Cardiology: Aortic Disease

• The aorta: The Aorta: Basics | Abdominal Aortic Aneurysm | Thoracic Aortic Aneurysm | Heritable Aortic Disease | After Aortic Dissection | Aortitis and Large-vessel Vasculitis
• Peripheral arterial disease: Peripheral Arterial Disease | Intermittent Claudication | Diagnosis and the ABPI | Managing Claudication | Chronic Limb-threatening Ischaemia | Acute Limb Ischaemia | The Diabetic Foot
• Other arterial disease: Carotid Artery Disease | Other Arterial Problems | Raynaud's Phenomenon
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🩸 Aortic and peripheral arterial disease are part of the same atherosclerotic process that causes heart attacks and strokes. People with leg artery disease have a very high risk of MI and stroke, so treating the whole patient matters as much as treating the legs. This chapter covers aortic aneurysms and inherited aortic disease, leg ischaemia (from claudication to the threatened limb), carotid disease and Raynaud's. Ruptured aneurysm and acute dissection are in the Cardiac Emergencies chapter.
Your four questions for every patient: Is there a threatened limb or a symptomatic aneurysm needing urgent referral? What is the ABPI or aneurysm size? Is cardiovascular risk fully treated (smoking, statin, antiplatelet, BP, diabetes)? Could this be inherited or inflammatory rather than atherosclerotic?

The Aorta: Basics

• Normal size: Ascending aorta under about 4 cm; abdominal aorta about 2 cm.
• Aneurysm: A permanent dilatation to at least 1.5 times normal (abdominal aorta 3.0 cm or more).
• Wall stress rises with diameter and BP (Laplace's law) - so bigger aneurysms grow faster and rupture more, and BP control matters.
• Causes of aortic disease:
  • Atherosclerosis and degeneration (most abdominal aneurysms).
  • Inherited connective tissue disorders (thoracic aneurysms in younger people).
  • Bicuspid aortic valve.
  • Inflammation (aortitis).
  • Infection (mycotic aneurysm).
  • Trauma.
• Aortic syndromes (acute): Dissection, intramural haematoma, penetrating aortic ulcer and rupture - all emergencies.

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Abdominal Aortic Aneurysm

Who: Older men (6 times commoner than in women).

Risk factors:

• Smoking - the strongest; it also doubles the growth rate.
• Hypertension.
• Family history (first-degree relative).
• Atherosclerotic disease.
• COPD.

Diabetes is surprisingly protective.

Clinical pattern:

• Usually asymptomatic - found on screening or incidentally (ultrasound, CT).
• A pulsatile, expansile abdominal mass (hard to feel in obesity).
• Symptomatic (tender, or back or abdominal pain) or ruptured aneurysms are emergencies.
• May embolise to the feet ("trash foot").
• Associated with popliteal aneurysms.

Screening - NHS AAA Screening Programme: A one-off ultrasound for men in their 65th year. Older men can self-refer. Screening reduces AAA deaths by about half.

Surveillance and referral (NICE NG156):

• 3.0–4.4 cm (small): Ultrasound every 12 months.
• 4.5–5.4 cm (medium): Ultrasound every 3 months.
• 5.5 cm or more: Refer to the vascular service, to be seen within 2 weeks.
• Symptomatic or ruptured at any size: Emergency referral.

Repair is offered for:

• Diameter of 5.5 cm or more.
• Growth of more than 1 cm a year.
• Symptoms.

Below 5.5 cm, the risk of rupture is lower than the risk of surgery.

Repair options:

• Open surgical repair - durable. NICE NG156 recommends it for most suitable people with unruptured AAA.
• Endovascular repair (EVAR) - a stent graft placed via the groin. Lower early risk, but needs lifelong imaging surveillance (endoleaks) and more re-interventions. Used when open surgery is unsuitable, and often for rupture.

Medical care - for everyone:

• Stop smoking.
• Statin; antiplatelet (aspirin).
• BP control.
• Exercise.
• Avoid fluoroquinolones where possible (MHRA - increased risk of aneurysm and dissection).

Driving (DVLA, group 1): Tell the DVLA if 6.0 cm or more. Disqualified at 6.5 cm or more.

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Thoracic Aortic Aneurysm

• Causes:
  • Ascending aorta and root: Degeneration with age and hypertension, bicuspid aortic valve, inherited aortopathies (Marfan and others), aortitis, syphilis (historical).
  • Descending aorta: Atherosclerosis; previous dissection.
• Clinical pattern:
  • Usually silent - found on echo, CT or chest X-ray (widened mediastinum).
  • Large aneurysms can cause chest or back pain, hoarseness (recurrent laryngeal nerve), stridor, dysphagia or SVC compression.
  • Aortic regurgitation from root dilatation.
• Surveillance: Echo, CT or MRI at intervals that depend on size and cause.
• Surgery thresholds (ESC 2024, approximate):
  • Ascending aorta about 5.5 cm in most people.
  • Lower (e.g. 5.0 cm) in Marfan syndrome, rapid growth or a family history of dissection.
  • Lower still in Loeys–Dietz syndrome.
• Medical care:
  • Strict BP control - beta-blockers or ARBs.
  • Avoid heavy isometric exercise (heavy weightlifting) and fluoroquinolones.
  • Screen first-degree relatives with echo if it is familial or young-onset.

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Heritable Aortic Disease

• Marfan syndrome (autosomal dominant, FBN1 - fibrillin-1):
  • Body: Tall stature, long arms and fingers (arachnodactyly), joint hypermobility, chest wall deformity, scoliosis.
  • Eyes: Lens dislocation (upwards), severe myopia.
  • Heart and aorta: Aortic root dilatation, dissection, aortic regurgitation, mitral valve prolapse.
  • Other: Spontaneous pneumothorax; dural ectasia.
  • Diagnosis: Ghent criteria; genetic testing.
  • Management:
    • Beta-blocker and/or ARB (losartan) to slow root growth.
    • Yearly imaging.
    • Root surgery at about 5.0 cm (lower with risk factors).
    • Avoid contact and isometric sports.
    • Pregnancy is high-risk - specialist cardio-obstetric care.
• Loeys–Dietz syndrome (TGF-beta pathway genes):
  • Wide-set eyes (hypertelorism), bifid uvula or cleft palate, twisted (tortuous) arteries.
  • Aneurysms throughout the arterial tree.
  • Dissection at smaller sizes - earlier surgery.
• Vascular Ehlers–Danlos syndrome (COL3A1 - type III collagen):
  • Thin, translucent skin; easy bruising.
  • Spontaneous rupture of arteries, bowel or uterus (pregnancy).
  • Avoid invasive procedures where possible.
  • Celiprolol may reduce events.
• Bicuspid aortic valve aortopathy: Dilatation of the ascending aorta. Screen first-degree relatives with echo.
• Turner syndrome: Coarctation, bicuspid valve, dilatation and dissection - use body-size-adjusted thresholds.
• Familial thoracic aortic aneurysm and dissection: Several genes. Screen family members.

💡 Clinical Pearl: A young person with an aortic dissection, or a thoracic aneurysm under 60, should prompt genetic assessment and screening of first-degree relatives - it may save a sibling's life.

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After Aortic Dissection

Acute management is in the Cardiac Emergencies chapter. After the acute phase:

• Type A (ascending, repaired surgically): The remaining aorta often has a persistent dissection flap - lifelong surveillance.
• Type B (descending, often managed medically or with TEVAR):
  • Risk of aneurysmal enlargement of the false channel over months to years.
  • Needs repeated CT or MRI (e.g. at 1, 6 and 12 months, then yearly).
  • Late TEVAR or surgery for growth.
• Lifelong care:
  • Strict BP control (target below about 130/80), usually including a beta-blocker.
  • Avoid heavy straining or lifting.
  • Stop smoking.
  • Avoid fluoroquinolones.
• Look for a cause in younger patients - genetic testing, family screening, cocaine use.

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Aortitis and Large-vessel Vasculitis

• Giant cell arteritis (GCA):
  • Over 50s.
  • As well as headache and visual loss, it can involve the aorta and its branches (large-vessel GCA), causing arm claudication, aneurysm and dissection years later.
  • PET-CT or vascular ultrasound helps diagnosis.
  • Steroids; tocilizumab for relapsing disease.
  • Long-term aortic imaging surveillance.
• Takayasu arteritis:
  • Young women, often of Asian origin.
  • "Pulseless disease":
    • Arm claudication.
    • Absent or weak arm pulses.
    • BP difference between arms.
    • Bruits over the subclavian arteries and aorta.
    • Renovascular hypertension.
    • Fever and fatigue early on.
  • Imaging: MR or CT angiography, PET-CT.
  • Treatment: Steroids plus a steroid-sparing drug (methotrexate, tocilizumab, anti-TNF). Revascularisation when the disease is inactive.
• Other causes of aortitis:
  • IgG4-related disease.
  • Behçet's disease.
  • Spondyloarthritis (aortic regurgitation).
  • Syphilis (tertiary - ascending aneurysm).
• Infected (mycotic) aneurysm:
  • Bacteria (e.g. Salmonella, S. aureus) infect the arterial wall, causing rapid growth and rupture.
  • Fever plus an enlarging, often saccular aneurysm.
  • Prolonged antibiotics plus surgery.

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Peripheral Arterial Disease

Mechanism: Atherosclerotic narrowing or blockage of the arteries to the legs (aorto-iliac, femoral, popliteal and tibial arteries), reducing blood flow - first on exercise, later at rest.

• How common: About 1 in 5 people over 60 have some PAD, but most have no symptoms.
• Risk factors:
  • Smoking - the strongest.
  • Diabetes - distal disease, calcified arteries, poor healing.
  • Hypertension.
  • High cholesterol.
  • CKD.
  • Older age.
• Why it matters: PAD is a marker of widespread atherosclerosis. Most people with PAD die from MI or stroke, not from their legs - so cardiovascular risk reduction is central.
• The spectrum: Asymptomatic, then intermittent claudication, then chronic limb-threatening ischaemia (rest pain, ulcers, gangrene). Separately, acute limb ischaemia.

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Intermittent Claudication

• Symptoms:
  • Cramping pain in the calf (or thigh or buttock) brought on by walking a predictable distance.
  • Relieved within minutes by standing still.
  • The level of pain points to the level of disease:
    • Calf - femoral or popliteal disease.
    • Thigh or buttock - aorto-iliac disease.
• Leriche syndrome (aorto-iliac occlusion): Buttock claudication, erectile dysfunction and absent femoral pulses.
• Signs:
  • Weak or absent pulses.
  • Cool, pale or shiny skin; hair loss.
  • Slow capillary refill.
  • Bruits.
  • Buerger's test - pallor on raising the leg, then redness (rubor) on hanging it down.
• Differential diagnosis - spinal stenosis ("neurogenic claudication"):
  • Pain with walking and standing.
  • Relieved by sitting or bending forward, not just stopping.
  • Variable distance.
  • Normal pulses.
• Outlook: Most people with claudication stay stable or improve with exercise and risk factor control. Only about 1–2% a year progress to limb-threatening ischaemia - but cardiovascular death rates are high.

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Diagnosis and the ABPI

• Ankle–brachial pressure index (ABPI): The ankle systolic pressure (by Doppler) divided by the higher arm systolic pressure.
  • 1.0–1.3 - normal.
  • Below 0.9 - PAD.
  • 0.5–0.9 - typical of claudication.
  • Below 0.5 - severe disease, possible limb-threatening ischaemia.
  • Above 1.3 - incompressible, calcified arteries (diabetes, CKD, older age). The ABPI is falsely reassuring - use toe pressures or toe–brachial index, and Doppler waveforms.
• Exercise ABPI: A fall after exercise confirms PAD when the resting ABPI is borderline.
• Duplex ultrasound: The first-line imaging test, to show the site and severity before planning revascularisation (NICE CG147).
• CT or MR angiography: For planning intervention if duplex is not enough.
• Cardiovascular risk assessment:
  • Lipids, HbA1c, U&E.
  • BP.
  • ECG.
  • Smoking status.

💡 Clinical Pearl: Before applying compression bandaging for a leg ulcer, always check the ABPI - compression on an ischaemic leg can cause gangrene. Compression is generally safe if the ABPI is 0.8 or more.

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Managing Claudication

Treat cardiovascular risk (for everyone with PAD):

• Stop smoking - the most important step for the legs and the heart.
• High-intensity statin (atorvastatin 80 mg).
• Antiplatelet: Clopidogrel 75 mg daily is preferred (NICE TA210). Aspirin if clopidogrel is unsuitable.
• Low-dose rivaroxaban (2.5 mg twice daily) plus aspirin reduces cardiovascular and limb events in people with PAD at high risk of ischaemic events and low bleeding risk (NICE TA607).
• BP control (ACE inhibitors or ARBs are suitable; beta-blockers are not contraindicated).
• Diabetes control; foot care.

Improve walking:

• Supervised exercise programme - first-line (NICE CG147). About 2 hours a week for 3 months, walking to near-maximal pain. It can roughly double walking distance.
• Naftidrofuryl oxalate (a vasoactive drug): Consider if exercise has not helped enough and the patient prefers not to have revascularisation. Review after 3–6 months and stop if there is no benefit.

Revascularisation - if symptoms still limit lifestyle despite exercise and risk factor treatment:

• Angioplasty, with or without stenting - particularly for aorto-iliac disease.
• Bypass surgery - e.g. femoro-popliteal bypass with the patient's own vein.

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Chronic Limb-threatening Ischaemia

Definition: PAD with:

• Ischaemic rest pain - usually in the forefoot, worse at night and on elevation, eased by hanging the leg over the bed or sleeping in a chair.
• Tissue loss - non-healing ulcers or gangrene.
• Usually for more than 2 weeks.

Typically the ABPI is below 0.5, or ankle pressure is below about 50 mmHg, or toe pressure is below about 30 mmHg.

Why it matters: Without revascularisation, many patients lose the leg, and mortality is high.

Management:

• Urgent referral to the vascular team.
• Imaging (duplex, CT or MR angiography) and revascularisation where possible - endovascular or surgical bypass.
• Treat infection (often with diabetic foot disease) and offload pressure.
• Analgesia - often opioids are needed.
• Full cardiovascular risk management.
• Amputation when revascularisation is not possible or fails, or for unsalvageable tissue or uncontrolled infection.
• Rehabilitation; palliative care for frail patients.

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Acute Limb Ischaemia

Mechanism: A sudden loss of blood supply to a limb. Muscle and nerve start to die within about 6 hours - a vascular emergency.

• Causes:
  • Embolus - usually from the heart (AF, recent MI with LV thrombus, endocarditis) or an aneurysm. Sudden onset, often in a previously normal limb.
  • Thrombosis on existing PAD, a bypass graft or a stent - often a slower onset, with a history of claudication.
  • Also popliteal aneurysm thrombosis, dissection, trauma, and drugs injected into an artery.
• The "6 Ps":
  • Pain.
  • Pallor.
  • Pulselessness.
  • Perishing cold.
  • Paraesthesia.
  • Paralysis.
  Sensory loss and muscle weakness mean the limb is immediately threatened. Fixed mottling and a hard, tender calf suggest it may be unsalvageable.
• Management:
  • Immediate vascular referral.
  • IV unfractionated heparin; analgesia; fluids.
  • Revascularisation - surgical embolectomy (embolic), catheter-directed thrombolysis or thrombectomy, or bypass.
  • Watch for reperfusion injury - compartment syndrome (fasciotomy), hyperkalaemia, rhabdomyolysis and AKI.
  • Afterwards: Find the source (ECG, echo) - long-term anticoagulation for AF or other cardiac emboli.

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The Diabetic Foot

Why diabetic feet are at risk - a combination of:

• Neuropathy - loss of protective sensation, so injuries go unnoticed; deformity; dry skin.
• Ischaemia - distal PAD, calcified arteries.
• Infection - poor immune response.

Assessment - at least yearly (NICE NG19):

• Inspect feet and footwear.
• Check sensation (10 g monofilament) and pulses.
• Classify risk (low, moderate, high, active).

Active foot problem - ulcer, spreading infection, critical ischaemia, gangrene, suspected Charcot foot: Refer to the multidisciplinary foot care service within 1 working day.

Diabetic foot infection:

• Antibiotics per severity.
• Probe to bone or X-ray or MRI for osteomyelitis.
• Urgent surgical review for abscess, gas or necrotising infection.

Charcot neuroarthropathy:

• A hot, red, swollen foot in a neuropathic patient, often with little pain - mistaken for cellulitis or gout.
• Bone and joint destruction can collapse the foot.
• Offload immediately (non-removable cast) and get an urgent specialist review. MRI shows early changes.

Prevention: Education, podiatry, proper footwear, glucose control, stopping smoking.

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Carotid Artery Disease

• Symptomatic carotid stenosis (TIA, minor stroke or amaurosis fugax in that territory):
  • Carotid endarterectomy for 50–99% stenosis (NASCET), ideally within 7 days of symptoms (NICE NG128).
  • Carotid stenting is an alternative in selected patients.
  • See the Stroke Emergencies chapter.
• Asymptomatic carotid stenosis (found on scans or bruits):
  • Best medical treatment - statin, antiplatelet, BP control and smoking cessation - is the mainstay.
  • The annual stroke risk is now low (about 1% or less).
  • Intervention is considered only in selected people with severe stenosis and features suggesting higher risk.
• Carotid bruits: Poor predictors of stenosis - investigate only if there are symptoms or other indications.
• Subclavian steal: Narrowing of the subclavian artery before the vertebral artery. Arm exercise "steals" blood from the brainstem, causing dizziness. There is a BP difference between the arms.

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Other Arterial Problems

• Popliteal artery aneurysm:
  • The commonest peripheral aneurysm - often bilateral, and associated with AAA (screen the aorta).
  • A prominent popliteal pulse.
  • Risk of thrombosis or emboli causing acute limb ischaemia.
  • Repair if large (e.g. 2–3 cm or more) or containing thrombus.
• Thromboangiitis obliterans (Buerger's disease):
  • Young male heavy smokers (also cannabis).
  • Inflammation and blockage of small and medium arteries of the hands and feet.
  • Rest pain, ulcers, gangrene of fingers and toes; Raynaud's; superficial thrombophlebitis.
  • Complete cessation of all tobacco is the only effective treatment - otherwise amputations follow.
• Popliteal artery entrapment: Young athletes with calf claudication - the artery is compressed by the calf muscle.
• Fibromuscular dysplasia: Young to middle-aged women - renal and carotid arteries ("string of beads"); hypertension, dissection, SCAD.
• Mesenteric and renal artery disease: See the Gastroenterology Emergencies and Hypertension chapters.
• Thoracic outlet syndrome (arterial): Compression of the subclavian artery by a cervical rib - arm ischaemia, emboli to the fingers.

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Raynaud's Phenomenon

Mechanism: Episodic spasm of the finger (and toe) arteries in response to cold or stress, with colour changes:

• White (ischaemia).
• Then blue (cyanosis).
• Then red (reperfusion), with tingling or pain.

Primary Raynaud's (most cases):

• Young women.
• Symmetrical.
• No ulcers.
• Normal nailfold capillaries.
• Negative autoantibodies.
• Benign.

Secondary Raynaud's - suspect if:

• Onset after 30–40.
• Asymmetrical.
• Digital ulcers or pits.
• Abnormal nailfold capillaries.
• Features of connective tissue disease.

Causes of secondary Raynaud's:

• Systemic sclerosis (present in over 90%).
• SLE; Sjögren's; myositis.
• Vibration tools ("vibration white finger").
• Drugs - beta-blockers, ergots, chemotherapy.
• Cervical rib.
• Cryoglobulinaemia; hypothyroidism.

Tests (if secondary is suspected): FBC, ESR, ANA, ENA (anti-centromere, anti-Scl-70), TFTs, and nailfold capillaroscopy.

Management:

• Keep warm - gloves, hand warmers, whole-body warmth.
• Stop smoking.
• Avoid triggers and culprit drugs.
• Nifedipine MR if frequent or severe. Alternatives: other calcium channel blockers, losartan, fluoxetine, sildenafil.
• Secondary Raynaud's with ulcers: Specialist care - IV iloprost, bosentan (to prevent new ulcers), botulinum toxin.
• Critical digital ischaemia (a white, painful finger that doesn't recover): Urgent admission.

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Drug Reference Table

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Spot the Diagnosis

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Exam-style Scenarios

1. A 71-year-old ex-smoker has a 5.8 cm AAA on ultrasound. He has no symptoms.
Answer: AAA of 5.5 cm or more - refer to the vascular service, to be seen within 2 weeks.

• Fitness assessment for repair (open or EVAR).
• Statin, antiplatelet, BP control.
• Tell him to seek emergency help with abdominal or back pain or collapse.

2. A 66-year-old smoker has calf pain after walking 150 m. ABPI is 0.65; duplex shows superficial femoral artery occlusion.
Answer: Intermittent claudication.

• Smoking cessation.
• Atorvastatin 80 mg and clopidogrel 75 mg.
• BP and diabetes control.
• Supervised exercise programme for 3 months.
• Revascularisation only if still lifestyle-limiting.

3. A 78-year-old woman with AF, not anticoagulated, has a sudden painful, cold, white right leg with no pulses below the femoral. She has reduced sensation in her toes.
Answer: Acute embolic limb ischaemia - immediately threatened.

• IV heparin; analgesia; emergency vascular referral for embolectomy.
• Watch for compartment syndrome after reperfusion.
• Long-term anticoagulation for AF.

4. A 24-year-old man has a family history of sudden death from aortic dissection. He is tall, with long fingers and a high-arched palate.
Answer: Suspected Marfan syndrome.

• Echo (aortic root), eye examination, genetic testing.
• Beta-blocker or ARB if the root is dilated.
• Advice on sport.
• Screen relatives.

5. A district nurse wants to start compression bandaging for a leg ulcer in a 75-year-old man with diabetes. ABPI is 1.4.
Answer: The ABPI is unreliable (calcified arteries). Do not assume it is safe.

• Check toe pressures and Doppler waveforms.
• Vascular referral if there is ischaemia.

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Key Points

• AAA screening: one-off ultrasound for men in their 65th year.
• AAA surveillance: 3.0–4.4 cm yearly; 4.5–5.4 cm every 3 months; 5.5 cm or more refer within 2 weeks; symptomatic means emergency.
• Repair at 5.5 cm or more, growth over 1 cm a year, or symptoms. Smoking doubles growth.
• Thoracic aneurysms in the young: think Marfan, Loeys–Dietz, vascular Ehlers–Danlos, bicuspid valve - screen relatives.
• Takayasu: young women, pulseless arms, unequal BPs. Large-vessel GCA in the over-50s.
• PAD is a marker of high MI and stroke risk - stop smoking, atorvastatin 80 mg, clopidogrel, BP and diabetes control.
• ABPI below 0.9 is PAD; below 0.5 is severe; above 1.3 means calcified vessels (check toe pressures).
• Claudication: supervised exercise first; revascularise only if still lifestyle-limiting.
• Rest pain, ulcers or gangrene (CLTI): urgent vascular referral.
• Acute limb ischaemia (6 Ps): heparin and emergency revascularisation; sensory or motor loss means the limb is threatened now.
• Diabetic foot: active problems go to the MDT foot service within 1 working day; think Charcot.
• Raynaud's: secondary if late onset, ulcers or autoantibodies - look for systemic sclerosis.

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Guidelines and Further Reading

• NICE NG156: Abdominal aortic aneurysm - diagnosis and management
• NHS AAA Screening Programme
• NICE CG147: Peripheral arterial disease - diagnosis and management
• NICE TA607: Rivaroxaban for preventing atherothrombotic events in coronary or peripheral artery disease
• NICE NG19: Diabetic foot problems - prevention and management
• ESC Guidelines for the management of peripheral arterial and aortic diseases (2024)
• Global Vascular Guidelines on chronic limb-threatening ischaemia
• BNF - for current doses

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