Angina pectoris is the name given to episodes of chest pain caused by myocar- dial ischemia secondary to CAD. Angina affects around 1% of the adult population and its prevalence rises with increasing age. The severity and prog- noses of angina depends upon the degree of coronary artery narrowing and has a varied clinical presentation. The average annual mortality rate in the UK is about 4% per year.
Angina is often unmistakable because the pain is precipitated by physical
exertion, particularly in cold weather, and is relieved by rest. Affected individuals
may describe a sense of tightness, heaviness, compression or constriction of the chest, sometimes radiating to the left arm or jaw. Emotion (anger or anxiety) and stress (fear or pain) can induce angina by leading to the release of
catecholamines (epinephrine [adrenaline] and norepinephrine [noradrenaline]) from the adrenal cortex. These hormones result in an increased heart rate (tachycardia), a raised blood pressure (reactive hypertension), and vasoconstriction of the coronary circulation. Consequently an increased cardiac workload is accom- panied by a paradoxical drop in blood flow and myocardial ischemia occurs – resulting in angina.
Variants of angina include:
- Stable angina: pain only on exertion and relieved in a few minutes by rest and sublingual glyceryl trinitrate (GTN)
- Decubitus angina: pain on lying down
- Vasospastic (variant or Prinzmetal) angina: caused by coronary artery spasm
- Acute coronary syndrome (unstable angina): angina at rest or of sudden onset with a rapid increase in severity. This is due to a transient subtotal
obstruction of a coronary vessel and is a medical emergency
- Cardiac syndrome X: clinical features of angina but normal coronary arter- ies on angiogram. It is thought to be due to a functional abnormality of the coronary microcirculation.
Some drugs such as nicorandil used in the management of unstable angina, can produce severe oral ulceration (Figure 1.5).
The diagnosis of angina is primarily a clinical one. Physical examination and investigations may be normal. The individual’s risk factors for CAD should be carefully assessed.
Investigations may include:
- Resting electrocardiogram (ECG): during pain there may be ST segment depression with a flat or inverted T-wave. The ECG is usually normal
between episodes of angina
- Exercise ECG testing: positive in approximately 75% of people with severe CAD
- Myocardial perfusion scans (thallium-201): to highlight ischemic myocardium
- Coronary angiography: to assess coronary blood flow in diagnostically challenging cases. Occasionally gastro-esophageal reflux disease (GORD) and chest wall disease may mimic angina.
Risk factors for CAD (cigarette smoking, physical inactivity, obesity,
hypertension, diabetes mellitus, hypercholesterolemia) should be identified and cor- rected. Prognostic therapies for angina include:
- Aspirin: inhibits platelet aggregation by preventing the synthesis of throm- boxane A2
- Glycoprotein IIb/IIIa receptor inhibitors: prevent adherence of fibrinogen to platelets and reduce thrombus formation, and are used in ‘high-risk’
individuals and patients with acute coronary syndrome
- Lipid-lowering drugs (e.g. statins): have been shown to lower mortality rates in patients with CAD.
During acute episodes of angina, pain is relieved by administering oxygen, sublingual GTN and reducing anxiety. When angina occurs more frequently long-acting nitrates (isosorbide mononitrate), b-adrenergic blocking drugs (atenolol), and calcium antagonists (amlodipine) are used to reduce cardiac oxygen demands. For angina that fails to respond to medical measures, cardiac revascularization techniques should be considered:
- Percutaneous transluminal coronary angioplasty (PTCA): stents (miniature wire coils) may be inserted into the coronary arteries to re-establish blood flow
- Coronary artery bypass grafts: to bridge severe obstructions in patients with extensive CAD.
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.
- Diabetes mellitus
- Obesity and lack of exercise.
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.
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’).
- 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.
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.
Atheroma (atherosclerosis) is character rised by the accumulation of cholesterol and lipids in the arterial intimal surface. Atheroma has a patchy distribution and, depending on the site and extent of disease, can give rise to a variety of clinical presentations (Table 1.1). A platelet–fibrin thrombus (clot) may form, break up and travel in the bloodstream (thrombo-embolism) with potentially life-threatening consequences. Alternatively, atheromatous plaques may rupture and ‘heal’ spontaneously.
Listen to pronunciation. A type of disease that affects the heart or blood vessels. The risk of certain cardiovascular diseases may be increased by smoking, high blood pressure, high cholesterol, unhealthy diet, lack of exercise, and obesity.
Includes Diseases: Heart failure
Risk Factors: Obesity; Hypertension