Heart

• 1. Introduction

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  The heart of an adult at rest beats close to 72 times every minute. This muscular organ, found in humans and other animals, pumps blood through the vessels that, together with it, form the circulatory system. Each beat sends oxygen and nutrients out to the tissues and carries waste such as carbon dioxide back toward the lungs. When the system falters, the toll is enormous. As of 2008, cardiovascular diseases were the most common cause of death across the world, responsible for 30% of all human deaths. How is the organ built so that blood flows in only one direction? What sets its rhythm, and what happens when that rhythm or its own blood supply fails? And how did physicians, who could not look inside a living chest, finally work out what it was doing?

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• 2. Chambers and Layers

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  An adult heart has a mass of 250-350 grams. It measures roughly 12 centimetres in length, 8 in width and 6 in thickness. Those figures are the basis of the familiar comparison with a closed fist, although the comparison is disputed and the true size is likely slightly larger. Well-trained athletes can have much bigger hearts, because exercise builds heart muscle much as it builds skeletal muscle. The organ sits in the middle compartment of the chest, the mediastinum, between the lungs. Its tip, the apex, points to the left, which is why the left lung is smaller and carries a cardiac notch to make room. In a rare congenital disorder called dextrocardia, the heart is offset to the right instead.

  Inside, four chambers do the work. The two upper atria receive blood, and the two lower ventricles discharge it. The right atrium and right ventricle are sometimes called the right heart, and their left counterparts the left heart. The septum between the ventricles is much thicker than the one between the atria, because the ventricles must generate greater pressure. The left ventricle is thicker than the right for a similar reason, since it must push blood to the entire body.

  Four valves keep that blood moving one way. The tricuspid valve, with three cusps, lies between the right atrium and right ventricle. The mitral valve lies between the left atrium and left ventricle, and it is also called the bicuspid valve because it has two cusps. Cords called chordae tendinae tie these cusps to papillary muscles in the ventricle wall. When the ventricles contract, the muscles tighten the cords, which stops the cusps from being blown back into the atria. A semilunar valve guards the exit of each ventricle, the pulmonary valve on the right and the aortic valve on the left. Each has three cusps and no papillary muscles. They seal when blood pressing back from the artery fills their pocket-like cusps.

  The wall itself has three layers. The inner endocardium is a lining of simple squamous epithelium that covers the chambers and valves. The middle myocardium is cardiac muscle, whose cells swirl and spiral around the chambers in figure 8 patterns that help the heart pump more effectively. The outer layer is the epicardium. Around all three hangs the pericardium, a double-membraned sac with a tough fibrous outside and an inner serous membrane that produces lubricating fluid. It steadies the heart's position, eases its movement against neighbouring structures, and protects it from infection.

  Almost all of the muscle is contractile, since such cells make up 99% of the cells in the atria and ventricles. The remaining 1% are pacemaker cells, much smaller and with few myofibrils, whose function resembles that of neurons. The muscle also needs a supply of its own. Two arteries arise just above the aortic valve, the left main coronary artery and the right coronary artery. The left main artery soon splits into the left anterior descending and the left circumflex, and the anatomy varies significantly from person to person. The right coronary artery feeds the atrioventricular node in about 90% of people and the sinoatrial node in about 60%, and those two nodes set the rhythm.

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• 3. Spark and Rhythm

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  Near the point where the superior vena cava joins the upper right atrium sits the sinoatrial node, the heart's own pacemaker. Its cells create an electrical signal that spreads through the right atrium and reaches the left atrium by way of Bachmann's bundle, so that both atria contract together. The signal then arrives at the atrioventricular node, low in the right atrium. It has no other route. The cardiac skeleton, a fibrous framework between atria and ventricles, contains collagen, and collagen cannot conduct electricity. From the node the signal runs along the bundle of His, divides into left and right bundle branches, and reaches the ventricular muscle through specialised tissue called Purkinje fibers.

  Inside a pacemaker cell, each beat begins on its own. A rapid influx of sodium ions turns the membrane's charge positive, a process called depolarisation. Calcium then enters, and potassium begins to leave. Calcium moving through slow channels gives the cells a prolonged plateau while they carry a positive charge. Later the calcium channels close and potassium channels open, returning the cell to a negative charge in repolarisation. When the membrane potential reaches approximately minus 60 millivolts, the potassium channels close and the cycle can start again. Calcium also binds to the regulatory protein troponin C, which allows the muscle to contract, and its release allows relaxation.

  The mechanical result is called the cardiac cycle. Systole is the period when the ventricles contract and force blood into the aorta and main pulmonary artery. Diastole is the period when they relax and refill. Just before contraction, the atria squeeze and prime the pump with extra blood. As pressure in the ventricles climbs, the mitral and tricuspid valves are forced shut. Once that pressure exceeds the pressure in the aorta and pulmonary arteries, the aortic and pulmonary valves open and blood is ejected.

  Cardiac output is the amount of blood pumped by each ventricle in one minute. It is found by multiplying stroke volume by heart rate. An average stroke volume of about 70 millilitres gives 5.25 litres per minute, within a normal range of 4.0-8.0 litres. The Frank-Starling mechanism adds a rule of its own, which says that a ventricle contracts more forcefully the more it is stretched.

  The rate shifts across a life and across a day. The adult resting rate ranges from 60 to 100 beats per minute, a newborn's can be 129, and an athlete's can fall below 60. During exercise it can reach 150, and maximum rates run from 200 to 220. The brain adjusts the pace through two nerve routes. The vagus nerve slows the heart, while nerves from the sympathetic trunk speed it up and strengthen each contraction. These nerves influence the heart but do not control it. Even a person's emotional state, body temperature and thyroid hormone levels can change the rate.

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• 4. Before Birth

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  About three weeks into embryonic development, around 22 days after conception, the heart begins to beat. It is the first functional organ to develop, and this early start is crucial for the embryonic and prenatal development that follows. Two endocardial tubes form in the cardiogenic region and fuse into a primitive tubular heart. Between the third and fourth week the tube lengthens and folds into an S-shape inside the pericardium, which brings the chambers and major vessels into the correct alignment. The septa are complete by the end of the fifth week, and the valves by the ninth week.

  A fetal heart carries a feature that disappears within moments of birth. An opening called the foramen ovale lets blood pass directly from the right atrium to the left atrium, so that some blood bypasses the lungs. Within seconds after birth, a flap of tissue called the septum primum closes the opening and establishes the typical pattern of circulation. A depression in the wall of the right atrium, the fossa ovalis, marks the spot where the opening once was.

  The embryonic heart starts at a rate near its mother's, about 75-80 beats per minute. It then accelerates to a peak of 165-185 beats per minute in the early 7th week. After 9 weeks, the start of the fetal stage, the rate begins to fall, slowing to around 145 beats per minute, give or take 25, at birth. Before birth, female and male hearts show no difference in rate.

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• 5. When It Fails

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  Smoking, being overweight, little exercise, high cholesterol, high blood pressure and poorly controlled diabetes all raise the risk of heart disease. Of the deaths from cardiovascular disease, more than three-quarters result from coronary artery disease and stroke. The condition often gives no symptoms, though it may cause chest pain or shortness of breath.

  Coronary artery disease is caused by atherosclerosis, a build-up of fatty material along the inner walls of the arteries. These plaques narrow the vessels. A minor narrowing may cause no symptoms, while a severe one can cause chest pain called angina, or breathlessness during exercise or even at rest. The thin covering of a plaque can rupture and expose its fatty centre to the blood. A clot then forms, blocks the artery and starves an area of heart muscle, causing a myocardial infarction, or heart attack. In the worst case the result is cardiac arrest, a sudden and utter loss of output from the heart.

  Heart failure is the condition in which the heart cannot pump enough blood to meet the body's demands. Patients may become breathless, especially when lying flat, and may have swollen ankles. It most commonly follows ischemic heart disease, valvular heart disease or high blood pressure. Despite better drugs, 30 to 40% of patients die within a year of the diagnosis.

  Diseases of the muscle itself, the cardiomyopathies, take four forms. Hypertrophic cardiomyopathy thickens the muscle, dilated cardiomyopathy makes the heart expand and weaken, restrictive cardiomyopathy leaves it stiff, and arrhythmogenic cardiomyopathy makes it prone to abnormal rhythms. Many are genetic, although dilated cardiomyopathy can be caused by toxins such as alcohol. Hypertrophic cardiomyopathy is linked to a higher risk of sudden cardiac death, particularly in athletes.

  A diseased valve may be narrowed, a condition called stenosis, or leaky, a condition called regurgitation. In the developed world the usual cause is degeneration with old age. In some parts of the world rheumatic heart disease is a major cause, and it begins when the immune system reacts to a streptococcal throat infection.

  Rhythm can fail as well. The most dangerous disturbance is ventricular fibrillation, in which the ventricles quiver rather than contract, and it is rapidly fatal if untreated. Atrial fibrillation, by contrast, raises the long-term risk of stroke. Some people are born with defects, ranging from patent foramen ovale, arguably a variant of normal, to the life-threatening hypoplastic left heart syndrome. Because every beat depends on ions crossing cell membranes, cardiac channelopathies form a major group of heart diseases. Long QT syndrome is the most common of them, and Brugada syndrome, a genetic disorder, is one of the most common causes of sudden cardiac death in young men.

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• 6. Diagnosis and Repair

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  A healthy heart makes only two audible sounds, called S1 and S2 and described as "lub" and "dub". The first is the closing of the atrioventricular valves during ventricular contraction, and the second is the closing of the semilunar valves. Extra sounds can signal trouble. Murmurs are graded by volume from 1, the quietest, to 6, the loudest, and they may come from damaged valves or be heard in perfectly normal hearts. A cardiac examination also includes taking the pulse, usually at the radial artery near the wrist, and measuring blood pressure.

  Blood tests add precision. Troponin is released 4-6 hours after injury and usually peaks at about 12-24 hours, so it is tested at presentation and again within 3-6 hours. A test for brain natriuretic peptide helps evaluate heart failure. An electrocardiogram records the heart's electrical activity through surface electrodes. Ten leads produce what is called a "12 lead" tracing, and a Holter monitor can record for 24 hours when a rhythm problem comes and goes. An echocardiogram uses ultrasound to measure function, assess valve disease and calculate the ejection fraction. A stress version uses exercise or, where exercise is impossible, a drug such as dobutamine.

  Treatment begins with lifestyle changes and drugs. For angina, medicines include nitroglycerin, beta blockers and calcium channel blockers, while aspirin and statins help prevent heart attacks. A percutaneous coronary intervention passes a balloon-tipped wire into the artery, inflates the balloon to widen the narrowing, and sometimes leaves behind a metal scaffold called a stent. When that is unsuitable, a coronary artery bypass graft uses a vessel from elsewhere in the body, such as the saphenous vein, radial artery or internal mammary artery, to redirect blood around the obstruction.

  Damaged valves may be replaced with a tissue or metallic prosthetic valve, and the tricuspid or mitral valves can sometimes be repaired instead. Transcatheter aortic valve replacement is increasingly used for patients at very high risk from open surgery. For arrhythmias, catheter ablation sends wires from a vein or artery in the leg to the abnormal tissue and damages it by heating or freezing. A cardioversion uses an electric shock to stun the heart out of an abnormal rhythm. Pacemakers treat abnormally slow rhythms, and implantable defibrillators monitor the heart and automatically deliver a shock if dangerous racing is detected.

  In heart failure, diuretics prevent fluid from accumulating in the lungs. In very severe cases a small pump called a ventricular assist device may be implanted. In the most severe cases of all, a cardiac transplant may be considered, and that operation has a history of its own.

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• 7. Centuries of Discovery

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  Erasistratos, who lived from 304 to 250 BCE, described the heart as a pump and discovered its valves, although he believed the vessels were filled with air rather than blood. Aristotle thought the heart created blood. Plato saw it as the source of circulating blood, and Hippocrates noted blood moving in a cycle from the body through the heart to the lungs. In the 2nd century CE, the Greek physician Galen concluded that the heart, as the hottest organ, supplied heat to the body. He held that the heart sucked blood in rather than pushing it out, and that blood crossed between the ventricles through pores. These ideas went unchallenged for almost a thousand years.

  The first break came in 1242, when Ibn al-Nafis wrote a commentary on Avicenna's Canon. He argued that blood passes through the lungs rather than moving from the right to the left ventricle, as Galen had believed. Andrea Alpago later translated his work into Latin. In Europe, Galen's teachings had been adopted as the official canon of the Church. Andreas Vesalius questioned some of them in De humani corporis fabrica in 1543, and was attacked for it. Michael Servetus wrote in 1553 that blood flows from one side of the heart to the other via the lungs.

  The breakthrough arrived in 1628 with De Motu Cordis by the English physician William Harvey. His book completely described the systemic circulation and the mechanical force of the heart, and it overhauled the Galenic doctrines. Later the German physiologist Otto Frank, who lived from 1865 to 1944, and the English physiologist Ernest Starling, who lived from 1866 to 1927, reached similar conclusions while working largely independently. Their names are joined in the Frank-Starling mechanism.

  The electrical wiring took longer to decode. Purkinje fibers and the bundle of His were known in the 19th century, but their role stayed unknown until Sunao Tawara published his monograph Das Reizleitungssystem des Säugetierherzens in 1906. His discovery of the atrioventricular node prompted Arthur Keith and Martin Flack to search for a similar structure, and they found the sinoatrial node several months later. These structures form the anatomical basis of the electrocardiogram, whose inventor, Willem Einthoven, was awarded the Nobel Prize in Medicine or Physiology in 1924.

  By the middle of the 20th century, heart disease had surpassed infectious disease as the leading cause of death in the United States. The Framingham Heart Study, begun in 1948 and still ongoing, has shed light on the effects of diet, exercise and common medications such as aspirin.

  Surgery reached the organ itself in 1964, when James Hardy transplanted a chimpanzee heart into a human, and the patient died within 2 hours. The first human to human transplant followed in 1967, performed by the South African surgeon Christiaan Barnard at Groote Schuur Hospital in Cape Town. It captured the attention of both the medical profession and the world. Its recipient, Louis Washkansky, died 18 days after the operation, and other early patients survived no more than a few weeks. Norman Shumway has been credited with improving transplantation techniques, along with pioneers Richard Lower, Vladimir Demikhov and Adrian Kantrowitz. By March 2000, more than 55,000 heart transplantations had been performed worldwide. On the 7th of January 2022 in Baltimore, surgeon Bartley P. Griffith transplanted a heart from a genetically modified pig into David Bennett, aged 57, who lived until the 8th of March 2022.

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• 8. Symbol and Soul

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  The Hebrew Bible uses the word lev for the heart in three senses at once: the seat of emotion, the mind, and the anatomical organ. Across cultures, the heart was long taken to be the center of the entire body and the seat of life, emotion, reason, will and purpose. In Islamic and Judeo-Christian thought it is the temple or throne of God. In Hinduism it holds the divine centre, the atman, and the third eye of transcendent wisdom. Buddhist tradition calls it the diamond of purity and the essence of the Buddha, and Taoism places the centre of understanding there.

  Ancient Egyptian religion built a whole idea of the soul around the heart, which it called ib. The ib was believed to be formed from one drop of blood taken from the mother's heart at conception. Egyptians treated it as the seat of emotion, thought, will and intention, and their language shows it. Awi-ib, meaning "happy", is literally "long of heart", and Xak-ib, meaning "estranged", is literally "truncated of heart".

  The heart was also the key to the afterlife. It was believed to survive death in the nether world, where it gave evidence for or against its owner. For that reason the heart was not removed from the body during mummification. In the Weighing of the Heart ceremony, Anubis and a variety of deities examined it, setting it against the feather of Maat, a symbol of the ideal standard.

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