Myocardial Infarction (Heart attack)

DEFINITION: The sudden death of heart muscle due to restricted flow of oxygenated blood to the heart muscle; characterized by intense chest pain, sweating, shortness of breath, or sometimes none of these symptoms.

ALSO KNOWN AS: Myocardial infarction (MI); heart attack

ANATOMY OR SYSTEM AFFECTED: Circulatory system, heart

Causes and Symptoms

Myocardial infarctions, better known as heart attacks, occur when there are interruptions in the delicately synchronized system that supplies blood to the heart and pumps blood from the heart to other vital organs. The heart is a highly specialized muscle whose function is to pump life-sustaining blood to all parts of the body. Its action involves generating pressure to propel blood through arriving and departing channels—veins and arteries—that must maintain that pressure at critical levels throughout the system.

The highest level of pressure in the total cardiovascular system is to be found closest to the two “pumping” chambers, or ventricles, in the right and left lower sections of the heart. Dark blood, emptied of its oxygen content and laden with carbon dioxide waste, flows into the upper portion of the heart via two large veins called the superior and inferior venae cavae. It then passes from the right atrium chamber into the right ventricle. Once in the ventricle, this blood cannot flow back the way it came because of one-way valves separating the “receiving” from the “pumping” sections of the total heart organ.

After this valve closes following a vitally synchronized timing system, constriction of the right ventricle by the myocardium muscle in the surrounding walls of the heart forces the blood from the heart, propelling it toward the oxygen-filled tissue of the lungs. Following reoxygenation, this blood, still under pressure from the thrust of the right ventricle, flows into the left atrium. Once channeled into the left ventricle, the pumping process that took place in the right ventricle is repeated on the left, and pressurized oxygenated blood flows out of the aortic valve and throughout the cardiovascular system to nourish the body’s cells. Because the force needed to supply enough pressure to circulate blood through the entire body is greater than the first-phase pumping force needed to move blood into the lungs, the myocardium surrounding the left ventricle is the thickest muscular layer in the heart’s wall.

A heart attack occurs when something slows or altogether prevents the flow of oxygen-rich blood into the heart. The lack of a constant supply of oxygen damages the heart muscle, and if blood flow is not quickly restored, the muscle will begin to die—hence the term "infarction," which refers to tissue death as a result of inadequate blood supply. The efficiency of blood circulation is tied to the maintenance of a reasonably constant level of blood pressure. If pulmonary problems, such as blockage caused by the effects of smoking or environmental pollution, make it harder for the right ventricle to push blood through the lungs, the heart must expend more energy in the first stage of the cardiovascular process. Similarly, and often in addition to the added work for the heart caused by pulmonary complications, the efficiency of the left ventricle in handling blood flow may be reduced by the presence of excessive plaque in the circulatory system, causing this ventricle to expend more energy to propel oxygenated blood into vital tissues.

Although factors such as these may be responsible for overworking the heart and thus contributing to eventual heart failure, other causes of heart attacks are to be found much closer to the working apparatus of the heart, particularly in the coronary arteries. The coronary arteries begin at the top of the heart and fan out along its sides. They are responsible for providing large quantities of blood to the myocardium muscle, which needs continual nourishment to carry out the pumping that forces blood forward from the ventricles. The passageways inside these and other key arteries are vulnerable to a condition known as atherosclerosis, which is the accumulation of waste material deposits inside an artery. The buildup of these deposits, called atheromas or plaque, narrows the arterial space and restricts the flow of blood through the affected artery.

A symptomatic condition called angina pectoris, characterized by intermittent chest pains, may develop if atherosclerosis sufficiently reduces blood (and therefore oxygen) supply to the heart. These danger signs can continue over a number of years. If diagnosis reveals a problem that might be resolved by preventive medication, exercise, or recommendations for heart surgery, then this condition, known as myocardial ischemia, may not necessarily end in a full heart attack.

Atherosclerosis of the coronary arteries, in particular, can lead to coronary artery disease (CAD), which in fact describes a group of several related conditions—including myocardial infarction—that can lead to heart failure. While any restriction of blood flow to the heart can result in a heart attack, the most common cause is the rupture of atherosclerotic plaque in a coronary artery, resulting in the artery being partly or completely blocked. Any such rupture that results in arterial blockage is considered a form of acute coronary syndrome (ACS), which has three main forms: unstable angina, which is a type of irregular angina pectoris; non-ST elevation myocardial infarction, or NSTEMI; and ST elevation myocardial infarction, or STEMI. As indicated by their names, NSTEMI and STEMI are both myocardial infarctions, named for their appearance in an electrocardiogram (ECG or EKG). In an ECG reading, the ST segment is the section between individual heartbeats, which in normal conditions is a flat line. During STEMI, the "classic" form of heart attack, the ST segment is no longer flat but raised (hence "ST elevation"); in NSTEMI, considered an "intermediate" form of heart attack, this segment remains flat (hence "non-ST elevation"). NSTEMI occurs when a minor coronary artery (rather than a major one) is blocked or when a major coronary artery is only partially obstructed. Though less severe, it still causes damage to the heart, though typically less damage than STEMI. NSTEMI accounts for approximately 70 percent of all heart attacks.

Another form of attack and disruption of the heart’s ability to deliver blood can come either independently of or in conjunction with an arterially induced heart attack. This form of attack involves a sustained interruption in the rate of heartbeats. The necessary pace or rate of myocardial contractions, which can vary depending on the person’s rate of physical exertion or age, is regulated in the sinoatrial node in the right atrium, which generates its own electrical impulses. The ultimate sources for the commands to the sinoatrial node are to be found in the network of nerves coming directly from the brain. There are, however, other so-called local pacemakers located in the atria and ventricles. If these sources of electrical charges begin giving commands to the myocardium that are not in rhythm with those coming from the sinoatrial node, then dysrhythmic or premature beats may confuse the heart muscle, causing it to beat wildly. In fact, the concentrated pattern of muscle contractions will not be coordinated and instead will be dispersed in different areas of the heart. The result is atrial fibrillation, a series of uncoordinated contractions that cannot combine to propel blood out of the ventricles. This condition may occur either as the aftershock of an arterially induced heart attack or suddenly and on its own, caused by the deterioration of the electrical impulse system commanding the heart rate. In patients whose potential vulnerability to this form of heart attack has been diagnosed in advance, a heart physician may decide to surgically implant an electronic pacemaker to ensure coordination of the necessary electrical commands to the myocardium.

Treatment and Therapy

Extraordinary medical advances have helped reduce the high death rates formerly associated with heart attacks. Many of these advances have been in the field of preventive medicine. The most widely recognized medical findings are related to diet, smoking cessation, and exercise. Although controversy remains, there is general agreement that cholesterol absorbed by the body from the ingestion of saturated fats plays a key role in the dangerous buildup of platelets inside arterial passageways. It has been accepted that regular, although not necessarily strenuous, exercise is an essential long-term preventive strategy that can reduce the risk of heart attacks. Exercise also plays a role in therapy after a heart attack. In both preventive and postattack contexts, it has been medically proven that the entire cardiovascular system profits from the natural muscle-strengthening process (in the heart’s case) and general cleansing effects (in the case of oxygen intake and stimulated blood flow) that result from controlled regular exercise.

The actual application of medical scientific knowledge to assist in the campaign against the deadly effects of heart disease involves multiple fields of specialization. These may range from the sophisticated use of ECGs to monitor the regularity of heartbeats, to specialized drug therapies aimed at preventing heart attacks in people who have been diagnosed as high-risk cases, to coronary bypass surgery or even heart transplants. In the 1980s, highly specialized surgeons at several university and private hospitals began performing operations to implant artificial hearts in human patients. While a patient cannot live indefinitely with a total artificial heart, which is a system of pumps, it can prolong their life while they wait for a donor heart.

In the case of ECGs, it has become possible, thanks to the use of portable units that record the heartbeat patterns of persons over an extended period of time, to gain a much more accurate impression of the actual functioning of the heart. Previous dependence on electrocardiographic data gathered during an appointed and limited examination provided only minimal information to doctors.

The domains of preventive surgery and specialized drug treatment to prevent dangerous blood clotting are vast. Statistically, the most important and widely practiced operations that were developed in the later decades of the twentieth century were replacement of the aortic valve, the coronary bypass operation, and, with greater or lesser degrees of success, the actual transplantation of donors’ hearts in the place of those belonging to heart disease patients. Coronary bypass operations involve the attachment to the myocardium of healthy arteries to carry the blood that can no longer pass through the patient’s clogged arterial passageways; these healthy arteries are taken by the heart surgeon from other areas of the patient’s own body.

Another sphere of medical technology, that of angioplasty, held out a major nonsurgical promise of preventing deterioration of the arteries leading to the heart. This sophisticated form of treatment involves the careful, temporary introduction of inflatable devices inside clogged arteries, which are then stretched to increase the space within the arterial passageway for blood to flow. By the 1990s, however, doctors recognized one disadvantage of balloon angioplasty: by stretching the essential blood vessels being treated, this procedure either stretches the plaque with the artery or breaks loose debris that remains behind, creating a danger of renewed clogging. Thus, although angioplasty remains a standard approach to treatment of heart disease, another technique, called atherectomy, was developed to clear certain coronary arteries, as well as arteries elsewhere in the body.

Atherectomy involves a motorized catheter device resembling a miniature drill that is inserted into clogged arteries. As the drill turns, material that is literally shaved off the interior walls of arteries is retrieved through a tiny collection receptacle. Atherectomy to treat the large anterior descending coronary artery on the left side of the heart, showed promise as being more effective than angioplasty to remove a blockage.

Perspective and Prospects

The modern conception of cardiology dates from William Harvey’s seventeenth-century discovery of the relationship between the heart’s function as a pump and the circulatory “restoration” of blood. Harvey’s much more scientific views replaced centuries-old conceptions of the heart as a blood-warming device only.

Although substantial anatomical advances were made over the next two centuries that helped explain most of the vital functions of the heart, it was not until the early decades of the twentieth century that science developed therapeutic methods to deal with problems that frequently cause heart attacks. Drugs that affect the liver’s production of substances necessary for normal coagulation of blood, for example, were discovered in the 1930s. A large variety of such anticoagulants have since been developed to help thin the blood of patients vulnerable to blood clotting. Other drugs, including certain antibiotics, are used to treat persons whose susceptibility to infection is known to be high. In these cases, the simple action of dislodging bacteria from the teeth when brushing and flossing can cause an invasion of the vital parts of the heart by an infection. This bacterial endocarditis, the result of the actual destruction of heart tissue or the sudden release of clots of infectious residue, could lead to a heart attack in such individuals although they have no other symptoms of identifiable heart disease.

The most spectacular advance in the scientific treatment of potential heart attack victims, however, has been in the field of cardiac surgery. Many advances in open heart surgery date from the late 1950s, when the development of heart and lung replacement machines made it safe enough to substitute electronic monitors for some of the organism’s normal body functions. Before the 1950s, operations had been limited to surgical treatment of the major blood vessels surrounding the heart.

Various technical methods have also been developed that help identify problems early enough for drug therapy to be attempted before the decision to perform surgery is made. The use of catheters, which are threaded into the coronary organ using the same vessels that transport blood, became the most effective way of locating problematic areas. The process known as angiography, which uses x-rays to trace the course of radiopaque dyes injected through a catheter into local heart areas under study, can actually tell doctors if drug therapy is having the desired effects. In cases where such tests show that preventive drug therapy is not effective, an early decision to perform surgery can be made, preventing the source of coronary trouble from multiplying the patient’s chances of suffering a heart attack. In the early decades of the twenty-first century, doctors found a combination approach to treating acute myocardial infarction using pharmacotherapy, procedures, and stents to be overwhelmingly effective. Further, research into the using of stem cells immediately following an acute myocardial infarction proved to restore cardiac function.

Early detection of an oncoming heart attack is critical to improving survival rates. According to the US Centers for Disease Control and Prevention (CDC), major warning signs and symptoms of a heart attack include chest pain; pain or discomfort in the arms, back, neck, and upper abdomen; shortness of breath; nausea; light-headedness; or cold sweats. Individuals experiencing these symptoms should seek emergency medical care immediately. Individuals who are at the highest risk of suffering a heart attack include those with high blood pressure, high LDL cholesterol, a history of smoking; are physically inactive; and are overweight or obese. A diet that is low in salt, fat, and cholesterol and regular exercise can significantly reduce a person's risk of heart attack.

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