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.