Although there are efforts to specify use of angina pectoris for chest area discomfort caused by myocardial ischaemia linked with coronary artery disease, there are also known causes like aortic stenosis and hypertrophic cardiomyopathy (Task Force of European Society of Cardiology 395; Fox et al. 3-9).
Angina pectoris is considered stable if it has been occurring for over a number of weeks without any major worsening. Stable angina pectoris normally occur in situations related to increased myocardial oxygen usage. Factors such as ambient temperature and emotional stress can, however, influence symptoms of stable angina pectoris from time to time (Crea & Gaspardone 3767; Christensen 10-11).
On the other hand, unstable angina pectoris is characterized by a suddenly deteriorating pre-existing angina pectoris or abrupt appearance of angina during rest or light work. This is generally caused by atherosclerotic plaque rupture which leads to intracoronary thrombus formation. Some patients experience heightened coronary artery tone or spasm (Fox et al 4).
The pathological condition giving rise to this imbalance is most often the atheromatous narrowing of the coronary arteries. To attain this medical condition, also referred to as stenosis, there must be at least 50 to 70 percent narrowing of the coronary artery. In such decrease in the inner diameter, the coronary blood flow is rendered inadequate to reach the metabolic demands of the heart during strenuous activities or exercise. The impact of stenosis is not limited to the degree of narrowing of the luminal diameter but also on the length and quantity of stenoses present in the coronary artery (Crea & Gaspardone 3767; Christensen 10-11).
Vasoconstriction at the area of the atheromatous narrowing normally results to segmental abnormal function and dilatation of the left ventricle which cause a sudden drop in coronary blood flow. Coronary vasoconstriction, on the other hand, occurs because of curtailed diastolic filling period due to tachycardia and different hormonal actions. Patients with coronary artery disease have the potential risk of acquiring fissuring or rupturing plaque which usually results in platelet aggregation, abnormality of coronary blood flow or thrombotic coronary occlusion. Increased vasomotor tone or spasm arises from the release of substances from activated platelets. This condition crosses the threshold in which a diagnosis of unstable angina pectoris or evolving myocardial infarction is given (Fox et al 5).
It is estimated that 30,000 to 40,000 per 1 million persons suffering from angina pectoris in countries with high number of patients with coronary heart disease. The incidence of angina pectoris is notably twice as high as in middle-aged men as in middle-aged women. This medical condition severely limits the lifestyle of patients such that those of working age are forced to apply for early retirement (Christensen 10; Fox et al. 3-9; Crea & Gaspardone 3767).
Stable angina pectoris symptoms are grouped into four major features. These are in terms of location, association with exercise, characteristics, and