Heart.

Heart. I INTRODUCTION Heart, in anatomy, hollow muscular organ that pumps blood through the body. The heart, blood, and blood vessels make up the circulatory system, which is responsible for distributing oxygen and nutrients to the body and carrying away carbon dioxide and other waste products. The heart is the circulatory system's power supply. It must beat ceaselessly because the body's tissues--especially the brain and the heart itself--depend on a constant supply of oxygen and nutrients delivered by the flowing blood. If the heart stops pumping blood for more than a few minutes, death will result. The human heart is shaped like an upside-down pear and is located slightly to the left of center inside the chest cavity. About the size of a closed fist, the heart is made primarily of muscle tissue that contracts rhythmically to propel blood to all parts of the body. This rhythmic contraction begins in the developing embryo about three weeks after conception and continues throughout an individual's life. The muscle rests only for a fraction of a second between beats. Over a typical life span of 76 years, the heart will beat nearly 2.8 billion times and move 169 million liters (179 million quarts) of blood. Since prehistoric times people have had a sense of the heart's vital importance. Cave paintings from 20,000 years ago depict a stylized heart inside the outline of hunted animals such as bison and elephant. The ancient Greeks believed the heart was the seat of intelligence. Others believed the heart to be the source of the soul or of the emotions--an idea that persists in popular culture and various verbal expressions, such as heartbreak, to the present day. II STRUCTURE OF THE HEART The human heart has four chambers. The upper two chambers, the right and left atria, are receiving chambers for blood. The atria are sometimes known as auricles. They collect blood that pours in from veins, blood vessels that return blood to the heart. The heart's lower two chambers, the right and left ventricles, are the powerful pumping chambers. The ventricles propel blood into arteries, blood vessels that carry blood away from the heart. A wall of tissue separates the right and left sides of the heart. Each side pumps blood through a different circuit of blood vessels: The right side of the heart pumps oxygen-poor blood to the lungs, while the left side of the heart pumps oxygen-rich blood to the body. Blood returning from a trip around the body has given up most of its oxygen and picked up carbon dioxide in the body's tissues. This oxygen-poor blood feeds into two large veins, the superior vena cava and inferior vena cava, which empty into the right atrium of the heart. The right atrium conducts blood to the right ventricle, and the right ventricle pumps blood into the pulmonary artery. The pulmonary artery carries the blood to the lungs, where it picks up a fresh supply of oxygen and eliminates carbon dioxide. The blood, now oxygen-rich, returns to the heart through the pulmonary veins, which empty into the left atrium. Blood passes from the left atrium into the left ventricle, from where it is pumped out of the heart into the aorta, the body's largest artery. Smaller arteries that branch off the aorta distribute blood to various parts of the body. A Heart Valves Four valves within the heart prevent blood from flowing backward in the heart. The valves open easily in the direction of blood flow, but when blood pushes against the valves in the opposite direction, the valves close. Two valves, known as atrioventricular valves, are located between the atria and ventricles. The right atrioventricular valve is formed from three flaps of tissue and is called the tricuspid valve. The left atrioventricular valve has two flaps and is called the bicuspid or mitral valve. The other two heart valves are located between the ventricles and arteries. They are called semilunar valves because they each consist of three half-moon-shaped flaps of tissue. The right semilunar valve, between the right ventricle and pulmonary artery, is also called the pulmonary valve. The left semilunar valve, between the left ventricle and aorta, is also called the aortic valve. B Myocardium Muscle tissue, known as myocardium or cardiac muscle, wraps around a scaffolding of tough connective tissue to form the walls of the heart's chambers. The atria, the receiving chambers of the heart, have relatively thin walls compared to the ventricles, the pumping chambers. The left ventricle has the thickest walls--nearly 1 cm (0.5 in) thick in an adult--because it must work the hardest to propel blood to the farthest reaches of the body. C Pericardium A tough, double-layered sac known as the pericardium surrounds the heart. The inner layer of the pericardium, known as the epicardium, rests directly on top of the heart muscle. The outer layer of the pericardium attaches to the breastbone and other structures in the chest cavity and helps hold the heart in place. Between the two layers of the pericardium is a thin space filled with a watery fluid that helps prevent these layers from rubbing against each other when the heart beats. D Endocardium The inner surfaces of the heart's chambers are lined with a thin sheet of shiny, white tissue known as the endocardium. The same type of tissue, more broadly referred to as endothelium, also lines the body's blood vessels, forming one continuous lining throughout the circulatory system. This lining helps blood flow smoothly and prevents blood clots from forming inside the circulatory system. E Coronary Arteries The heart is nourished not by the blood passing through its chambers but by a specialized network of blood vessels. Known as the coronary arteries, these blood vessels encircle the heart like a crown. About 5 percent of the blood pumped to the body enters the coronary arteries, which branch from the aorta just above where it emerges from the left ventricle. Three main coronary arteries--the right, the left circumflex, and the left anterior descending--nourish different regions of the heart muscle. From these three arteries arise smaller branches that enter the muscular walls of the heart to provide a constant supply of oxygen and nutrients. Veins running through the heart muscle converge to form a large channel called the coronary sinus, which returns blood to the right atrium. III FUNCTION OF THE HEART The heart's duties are much broader than simply pumping blood continuously throughout life. The heart must also respond to changes in the body's demand for oxygen. The heart works very differently during sleep, for example, than in the middle of a 5-km (3-mi) run. Moreover, the heart and the rest of the circulatory system can respond almost instantaneously to shifting situations--when a person stands up or lies down, for example, or when a person is faced with a potentially dangerous situation. A Cardiac Cycle Although the right and left halves of the heart are separate, they both contract in unison, producing a single heartbeat. The sequence of events from the beginning of one heartbeat to the beginning of the next is called the cardiac cycle. The cardiac cycle has two phases: diastole, when the heart's chambers are relaxed, and systole, when the chambers contract to move blood. During the systolic phase, the atria contract first, followed by contraction of the ventricles. This sequential contraction ensures efficient movement of blood from atria to ventricles and then into the arteries. If the atria and ventricles contracted simultaneously, the heart would not be able to move as much blood with each beat. During diastole, both atria and ventricles are relaxed, and the atrioventricular valves are open. Blood pours from the veins into the atria, and from there into the ventricles. In fact, most of the blood that enters the ventricles simply pours in during diastole. Systole then begins as the atria contract to complete the filling of the ventricles. Next, the ventricles contract, forcing blood out through the semilunar valves and into the arteries, and the atrioventricular valves close to prevent blood from flowing back into the atria. As pressure rises in the arteries, the semilunar valves snap shut to prevent blood from flowing back into the ventricles. Diastole then begins again as the heart muscle relaxes--the atria first, followed by the ventricles--and blood begins to pour into the heart once more. A health-care professional uses an instrument known as a stethoscope to detect internal body sounds, including the sounds produced by the heart as it is beating. The characteristic heartbeat sounds are made by the valves in the heart--not by the contraction of the heart muscle itself. The sound comes from the leaflets of the valves slapping together. The closing of the atrioventricular valves, just before the ventricles contract, makes the first heart sound. The second heart sound is made when the semilunar valves snap closed. The first heart sound is generally longer and lower than the second, producing a heartbeat that sounds like lub-dup, lub-dup, lub-dup. Blood pressure, the pressure exerted on the walls of blood vessels by the flowing blood, also varies during different phases of the cardiac cycle. Blood pressure in the arteries is higher during systole, when the ventricles are contracting, and lower during diastole, as the blood ejected during systole moves into the body's capillaries. Blood pressure is measured in millimeters (mm) of mercury using a sphygmomanometer, an instrument that consists of a pressure-recording device and an inflatable cuff that is usually placed around the upper arm. Normal blood pressure in an adult is less than 120 mm of mercury during systole, and less than 80 mm of mercury during diastole. Blood pressure is usually noted as a ratio of systolic pressure to diastolic pressure--for example, 120/80. A person's blood pressure may increase for a short time during moments of stress or strong emotions. However, a prolonged or constant elevation of blood pressure, a condition known as hypertension, can increase a person's risk for heart attack, stroke, heart and kidney failure, and other health problems. B Generation of the Heartbeat Unlike most muscles, which rely on nerve impulses to cause them to contract, heart muscle can contract of its own accord. Certain heart muscle cells have the ability to contract spontaneously, and these cells generate electrical signals that spread to the rest of the heart and cause it to contract with a regular, steady beat. The heartbeat begins with a small group of specialized muscle cells located in the upper right-hand corner of the right atrium. This area is known as the sinoatrial (SA) node. Cells in the SA node generate their electrical signals more frequently than cells elsewhere in the heart, so the electrical signals generated by the SA node synchronize the electrical signals traveling to the rest of the heart. For this reason, the SA node is also known as the heart's pacemaker. Impulses generated by the SA node spread rapidly throughout the atria, so that all the muscle cells of the atria contract virtually in unison. Electrical impulses cannot be conducted through the partition between the atria and ventricles, which is primarily made of fibrous connective tissue rather than muscle cells. The impulses from the SA node are carried across this connective tissue partition by a small bridge of muscle called the atrioventricular conduction system. The first part of this system is a group of cells at the lower margin of the right atrium, known as the atrioventricular (AV) node. Cells in the AV node conduct impulses relatively slowly, introducing a delay of about two-tenths of a second before an impulse reaches the ventricles. This delay allows time for the blood in the atria to empty into the ventricles before the ventricles begin contracting. After making its way through the AV node, an impulse passes along a group of muscle fibers called the bundle of His, which span the connective tissue wall separating the atria from the ventricles. Once on the other side of that wall, the impulse spreads rapidly among the muscle cells that make up the ventricles. The impulse travels to all parts of the ventricles with the help of a network of fast-conducting fibers called Purkinje fibers. These fibers are necessary because the ventricular walls are so thick and massive. If the impulse had to spread directly from one muscle cell to another, different parts of the ventricles would not contract together, and the heart would not pump blood efficiently. Although this complicated circuit has many steps, an electrical impulse spreads from the SA node throughout the heart in less than one second. The journey of an electrical impulse around the heart can be traced by a machine called an electrocardiograph (see Electrocardiography). This instrument consists of a recording device attached to electrodes that are placed at various points on a person's skin. The recording device measures different phases of the heartbeat and traces these patterns as peaks and valleys in a graphic image known as an electrocardiogram (ECG, sometimes known as EKG). Changes or abnormalities in the heartbeat or in the heart's rate of contraction register on the ECG, helping doctors diagnose heart problems or identify damage from a heart attack. C Control of the Heart Rate In an adult, resting heart rate is normally about 70 beats per minute. However, the heart can beat up to three times faster--at more than 200 beats per minute--when a person is exercising vigorously. Younger people have faster resting heart rates than adults do. The normal heart rate is about 120 beats per minute in infants and about 100 beats per minute in young children. Many athletes, by contrast, often have relatively slow resting heart rates because physical training makes the heart stronger and enables it to pump the same amount of blood with fewer beats. An athlete's resting heart rate may be only 40 to 60 beats per minute. Although the SA node generates the heartbeat, impulses from nerves cause the heart to speed up or slow down almost instantaneously (see Nervous System). The nerves that affect heart rate are part of the autonomic nervous system, which directs activities of the body that are not under conscious control. The autonomic nervous system is made up of two types of nerves, sympathetic and parasympathetic fibers. These fibers come from the spinal cord or brain and deliver impulses to the SA node and other parts of the heart. Sympathetic nerve fibers increase the heart rate. These fibers are activated in times of stress, and they play a role in the fight or flight response that prepares humans and other animals to respond to danger. In addition to fear or physical danger, exercising or experiencing a strong emotion can also activate sympathetic fibers and cause an increase in heart rate. In contrast, parasympathetic nerve fibers slow the heart rate. In the absence of nerve impulses the SA node would fire about 100 times each minute--parasympathetic fibers are responsible for slowing the heart to the normal rate of about 70 beats per minute. Chemicals known as hormones carried in the bloodstream also influence the heart rate. Hormones generally take effect more slowly than nerve impulses. They work by attaching to receptors, proteins on the surface of heart muscle cells, to change the way the muscle cells contract. Epinephrine (also called adrenaline) is a hormone made by the adrenal glands, which are located on top of the kidneys. Released during times of stress, epinephrine increases the heart rate much as sympathetic nerve fibers do. Thyroid hormone, which regulates the body's overall metabolism, also increases the heart rate. Other chemicals--especially calcium, potassium, and sodium--can affect heart rate and rhythm. D Cardiac Output To determine overall heart function, doctors measure cardiac output, the amount of blood pumped by each ventricle in one minute. Cardiac output is equal to the heart rate multiplied by the stroke volume, the amount of blood pumped by a ventricle with each beat. Stroke volume, in turn, depends on several factors: the rate at which blood returns to the heart through the veins; how vigorously the heart contracts; and the pressure of blood in the arteries, which affects how hard the heart must work to propel blood into them. Normal cardiac output in an adult is about 3 liters per minute per square meter of body surface. An increase in either heart rate or stroke volume--or both--will increase cardiac output. During exercise, sympathetic nerve fibers increase heart rate. At the same time, stroke volume increases, primarily because venous blood returns to the heart more quickly and the heart contracts more vigorously. Many of the factors that increase heart rate also increase stroke volume. For example, impulses from sympathetic nerve fibers cause the heart to contract more vigorously as well as increasing the heart rate. The simultaneous increase in heart rate and stroke volume enables a larger and more efficient increase in cardiac output than if, say, heart rate alone increased during exercise. In a healthy adult during vigorous exercise, cardiac output can increase six-fold, to 18 liters per minute per square meter of body surface. IV DISEASES OF THE HEART In the United States and many other industrialized countries, heart disease is the leading cause of death. According to the United States Centers for Disease Control and Prevention (CDC), more than 710,000 people in the United States die of heart disease each year. By far the most common type of heart disease in the United States is coronary heart disease, in which the arteries that nourish the heart become narrowed and unable to supply enough blood and oxygen to the heart muscle. However, many other problems can also affect the heart, including congenital defects (physical abnormalities that are present at birth), malfunction of the heart valves, and abnormal heart rhythms. Any type of heart disease may eventually result in heart failure, in which a weakened heart is unable to pump sufficient blood to the body. A Coronary Heart Disease Coronary heart disease, the most common type of heart disease in most industrialized countries, is responsible for over 515,000 deaths in the United States yearly. It is caused by atherosclerosis, the buildup of fatty material called plaque on the inside of the coronary arteries (see Arteriosclerosis). Over the course of many years, this plaque narrows the arteries so that less blood can flow through them and less oxygen reaches the heart muscle. The most common symptom of coronary heart disease is angina pectoris, a squeezing chest pain that may radiate to the neck, jaw, back, and left arm. Angina pectoris is a signal that blood flow to the heart muscle falls short when extra work is required from the heart muscle. An attack of angina is typically triggered by exercise or other physical exertion, or by strong emotions. Coronary heart disease can also lead to a heart attack, which usually develops when a blood clot forms at the site of a plaque and severely reduces or completely stops the flow of blood to a part of the heart. In a heart attack, also known as myocardial infarction, part of the heart muscle dies because it is deprived of oxygen. This oxygen deprivation also causes the crushing chest pain characteristic of a heart attack. Other symptoms of a heart attack include nausea, vomiting, and profuse sweating. About one-third of heart attacks are fatal, but patients who seek immediate medical attention when symptoms of a heart attack develop have a good chance of surviving. One of the primary risk factors for coronary heart disease is the presence of a high level of a fatty substance called cholesterol in the bloodstream. High blood cholesterol is typically the result of a diet that is high in cholesterol and saturated fat, although some genetic disorders also cause the problem. Other risk factors include smoking, high blood pressure, diabetes mellitus, obesity, and a sedentary lifestyle. Coronary heart disease was once thought to affect primarily men, but this is not the case. The disease affects an equal number of men and women, although women tend to develop the disease later in life than men do. Coronary heart disease cannot be cured, but it can often be controlled with a combination of lifestyle changes and medications. Patients with coronary heart disease are encouraged to quit smoking, exercise regularly, and eat a low-fat diet. Doctors may prescribe a drug such as lovastatin, simvastatin, or pravastatin to help lower blood cholesterol. A wide variety of medications can help relieve angina, including nitroglycerin, beta blockers, and calcium channel blockers. Doctors may recommend that some patients take a daily dose of aspirin, which helps prevent heart attacks by interfering with platelets, tiny blood cells that play a critical role in blood clotting. In some patients, lifestyle changes and medication may not be sufficient to control angina. These patients may undergo coronary artery bypass surgery or percutaneous transluminal coronary angioplasty (PTCA) to help relieve their symptoms. In bypass surgery, a length of blood vessel is removed from elsewhere in the patient's body--usually a vein from the leg or an artery from the wrist. The surgeon sews one end to the aorta and the other end to the coronary artery, creating a conduit for blood to flow that bypasses the narrowed segment. Surgeons today commonly use an artery from the inside of the chest wall because bypasses made from this artery are very durable. In PTCA, commonly referred to as balloon angioplasty, a deflated balloon is threaded through the patient's coronary arteries to the site of a blockage. The balloon is then inflated, crushing the plaque and restoring the normal flow of blood through the artery. See also Coronary Heart Disease. B Congenital Defects Each year about 25,000 babies in the United States are born with a congenital heart defect (see Birth Defects). A wide variety of heart malformations can occur. One of the most common abnormalities is a septal defect, an opening between the right and left atrium or between the right and left ventricle. In other infants, the ductus arteriosus, a fetal blood vessel that usually closes soon after birth, remains open. In babies with these abnormalities, some of the oxygen-rich blood returning from the lungs is pumped to the lungs again, placing extra strain on the right ventricle and on the blood vessels leading to and from the lung. Sometimes a portion of the aorta is abnormally narrow and unable to carry sufficient blood to the body. This condition, called coarctation of the aorta, places extra strain on the left ventricle because it must work harder to pump blood beyond the narrow portion of the aorta. With the heart pumping harder, high blood pressure often develops in the upper body and may cause a blood vessel in the brain to burst, a complication that is often fatal. An infant may be born with several different heart defects, as in the condition known as tetralogy of Fallot. In this condition, a combination of four different heart malformations allows mixing of oxygenated and deoxygenated blood pumped by the heart. Infants with tetralogy of Fallot are often known as "blue babies" because of the characteristic bluish tinge of their skin, a condition caused by lack of oxygen. In many cases, the cause of a congenital heart defect is difficult to identify. Some defects may be due to genetic factors, while others may be the result of viral infections or exposure to certain chemicals during the early part of the mother's pregnancy. Regardless of the cause, most congenital malformations of the heart can be treated successfully with surgery, sometimes performed within a few weeks or months of birth. For example, a septal defect can be repaired with a patch made from pericardium or synthetic fabric that is sewn over the hole. An open ductus arteriosus is cut, and the pulmonary artery and aorta are stitched closed. To correct coarctation of the aorta, a surgeon snips out the narrowed portion of the vessel and sews the normal ends together, or sews in a tube of fabric to connect the ends. Surgery for tetralogy of Fallot involves procedures to correct each part of the defect. Success rates for many of these operations are well above 90 percent, and with treatment most children with congenital heart defects live healthy, normal lives. C Heart Valve Malfunction Malfunction of one of the four valves within the heart can cause problems that affect the entire circulatory system. A leaky valve does not close all the way, allowing some blood to flow backward as the heart contracts. This backward flow decreases the amount of oxygen the heart can deliver to the tissues with each beat. A stenotic valve, which is stiff and does not open fully, requires the heart to pump with increased force to propel blood through the narrowed opening. Over time, either of these problems can lead to damage of the overworked heart muscle. Some people are born with malformed valves. Such congenital malformations may require treatment soon after birth, or they may not cause problems until a person reaches adulthood. A heart valve may also become damaged during life, due to infection, connective tissue disorders such as Marfan syndrome, hypertension, heart attack, or simply aging. A well-known, but poorly understood, type of valve malfunction is mitral valve prolapse. In this condition, the leaflets of the mitral valve fail to close properly and bulge backward like a parachute into the left atrium. Mitral valve prolapse is the most common type of valve abnormality, affecting 5 to 10 percent of the United States population, the majority of them women. In most cases, mitral valve prolapse does not cause any problems, but in a few cases the valve's failure to close properly allows blood to leak backwards through the valve. Another common cause of valve damage is rheumatic fever, a complication that sometimes develops after an infection with common bacteria known as streptococci. Most common in children, the illness is characterized by inflammation and pain in the joints. Connective tissue elsewhere in the body, including in the heart, heart valves, and pericardium, may also become inflamed. This inflammation can result in damage to the heart, most commonly one of the heart valves, that remains after the other symptoms of rheumatic fever have gone away. Valve abnormalities are often detected when a health-care professional listens to the heart with a stethoscope. Abnormal valves cause extra sounds in addition to the normal sequence of two heart sounds during each heartbeat. These extra heart sounds are often known as heart murmurs, and not all of them are dangerous. In some cases, a test called echocardiography may be necessary to evaluate an abnormal valve. This test uses ultrasound waves to produce images of the inside of the heart, enabling doctors to see the shape and movement of the valves as the heart pumps. Damaged or malformed valves can sometimes be surgically repaired. More severe valve damage may require replacement with a prosthetic valve. Some prosthetic valves are made from pig or cow valve tissue, while others are mechanical valves made from silicone and other synthetic materials. D Arrhythmias Arrhythmias, or abnormal heart rhythms, arise from problems with the electrical conduction system of the heart. Arrhythmias can occur in either the atria or the ventricles. In general, ventricular arrhythmias are more serious than atrial arrhythmias because ventricular arrhythmias are more likely to affect the heart's ability to pump blood to the body. Some people have minor arrhythmias that persist for long periods and are not dangerous--in fact, they are simply heartbeats that are normal for that particular person's heart. A temporary arrhythmia can be caused by alcohol, caffeine, or simply not getting a good night's sleep. Often, damage to the heart muscle results in a tendency to develop arrhythmias. This heart muscle damage is frequently the result of a heart attack, but can also develop for other reasons, such as after an infection or as part of a congenital defect. Arrhythmias may involve either abnormally slow or abnormally fast rhythms. An abnormally slow rhythm sometimes results from slower firing of impulses from the SA node itself, a condition known as sinus bradycardia. An abnormally slow heartbeat may also be due to heart block, which arises when some or all of the impulses generated by the SA node fail to be transmitted to the ventricles. Even if impulses from the atria are blocked, the ventricles continue to contract because fibers in the ventricles can generate their own rhythm. However, the rhythm they generate is slow, often only about 40 beats per minute. An abnormally slow heartbeat is dangerous if the heart does not pump enough blood to supply the brain and the rest of the body with oxygen. In this case, episodes of dizziness, lightheadedness, or fainting may occur. Episodes of fainting caused by heart block are known as Stokes-Adams attacks. Some types of abnormally fast heart rhythms--such as atrial tachycardia, an increased rate of atrial contraction--are usually not dangerous. Atrial fibrillation, in which the atria contract in a rapid, uncoordinated manner, may reduce the pumping efficiency of the heart. In a person with an otherwise healthy heart, this may not be dangerous, but in a person with other heart disease the reduced pumping efficiency may lead to heart failure or stroke. By far the most dangerous type of rapid arrhythmia is ventricular fibrillation, in which ventricular contractions are rapid and chaotic. Fibrillation prevents the ventricles from pumping blood efficiently, and can lead to death within minutes. Ventricular fibrillation can be reversed with an electrical defibrillator, a device that delivers a shock to the heart. The shock briefly stops the heart from beating, and when the heartbeat starts again the SA node is usually able to resume a normal beat. Most often, arrhythmias can be diagnosed with the use of an ECG. Some arrhythmias do not require treatment. Others may be controlled with medications such as digitalis, propanolol, or disopyramide. Patients with heart block or several other types of arrhythmias may have an artificial pacemaker implanted in their chest. This small, battery-powered electronic device delivers regular electrical impulses to the heart through wires attached to different parts of the heart muscle. Another type of implantable device, a miniature defibrillator, is used in some patients at risk for serious ventricular arrhythmias. This device works much like the larger defibrillator used by paramedics and in the emergency room, delivering an electric shock to reset the heart when an abnormal rhythm is detected. E Other Forms of Heart Disease In addition to the relatively common heart diseases described above, a wide variety of other diseases can also affect the heart. These include tumors, heart damage from other diseases such as syphilis and tuberculosis, and inflammation of the heart muscle, pericardium, or endocardium. Myocarditis, or inflammation of the heart muscle, was commonly caused by rheumatic fever in the past. Today, many cases are due to a viral infection or their cause cannot be identified. Sometimes myocarditis simply goes away on its own. In a minority of patients, who often suffer repeated episodes of inflammation, myocarditis leads to permanent damage of the heart muscle, reducing the heart's ability to pump blood and making it prone to developing abnormal rhythms. Cardiomyopathy encompasses any condition that damages and weakens the heart muscle. Scientists believe that viral infections cause many cases of cardiomyopathy. Other causes include vitamin B deficiency, rheumatic fever, underactivity of the thyroid gland, and a genetic disease called hemochromatosis in which iron builds up in the heart muscle cells. Some types of cardiomyopathy can be controlled with medication, but others lead to progressive weakening of the heart muscle and sometimes result in heart failure. In pericarditis, the most common disorder of the pericardium, the saclike membrane around the heart becomes inflamed. Pericarditis is most commonly caused by a viral infection, but may also be due to arthritis or an autoimmune disease such as systemic lupus erythematosus. It may be a complication of late-stage kidney disease, lung cancer, or lymphoma; it may be a side effect of radiation therapy or certain drugs. Pericarditis sometimes goes away without treatment, but it is often treated with anti-inflammatory drugs. It usually causes no permanent damage to the heart. If too much fluid builds up around the heart during an attack of pericarditis, the fluid may need to be drained with a long needle or in a surgical procedure. Patients who suffer repeated episodes of pericarditis may have the pericardium surgically removed. Endocarditis is an infection of the inner lining of the heart, but damage from such an infection usually affects only the heart valves. Endocarditis often develops when bacteria from elsewhere in the body enter the bloodstream, settle on the flaps of one of the heart valves, and begin to grow there. The infection can be treated with antibiotics, but if untreated, endocarditis is often fatal. People with congenital heart defects, valve damage due to rheumatic fever, or other valve problems are at greatest risk for developing endocarditis. They often take antibiotics as a preventive measure before undergoing dental surgery or certain other types of surgery that can allow bacteria into the bloodstream. Intravenous drug users who share needles are another population at risk for endocarditis. People who use unclean needles, which allow bacteria into the bloodstream, frequently develop valve damage. F Heart Failure The final stage in almost any type of heart disease is heart failure, also known as congestive heart failure, in which the heart muscle weakens and is unable to pump enough blood to the body. In the early stages of heart failure, the muscle may enlarge in an attempt to contract more vigorously, but after a time this enlargement of the muscle simply makes the heart inefficient and unable to deliver enough blood to the tissues. In response to this shortfall, the kidneys conserve water in an attempt to increase blood volume, and the heart is stimulated to pump harder. Eventually excess fluid seeps through the walls of tiny blood vessels and into the tissues. Fluid may collect in the lungs, making breathing difficult, especially when a patient is lying down at night. Many patients with heart failure must sleep propped up on pillows to be able to breathe. Fluid may also build up in the ankles, legs, or abdomen. In the later stages of heart failure, any type of physical activity becomes next to impossible. Almost any condition that overworks or damages the heart muscle can eventually result in heart failure. The most common cause of heart failure is coronary heart disease. Heart failure may develop when the death of heart muscle in a heart attack leaves the heart with less strength to pump blood, or simply as a result of longterm oxygen deprivation due to narrowed coronary arteries. Hypertension or malfunctioning valves that force the heart to work harder over extended periods of time may also lead to heart failure. Viral or bacterial infections, alcohol abuse, and certain chemicals (including some lifesaving drugs used in cancer chemotherapy), can all damage the heart muscle and result in heart failure. Despite its ominous name, heart failure can sometimes be reversed and can often be effectively treated for long periods with a combination of drugs. About 4.6 million people with heart failure are alive in the United States today. Medications such as digitalis are often prescribed to increase the heart's pumping efficiency, while beta blockers may be used to decrease the heart's workload. Drugs known as vasodilators relax the arteries and veins so that blood encounters less resistance as it flows. Diuretics stimulate the kidneys to excrete excess fluid. A last resort in the treatment of heart failure is heart transplantation, in which a patient's diseased heart is replaced with a healthy heart from a person who has died of other causes (see Medical Transplantation). Heart transplantation enables some patients with heart failure to lead active, healthy lives once again. However, a person who has received a heart transplant must take medications to suppress the immune system for the rest of his or her life in order to prevent rejection of the new heart. These drugs can have serious side effects, making a person more vulnerable to infections and certain types of cancer. The first heart transplant was performed in 1967 by South African surgeon Christiaan Barnard. However, the procedure did not become widespread until the early 1980s, when the immune-suppressing drug cyclosporine became available. This drug helps prevent rejection without making patients as vulnerable to infection as they had been with older immune-suppressing drugs. About 3,500 heart transplants are performed worldwide each year, about 2,500 of them in the United States. Today, about 83 percent of heart transplant recipients survive at least one year, and 71 percent survive for four years. A shortage of donor hearts is the main limitation on the number of transplants performed today. Some scientists are looking for alternatives to transplantation that would help alleviate this shortage of donor hearts. One possibility is to replace a human heart with a mechanical one. A permanent artificial heart was first implanted in a patient in 1982. Artificial hearts have been used experimentally with mixed success. They are not widely used today because of the risk of infection and bleeding and concerns about their reliability. In addition, the synthetic materials used to fashion artificial hearts can cause blood clots to form in the heart. These blood clots may travel to a vessel in the neck or head, resulting in a stroke. Perhaps a more promising option is the left ventricular assist device (LVAD). This device is implanted inside a person's chest or abdomen to help the patient's own heart pump blood. LVADs are used in many people waiting for heart transplants, and could one day become a permanent alternative to transplantation. Some scientists are working to develop xenotransplantation, in which a patient's diseased heart would be replaced with a heart from a pig or another species. However, this strategy still requires a great deal of research to prevent the human immune system from rejecting a heart from a different species. Some experts have also raised concerns about the transmission of harmful viruses from other species to humans as a result of xenotransplantation. V HISTORY OF HEART RESEARCH Scientific knowledge of the heart dates back almost as far as the beginnings of recorded history. The Egyptian physician Imhotep made observations on the pulse during the 2600s BC. During the 300s BC the Greek physician Hippocrates studied and wrote about various signs and symptoms of heart disease, and the Greek philosopher Aristotle described the beating heart of a chick embryo. Among the first people to investigate and write about the anatomy of the heart was another Greek physician, Erasistratus, around 250 BC. Erasistratus described the appearance of the heart and the four valves inside it. Although he correctly deduced that the valves prevent blood from flowing backward in the heart, he did not understand that the heart was a pump. Galen, a Greek-born Roman physician, also wrote about the heart during the second century AD. He recognized that the heart was made of muscle, but he believed that the liver was responsible for the movement of blood through the body. Heart research did not greatly expand until the Renaissance in Europe (14th century to 16th century). During that era, scientists began to connect the heart's structure with its function. During the early 16th century the Spanish physician and theologian Michael Servetus described how blood passes through the four chambers of the heart and picks up oxygen in the lungs. Perhaps the most significant contributions were made by English physician William Harvey, who discovered the circulation of blood in 1628. Harvey was the first to realize that the heart is a pump responsible for the movement of blood through the body. His work revealed how the heart works with the blood and blood vessels to nourish the body, establishing the concept of the circulatory system. The 20th century witnessed extraordinary advances in the diagnosis of heart diseases, corrective surgeries, and other forms of treatment for heart problems. Many doctors had become interested in measuring the pulse and abnormal heartbeats. This line of research culminated in the 1902 invention of the electrocardiograph by Dutch physiologist Willem Einthoven, who received the Nobel Prize for this work in 1924. Another major advance in diagnosis was cardiac catheterization, which was pioneered in 1929 by German physician Werner Forssmann. After performing experiments on animals, Forssmann inserted a catheter through a vein in his arm and into his own heart--a stunt for which he was fired from his job. Two American physicians, André Cournand and Dickinson Richards, later continued research on catheterization, and the technique became commonly used during the 1940s. The three scientists received the Nobel Prize in 1956 for their work. At the beginning of the 20th century, most doctors believed that surgery on the heart would always remain impossible, as the heart was thought to be an extremely delicate organ. Most of the first heart operations were done in life-or-death trauma situations. American physician L. L. Hill performed the first successful heart surgery in the United States in 1902, sewing up a stab wound in the left ventricle of an 8-year-old boy. The next year, French surgeon Marin Théodore Tuffier removed a bullet from a patient's left atrium. Surgery to correct some congenital defects involving blood vessels also helped lay the foundations for surgery on the heart itself. In 1938 American surgeon Robert Gross performed the first successful surgery to treat an open ductus arteriosus, tying the vessel closed with thread. In 1944 Gross and Swedish surgeon Clarence Crafoord each performed successful surgery for coarctation of the aorta. The same year, American surgeon Alfred Blalock and surgical assistant Vivien Thomas performed the first successful operation to correct tetralogy of Fallot. But the greatest leap forward came in 1953, when American physician John Gibbon introduced the heart-lung machine, a device to oxygenate and pump blood during surgery on the heart. This invention made open-heart surgery--with the heart stopped for the duration of the operation--possible. It led to now-routine surgical techniques such as valve replacement, correction of congenital defects, and bypass surgery. The rapid pace of scientific discovery during the 20th century has also led to many nonsurgical treatments for diseases of the heart. The introduction of antibiotics to treat bacterial infections greatly reduced sickness and deaths due to heart disease from rheumatic fever, endocarditis, and other infections involving the heart, although these infections remain a significant threat in many developing nations. Many effective drugs to control hypertension, reduce cholesterol, relieve angina, limit damage from heart attacks, and treat other forms of heart disease have also been developed. Advances in electronics led to implantable pacemakers in 1959 and implantable defibrillators in 1982. VI HEARTS IN OTHER ANIMALS Among different groups of animals, hearts vary greatly in size and complexity. In insects, the heart is a hollow bulb with muscular walls that contract to push blood into an artery. Many insects have several such hearts arranged along the length of the artery. When the artery ends, blood percolates among the cells of the insect's body, eventually making its way back to the heart. In an insect, blood may take as long as an hour to complete a trip around the body. In earthworms and other segmented worms, known as annelids, blood flows toward the back of the body through the ventral blood vessel and toward the front of the body through the dorsal blood vessel. Five pairs of hearts, or aortic arches, help pump blood. The hearts are actually segments of the dorsal blood vessel and are similar in structure to those of insects. In vertebrates, or animals with a backbone, the heart is a separate, specialized organ rather than simply a segment of a blood vessel. In fish, the heart has two chambers: an atrium (receiving chamber) and a ventricle (pumping chamber). Oxygen-depleted blood returning from the fish's body empties into the atrium, which pumps blood into the ventricle. The ventricle then pumps the blood to the gills, the respiratory organs of fish. In the gills, the blood picks up oxygen from the water and gets rid of carbon dioxide. The freshly oxygenated blood leaves the gills and travels to various parts of the body. In fish, as in humans, blood passes through the respiratory organs before it is distributed to the body. Unlike in humans, the blood does not return to the heart between visiting the respiratory organs and being distributed to the tissues. Without the added force from a second trip through the heart, blood flows relatively slowly in fish compared to humans and other mammals. However, this sluggish flow is enough to supply the fish's relatively low oxygen demand. As vertebrates moved from life in the sea to life on land, they evolved lungs as new respiratory organs for breathing. At the same time, they became more active and developed greater energy requirements. Animals use oxygen to release energy from food molecules in a process called cellular respiration, so land-dwelling vertebrates also developed a greater requirement for oxygen. These changes, in turn, led to changes in the structure of the heart and circulatory system. Amphibians and most reptiles have a heart with three chambers--two atria and a single ventricle. These animals also have separate circuits of blood vessels for oxygenating blood and delivering it to the body. Deoxygenated blood returning from the body empties into the right atrium. From there, blood is conducted to the ventricle and is then pumped to the lungs. After picking up oxygen and getting rid of carbon dioxide in the lungs, blood returns to the heart and empties into the left atrium. The blood then enters the ventricle a second time and is pumped out to the body. The second trip through the heart keeps blood pressure strong and blood flow rapid as blood is pumped to the tissues, helping the blood deliver oxygen more efficiently. The three-chambered heart of amphibians and reptiles also creates an opportunity for blood to mix in the ventricle which pumps both oxygenated and deoxygenated blood with each beat. While in birds and mammals this would be deadly, scientists now understand that a three-chambered heart is actually advantageous for amphibians and reptiles. These animals do not breathe constantly--for example, amphibians absorb oxygen through their skin when they are underwater--and the three-chambered heart enables them to adjust the proportions of blood flowing to the body and the lungs depending on whether the animal is breathing or not. The three-chambered heart actually results in more efficient oxygen delivery for amphibians and reptiles. Birds and mammals have high energy requirements even by vertebrate standards, and a corresponding high demand for oxygen. Their hearts have four chambers--two atria and two ventricles--resulting in a complete separation of oxygenated and deoxygenated blood and highly efficient delivery of oxygen to the tissues. Small mammals have more rapid heart rates than large mammals because they have the highest energy needs. The resting heart rate of a mouse is 500 to 600 beats per minute, while that of an elephant is 30 beats per minute. Blood pressure also varies among different mammal species. Blood pressure in a giraffe's aorta is about 220 mm of mercury when the animal is standing. This pressure would be dangerously high in a human, but is necessary in a giraffe to lift blood up the animal's long neck to its brain. Although other groups of vertebrates have hearts with a different structure than those of humans, they are still sufficiently similar that scientists can learn about the human heart from other animals. Scientists use a transparent fish, the zebra fish, to learn how the heart and the blood vessels that connect to it form before birth. Fish embryos are exposed to chemicals known to cause congenital heart defects, and scientists look for resulting genetic changes. Researchers hope that these studies will help us understand why congenital heart malformations occur, and perhaps one day prevent these birth defects. Contributed By: Eugene Passamani Microsoft ® Encarta ® 2009. © 1993-2008 Microsoft Corporation. All rights reserved.