Coronary artery disease (CAD) is caused by atheroma. It is the leading cause of death in the UK and results from a combination of genetic and lifestyle factors. Irreversible (fixed) risk factors include:

• Increasing age
• Gender: men are at greater risk than premenopausal women
• Family history of CAD.

Potentially reversible (modifiable) risk factors for CAD include:

• Cigarette smoking
• High blood cholesterol level: low density lipoproteins (LDL) are associated with a high risk of CAD, whilst high density lipoproteins (HDL) appear to be anti-atherogenic.

• Hypertension
• Diabetes mellitus
• Obesity and lack of exercise.

Clinical Features:

The clinical presentation of CAD is reflective of the degree and duration of impaired coronary blood flow. Features include dizziness, shortness of breath, decreased exercise tolerance, chest pain (angina pectoris) and sometimes sudden death due to a catastrophic myocardial infarction (irreversible damage to cardiac muscle). Xanthelasmata may signify hyperlipidaemia. A chronically reduced blood supply to the myocardium progressively damages the heart muscle and may lead to cardiac arrhythmias and cardiac failure.

Clinical Signs:

Distended neck veins (Figure 1.1) due to increased jugular venous pressure (JVP), are a classic sign of right-sided cardiac failure, although it may also be seen in hypervolaemic states, superior vena cava obstruction and cardiac tam- ponade. The causes of cardiac failure may also include cardiac valvular disease

and chronic obstructive pulmonary disease. Pitting oedema may be demon- started by applying firm digital pressure over the lower legs or ankles.

Hyperlipidemia may predispose to CAD [sometimes premature]. The com- bination of corneal arcus with xanthelasma (Figure 1.2) should suggest the possibility of hyperlipidemia. This is especially the case in young people where autosomal dominant familial hypercholesterolemia may be the underlying cause. Other causes of xanthelasma (but not corneal arcus) include hypothy- roidism and primary biliary cirrhosis.

It is thought that if an individual has diagonal creases (Figure 1.3) on both ear lobes, there may be some benefit in undergoing screening to exclude the possibility of cardiovascular disease. The actual cause of earlobe creasing is unknown but it is possible that chronic circulatory problems allow the vascular bed in the earlobe to collapse and the telltale earlobe crease to appear. In one study the presence of a unilateral earlobe crease was associated with a 33% increase in the risk of a myocardial infarct; the risk increased to 77% when the earlobe crease appeared bilaterally.

Vertex baldness also appears to be a valid marker for an increased risk of cardiovascular disease, particularly when clustered with other factors such as hypertension or hypercholesterolemia. Other factors include being short and having an ‘apple-shaped’ physique.

The American Academy of Periodontology recently showed that people with periodontal disease are 200–300% more likely to experience a heart attack than those with healthy periodontium, making periodontal disease a possible risk for cardiovascular disease.

Atheroma, trauma, orbital apex disease, cavernous sinus disease, aneurysm of the posterior communicating artery, raised intracranial pressure and diabetes (often a partial palsy) are all possible causes of a third nerve (oculomotor) palsy

(Figure 1.4). The third nerve supplies all of the muscles of the orbit apart from the superior oblique (IV cranial nerve) and the lateral rectus (VI). Unopposed action of these muscles leads to the eye pointing ‘down and out’. It is also the muscle that raises the eyelid (levator palpebrae), the ciliary muscle and constric- tor of the pupil, hence there is a complete ptosis (drooping of the eyelid) and dilatation of the pupil. The left eye would be looking inferolaterally (‘down and out’) giving a divergent squint and the pupil would be dilated (complete paralysis) or normal (‘partial third nerve palsy’).

Diagnosis

• Clinical history.
  • Electrocardiogram (ECG): the resting ECG may be normal and so an exer- cise ECG is also indicated.
  • Myocardial perfusion scans (thallium-201) show ischaemic areas as ‘cold spots’ during exercise.
  • Coronary angiography assesses the coronary artery anatomy and patency.

Management

Emphasis should be on lifestyle changes with the primary aim to prevent, or reduce progression of, coronary atheroma. These include:

• Dietary modification: reduction of cholesterol and saturated fat intake
  • Regular exercise
  • Weight loss
  • Smoking cessation.

Pharmacological measures for the management of CAD include:

• Anti-platelet drugs (aspirin or clopidogrel)
  • Anti-hypertensive treatment with beta-blockers (atenolol), diuretics (furo- semide) and angiotensin converting enzyme (ACE) inhibitors (enalapril)
  • Cholesterol lowering drugs such as statins (simvastatin)
  • Good control of blood glucose levels if diabetic.

When CAD is extensive and an individual’s symptoms are worsening despite general measures and optimal medical management, cardiac revascularisation techniques that should be considered include:

• Coronary angioplasty: stents may be placed percutaneously (percutaneous coronary intervention [PCI]), to re-establish coronary blood flow and

improve myocardial perfusion

• Coronary artery bypass grafts (CABGs) to bridge severe obstructions in the coronary blood vessels.