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Any increase in oxygen demand beyond the capacity of the compromised coronary circulation results in precipitating angina pain. Such a situation may arise with a variety of conditions including physical exertion or after a heavy meal or with an emotional upset.Cessation of the activity arousing increase in oxygen demand by the heart leads to prompt cessation of pain. Nitroglycerin is also effective in providing rapid relief from the pain. What is often not realized is that angina is commoner in women than in men. Also, atypical symptoms are commoner in women. Prognosis too is worse in women partly because angina occurs at a later age in women with resultant worse outcome and partly because atypical symptoms are commoner in them which often delay diagnosis. Both the location of pain and its character vary in different cases. Rather than pain on the left side of the chest, the commonest site of pain is the centre of the chest in the sternal area. The pain may radiate to the left side of the chest or to the jaw or to the left arm and down to the fingers along the inner side of the arm. The pain may also radiate to the back or to the upper abdomen. It may be described as of a pressure or heaviness or as if someone is squeezing the chest. Other people report a feeling of discomfort rather than pain, as if they are choking. It is usually not described as being sharp or like the pricking of a pin. Quite a few people with angina will place their clenched right fist over the sternum to demonstrate the location and type of pain. This is known as Levine sign. The pain lasts for a period usually between a minute to may be 5 minutes or so and is often precipitated by a specific activity such as physical exertion or a heavy meal or an emotional upset. Exposure to cold is another common aggravating factor. Especially classical is the onset of pain with walking uphill in cold weather after a heavy meal. The pain subsides shortly after cessation of the activity precipitating it or after administration of nitroglycerin.To be noted is that the pain does not change with breathing or movements of the chest or change in position or with coughing. The above description of angina pain applies to most patients. However, there are many exceptions with regard to symptoms and any pain over the chest, abdomen, head and neck and the upper limbs brought on by exertion and subsiding with rest needs evaluation to exclude angina as the cause. Some of the conditions needing to be differentiated from angina are oesophageal pain from reflux of acid into the food-pipe, asthmatic attacks, anxiety, musculoskeletal pain, etc. Angina is not a heart attack. Rather both entities are part of the spectrum of ischaemic heart disease. In a heart attack or myocardial infarction the affected heart muscle is deprived of blood for a more extended period of time thereby resulting in its death. In angina, on the other hand, the lack of oxygen is temporary and the muscle recovers. However, angina is a warning that circulation to the heart is compromised, the commonest cause being narrowed coronary arteries because of atherosclerosis. Angina not only needs to be treated for relief of symptoms but even more importantly to prevent progression to irreversible changes as manifested by a myocardial infarction or even sudden death. While all angina patients are at higher risk for a heart attack, a subset has a particularly high risk. These are the people with what is termed unstable angina.Most people with angina have quite stable symptoms. They know how much exertion they can do without bringing on pain and using nitroglycerine before any additional exertion becomes almost second nature to them. In unstable angina, however, symptoms may occur at rest, may last for longer than a few minutes, may not respond rapidly to nitroglycerine and may show an incremental pattern with increasing severity, frequency or duration. Symptoms suggestive of unstable angina require early and aggressive treatment to prevent development of complications such as myocardial infarction or heart rhythm disturbance.The history is often highly suggestive in people with angina. During an angina episode, careful examination may reveal some abnormalities. However, clinical examination between attacks is usually normal except for abnormalities related to risk factors. Major risk factors for ischaemic heart disease have been well identified and include non-modifiable factors such as age, sex, race and family history as well as modifiable factors such as hypertension, diabetes, elevated LDL cholesterol, low HDL cholesterol, high triglycerides, obesity, lack of regular physical exercise, smoking and stress. Increasing age is probably the most important risk factor but there is nothing that can be done about it. Women enjoy substantial protection from ischaemic heart disease till menopause when their menstrual cycles cease. Many of the modifiable risk factors are interrelated with obesity, lack of regular physical exercise, high blood pressure, type-2 diabetes often occurring in a cluster pattern. Smoking is a particularly undesirable habit with wide ranging deleterious effects on one s health and there is really no justification for tobacco use in any form. Most of the modifiable risk factors are highly amenable to control by lifestyle changes combined with medications where indicated. A majority of cases of angina are due to atherosclerotic changes in the coronary arteries. This is a complex process in which there is thickening of the arterial wall associated with deposition of fatty substances including cholesterol and triglycerides along with inflammation. These deposits are called atherosclerotic plaques. Atherosclerosis results in narrowing of the internal diameter or lumen of affected blood vessels. The capacity to distend in response to metabolic demands is also hampered as elasticity is reduced. Atherosclerosis is a process that affects arteries, with special predilection for some of the larger arteries such as the coronary arteries supplying the heart, internal carotid arteries and their branches the cerebral arteries the brain, femoral arteries the lower limbs and renal arteries the kidneys. Areas of the inner lining of arteries under which atherosclerotic plaques are deposited may become irregular or ulcerate with formation of a clot or thrombus. This thrombus can block the lumen of the artery substantially thereby interfering with circulation beyond this block. If the affected artery is the sole or major source of blood supply to a tissue, that tissue suffers ischaemia and possibly infarction or death.Another possible course of events is for the thrombus to shear off from the site where it forms, and be carried along with blood to a smaller branch where it is too big to pass further. This process is called thromoembolism. A third way for atherosclerosis to block the artery is by the bulk of the deposits itself. A critical stage is usually reached when about 80 per cent of the lumen is blocked when effective circulation through it is no longer possible. All three mechanisms serve to impede circulation through the affected artery. If the affected artery is a coronary artery or one of its branches, the resultant compromise of circulation may cause angina or myocardial infarction. A special type of angina is called Prinzmetal angina. Anginal pain occurs at rest and while there may be underlying or associated atherosclerosis, the immediate event is spasm of the coronary artery. In fact, even coronary angiography may fail to detect any block in such patients. Cigarette smoking and cocaine use are amongst the predisposing factors causing this type of angina. Another condition in which coronary arteries may be normal on angiography is called syndrome X. Angina occurs due to dysfunction of smaller branches of coronary arteries and arterioles which are even smaller. The condition is commoner in women past menopause. Although problems in coronary arteries, usually atherosclerosis, are by far the leading cause of angina, undue enlargement of heart muscle with relatively healthy coronary arteries may also cause angina. This is because a relatively normal circulation may no longer be adequate to satisfy increased oxygen demand of higher cardiac muscle bulk. 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