This term is most often used to describe the signs and symptoms associated with acute myocardial infarction, the sudden interruption or inadequacy of blood flow (ischaemia) to sections of the heart itself. If the inadequate blood flow persists for several minutes it can cause the affected section of heart muscle to die. The dead cells become replaced with scar tissue, and the dead area is known as an infarct. The immediate problem, however, is that the effectiveness of the heart's pumping action is abruptly reduced. Loss of function in any part of the heart will obviously reduce the strength of the pump. But a potentially greater threat is that damage, even to a small area, can induce within it erratic, spontaneous electrical activity. (Similar, but not dangerous, phenomena are sometimes seen in limb muscles when they twitch involuntarily if they or their associated nerve fibres, are underperfused with blood.) Since each heart cell is in electrical contact with its neighbours, the erratic activity is conducted to other, non-infarcted regions. If the electrical disturbance is serious enough, it can cause cardiac arrest.
Heart attack is a distressingly common clinical problem in many (but not all) Western developed societies. The incidence in the UK is about 150 000 per annum, of which nearly half prove fatal. (This can be judged against a total UK mortality of about half a million per annum.) The major cause of myocardial infarction in Western society is progressive coronary artery disease. The coronary arteries are the first blood vessels to branch from the aorta (the large artery leaving the heart). Although only two coronary arteries arise directly from the aorta, these branch extensively, forming an intricate network of vessels supplying all areas of the heart muscle with oxygenated blood. The arrangement of this ‘plumbing’ system makes the heart peculiarly vulnerable to interruptions of supply. In most other tissues, there are significant alternative routes by which arterial blood can reach any one region; so-called collateral supplies. Thus the cells of the heart are like leaves on a tree; they are at the end of the furthest twigs of the supply system. By contrast, in other tissues, the supply is more like a road network; very few houses are at the end of cul-de-sacs, most can be reached from several directions. If the flow of blood is stopped in one of the branches in our ‘tree’ analogy, the heart cells downstream, beyond the block, will inevitably suffer. (It is sobering to note that many other mammalian species do not have their hearts ‘plumbed’ so extensively this way. But the pig and several breeds of dog do suffer the risks of this ‘design flaw’ much like us.)
Typical signs of coronary artery disease include a painful feeling of ‘tightness’ in the chest or ‘heaviness’ brought on by physical effort, heavy meals, cold weather, or emotional stress. The sensation starts behind the breast bone and radiates across the chest. The pain is frequently confused with that of severe indigestion. Frequently, it is associated with a leaden feeling in the arms. Occasionally the sensation may be perceived in more unusual sites (e.g. in the jaws or teeth). An abnormal sensation of breathlessness on effort or at rest can occur, known as dyspnoea. Patients often feel cool, yet clammy or sticky to touch, and sometimes have dilated hand veins. If the symptoms are relieved by rest then this tends to indicate a serious narrowing of the coronary artery circulation (stable angina pectoris) rather than actual blockage. If the symptoms occur whilst at rest, or are not relieved by rest, they could indicate a heart attack. The severity of the symptoms is often indicative; patients may report a sense of impending doom, the chest pains are severe, vice-like, and persistent; the attack itself may provoke collapse, often without warning.
Coronary artery disease, with its ultimate sequel of myocardial infarction, is almost always due to atherosclerosis. The initiating event in the development of atherosclerosis is thought to be damage to the layer of cells lining the inner surface of the artery. Such injury triggers blood-borne factors to stimulate proliferation of cells within the wall of the artery and deposition of protein and cholesterol, known as an atheromatous plaque, that narrows the artery. In the majority of cases, the cracking of the atheromatous plaque causing a sudden blockage of the artery is the event which results in progression from atherosclerosis to infarction. Only very rarely is a myocardial infarction produced by other factors (e.g. a spasm within artery). It should be clear that if ejection of blood from the heart is suddenly reduced for any reason, the heart itself will receive an inadequate supply which can precipitate heart attack. In this category comes a variety of causes such as drug overdose, major haemorrhage, electric shock, and so on.
Treatment of coronary artery disease, thereby reducing the risk of heart attack, has many elements. It involves alterations to lifestyle, exclusion or treatment of precipitating factors, drug treatment, and surgery if medical treatment fails. Alteration in lifestyle involves a reduction in physical activity in work and the home. It may require a change of job. Smoking must stop and weight reduction may be required. Many socially related activities can be continued with medical treatment. The most important precipitating factors for coronary artery disease are high blood pressure, diabetes, and high cholesterol levels in the blood. These factors can largely be treated or controlled by diet and drugs; such treatment could prevent the progression of coronary artery disease to myocardial infarction. In the main, drug therapy involves drugs that act to dilate the blood vessels or reduce the contractility (and thereby oxygen requirements) of the heart muscle receiving a reduced blood supply. Surgical approaches to coronary artery disease include coronary artery bypass (where a vein is connected to the aorta and to the coronary artery beyond the narrowed region to improve blood flow) and coronary angioplasty (where a catheter containing a fine, elongated balloon is guided from the main leg artery into the coronary artery, positioned within the region of narrowing, and then briefly inflated, forcing open the narrowing).
— David J. Miller, Niall G. MacFarlane
See also coronary artery bypass; heart.
