night/elevation, relieved by dependency

  • Ulceration, gangrene

• Acute limb ischaemia: “6 P’s” — Pain, Pallor, Pulselessness, Paraesthesia, Paralysis (late), Poikilothermia (cold)

• Clinical signs: Cool limb, hair loss, prolonged cap refill, absent pulses, bruits, neuropathic changes.

Pathophysiology

• Atherosclerosis → intimal plaque → Lumen narrowing (Stenosis) or complete occlusion

• ↓ perfusion pressure → inability to meet metabolic demands:

  • At rest: only in severe disease (rest pain)

  • On exertion: increased demand → ischaemic pain (claudication)

• Gradual onset → collateral circulation may delay symptoms

• Acute limb ischaemia: embolism (carotid, heart), plaque rupture, thrombosis

Cerebrovascular atherosclerosis

• Cause: Mainly atherosclerosis at carotid bifurcation → plaque rupture or thrombus → emboli to brain

• Presentations:

  • Stroke (CVA): Focal neurological deficit >24h (80% ischaemic)

  • Transient Ischaemic Attack (TIA): Focal deficit<24h; high early stroke risk (up to 10% in 7 days)

  • Symptoms:

    • Hemiparesis (Weakness affecting one side of the body)

    • Hemisensory (reduced or absent sensation on one side of the body) loss

    • Dysphasia (Impaired ability to understand or produce language)

    • Dysarthria (Slurred or unclear speech due to weakness or poor coordination of the speech muscles)

    • Amaurosis fugax (Sudden, temporary loss of vision in one eye, usually from reduced blood flow to the retina), neglect

• Investigations:

  • Duplex ultrasound (first line)

  • CTA, MRA for anatomy

  • DSA = gold standard (invasive)

• Management:

  • Best medical therapy (BMT) for all: stop smoking, antiplatelet, statin, BP <140/90, HbA1c ~6.5% if diabetic

  • Surgery: Carotid endarterectomy if symptomatic ICA stenosis >50% (within 2 weeks, ideally 48h)

  • Stenting: Higher peri-op stroke risk; for select cases only

Mechanism of claudication

1. Exercise → ↑ O₂ demand in muscle.

2. Stenosed artery → flow limitation (can’t increase supply).

3. Ischaemia → anaerobic metabolism → lactate, adenosine, potassium → pain.

4. Rest → demand ↓ → pain resolves rapidly.

Management overview (PAD & cerebrovascular atherosclerosis)

1. Best Medical Therapy (all patients)

• Smoking cessation (most important modifiable factor; OR ~4–5).

• Control diabetes (HbA1c ~6.5%).

• BP control (<140/90; reduces stroke, MI, PAD progression).

• Lipid lowering (statins for all PAD/CVD patients; LDL <2.0 mmol/L).

• Antiplatelets (aspirin/clopidogrel; ↓ CV events by ~23%).

• Exercise therapy (supervised treadmill for claudication).

2. Revascularisation (if lifestyle‑limiting claudication, CLTI, or acute limb ischaemia)

• Endovascular: Balloon angioplasty ± stent (drug‑eluting or bare metal), atherectomy, intravascular lithotripsy.

• Surgical: Endarterectomy, bypass grafts (vein > prosthetic), amputation if non‑salvageable.

• Carotid disease: CEA preferred over stenting except in special situations.