How many chambers has the heart?
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Heart Cardiovascular disease
The heart is a muscular organ in humans and other animals, which pumps blood through the blood vessels of the circulatory system.  Blood provides the body with oxygen and nutrients, and also assists in the removal of metabolic wastes. The heart is located in the middle compartment of the mediastinum in the chest. 

In humans, other mammals, and birds, the heart is divided into four chambers: upper left and right atria; and lower left and right ventricles.  Commonly the right atrium and ventricle are referred together as the right heart and their left counterparts as the left heart. Fish in contrast have two chambers, an atrium and a ventricle, while reptiles have three chambers. In a healthy heart blood flows one way through the heart due to heart valves, which prevent backflow. The heart is enclosed in a protective sac, the pericardium, which also contains a small amount of fluid. The wall of the heart is made up of three layers: epicardium, myocardium, and endocardium. 

The heart pumps blood through the body. Blood low in oxygen from the systemic circulation enters the right atrium from the superior and inferior venae cavae and passes to the right ventricle. From here it is pumped into the pulmonary circulation, through the lungs where it receives oxygen and gives off carbon dioxide. Oxygenated blood then returns to the left atrium, passes through the left ventricle and is pumped out through the aorta to the systemic circulation−where the oxygen is used and metabolized to carbon dioxide. In addition the blood carries nutrients from the digestive tract to various organs of the body, while transporting waste to the liver and kidneys. Normally with each heartbeat  the right ventricle pumps the same amount of blood into the lungs as the left ventricle pumps to the body. Veins transport blood to the heart and carry deoxygenated blood - except for the pulmonary and portal veins. Arteries transport blood away from the heart, and apart from the pulmonary artery hold oxygenated blood. Their increased distance from the heart cause veins to have lower pressures than arteries. The heart contracts at a resting rate close to 72 beats per minute. Exercise temporarily increases the rate, but lowers resting heart rate in the long term, and is good for heart health.

Cardiovascular diseases (CVD) are the most common cause of death globally as of 2008, accounting for 30% of deaths.  Of these more than three quarters follow coronary artery disease and stroke.  Risk factors include: smoking, being overweight, little exercise, high cholesterol, high blood pressure, and poorly controlled diabetes, among others.  Diagnosis of CVD is often done by listening to the heart-sounds with a stethoscope, ECG or by ultrasound. Specialists who focus on diseases of the heart are called cardiologists, although many specialties of medicine may be involved in treatment.

Structure

Location and shape

The human heart is situated in the middle mediastinum, at the level of thoracic vertebrae T5-T8. A double-membraned sac called the pericardium surrounds the heart and attaches to the mediastinum.  The back surface of the heart lies near the vertebral column, and the front surface sits behind to the sternum and rib cartilages. The upper part of the heart is the attachment point for several large blood vessels - the venae cavae,  aorta and pulmonary trunk. The upper part of the heart is located at the level of the third costal cartilage. The lower tip of the heart, the apex, lies to the left of the sternum (8 to 9 cm from the midsternal line) between the junction of the fourth and fifth ribs near their articulation with the costal cartilages. 

The largest part of the heart is usually slightly offset to the left side of the chest (though occasionally it may be offset to the right) and is felt to be on the left because the left heart is stronger and larger, since it pumps to all body parts. Because the heart is between the lungs, the left lung is smaller than the right lung and has a cardiac notch in its border to accommodate the heart. 
The heart is cone-shaped, with its base positioned upwards and tapering down to the apex. An adult heart has a mass of 250–350 grams (9–12 oz).  The heart is typically the size of a fist: 12 cm (5 in) in length, 8 cm (3.5 in) wide, and 6 cm (2.5 in) in thickness. Well-trained athletes can have much larger hearts due to the effects of exercise on the heart muscle, similar to the response of skeletal muscle. 

Chambers

The heart has four chambers, two upper atria, the receiving chambers, and two lower ventricles, the discharging chambers. The atria open into the ventricles via the atrioventricular valves, present in the atrioventricular septum. This distinction is visible also on the surface of the heart as the coronary sulcus. There is an ear-shaped structure in the upper right atrium called the right atrial appendage, or auricle, and another in the upper left atrium, the left atrial appendage. The right atrium and the right ventricle together are sometimes referred to as the right heart. Similarly, the left atrium and the left ventricle together are sometimes referred to as the left heart. The ventricles are separated from each other by the interventricular septum, visible on the surface of the heart as the anterior longitudinal sulcus and the posterior interventricular sulcus.

The cardiac skeleton is made of dense connective tissue and this gives structure to the heart. It forms the atrioventricular septum which separates the atria from the ventricles, and the fibrous rings which serve as bases for the four heart valves.  The cardiac skeleton also provides an important boundary in the heart's electrical conduction system since collagen cannot conduct electricity. The interatrial septum separates the atria and the interventricular septum separates the ventricles. The interventricular septum is much thicker than the interatrial septum, since the ventricles need to generate greater pressure when they contract.

Valves

The heart has four valves, which separate its chambers. The valves ensure blood flows in the correct direction through the heart and prevents backflow. Each valve consists of two to three cusps. The valves between the atria and ventricles connected to cartilaginous strings called chordae tendinae which in turn connect to muscles on the heart wall called papillary muscles.

The valves between the atria and ventricles are called the atrioventricular valves. Between the right atrium and the right ventricle is the tricuspid valve. The tricuspid valve has three cusps, which connect to chordae tendinae and three papillary muscles named the anterior, posterior, and septal muscles, after their relative positions. The mitral valve lies between the left atrium and left ventricle. It is also known as the bicuspid valve due to its having two cusps, an anterior and a posterior cusp. These cusps are also attached via chordae tendinae to two papillary muscles projecting from the ventricular wall.

The papillary muscles extends from the walls of the heart to the chordae tendinae of valves. These muscles prevent the valves from falling too far back when they close. During the relaxation phase of the cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight. As the heart chambers contract, so do the papillary muscles. This creates tension on the chordae tendineae, helping to hold the cusps of the atrioventricular valves in place and preventing them from being blown back into the atria. 

Two additional semilunar valves sit at the exit of each of the ventricles. The pulmonary valve is located at the base of the pulmonary artery. This has three cusps which are not attached to any papillary muscles. When the ventricle relaxes blood flows back into the ventricle from the artery and this flow of blood fills the pocket-like valve, pressing against the cusps which close to seal the valve. The semilunar aortic valve is at the base of the aorta and also is not attached to papillary muscles. This too has three cusps which close with the pressure of the blood flowing back from the aorta.

Right heart

The right heart consists of two chambers, the right atrium and the right ventricle, separated by a valve, the tricuspid valve.

The right atrium receives blood almost continuously from the body's two major veins, the superior and inferior venae cavae. A small amount of blood from the coronary circulation also drains into the right atrium via the coronary sinus, which is immediately above and to the middle of the opening of the inferior vena cava. In the wall of the right atrium is an oval-shaped depression known as the fossa ovalis, which is a remnant of an opening in the fetal heart known as the foramen ovale. Most of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and the anterior surface has prominent ridges of pectinate muscles, which are also present in the right atrial appendage.

The right atrium is connected to the right ventricle by the tricuspid valve. The walls of the right ventricle are lined with trabeculae carneae, ridges of cardiac muscle covered by endocardium. In addition to these muscular ridges, a band of cardiac muscle, also covered by endocardium, known as the moderator band reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction. It arises from the lower part of the interventricular septum and crosses the interior space of the right ventricle to connect with the inferior papillary muscle. The right ventricle tapers into the pulmonary trunk, into which it ejects blood when contracting. The pulmonary trunk  branches into the left and right pulmonary arteries that carry the blood to each lung. The pulmonary valve lies between the right lung and the pulmonary trunk.

Left heart

The left heart has two chambers: the left atrium, and the left ventricle, separated by the mitral valve.

The left atrium receives oxygenated blood back from the lungs via one of the four pulmonary veins. The left atrium has an outpouching called the left atrial appendage. Like the right atrium, the left atrium is lined by pectinate muscles.  The left atrium is connected to the left ventricle by the mitral valve.

The left ventricle is much thicker as compared with the right, due to the greater force needed to pump blood to the entire body. Like the right ventricle, the left also has trabeculae carneae, but there is no moderator band. The left ventricle pumps blood to the body through the aortic valve and into the aorta. Two small openings above the aortic valve carry blood to the heart itself, the left main coronary artery and the right coronary artery.

Heart wall

The heart wall is made up of three layers: the inner endocardium, middle myocardium and outer epicardium. These are surrounded by a double-membraned sac called the pericardium.

The innermost layer of the heart is called the endocardium. It is made up of a lining of simple squamous epithelium, and covers heart chambers and valves. It is continuous with the endothelium of the veins and arteries of the heart, and is joined to the myocardium with a thin layer of connective tissue. The endocardium, by secreting endothelins, may also play a role in regulating the contraction of the myocardium.

The middle layer of the heart wall is the myocardium, which is the cardiac muscle – a layer of involuntary striated muscle tissue surrounded by a framework of collagen. The cardiac muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart, with the outer muscles forming a figure 8 pattern around the atria and around the bases of the great vessels, and inner muscles formining a figure 8 around the two ventricles and proceed toward the apex. This complex swirling pattern allows the heart to pump blood more effectively. 

There are two types of cells in cardiac muscle: muscle cells which have the ability to contract easily, and pacemaker cells of the conducting system. The muscle cells make up the bulk (99%) of cells in the atria and ventricles. These contractile cells are connected by intercalated discs which allow a rapid response to impulses of action potential from the pacemaker cells. The intercalated discs allow the cells to act as a syncytium and enable the contractions that pump blood through the heart and into the major arteries. The pacemaker cells make up 1% of cells and form the conduction system of the heart. They are generally much smaller than the contractile cells and have few myofibrils which gives them limited contractibility. Their function is similar in many respects to neurons. Cardiac muscle tissue has autorhythmicity, the unique ability to initiate a cardiac action potential at a fixed rate – spreading the impulse rapidly from cell to cell to trigger the contraction of the entire heart.

The pericardium surrounds the heart. It consists of two membranes: an inner serous membrane called the epicardium, and an outer fibrous membrane.  Blood vessels and nerves reach the cardiac muscle from the epicardium. These help influence the heart rate. These enclose the pericardial cavity which contains the  pericardial fluid that lubricates the surface of the heart.

Coronary circulation

Heart tissue, like all cells in the body, need to be supplied with oxygen, nutrients and a way of removing metabolic wastes. This is achieved by the coronary circulation, which includes arteries, veins, and lymphatic vessels, Blood circulates through the coronary circulation cyclically, in peaks and troughs relating to the heart muscle's relaxation or contraction.

Heart tissue receives blood from two arteries which arise just above the aortic valve. These are the left main coronary artery and the right coronary artery. The left main coronary artery splits shortly after leaving the aorta into two vessels, the left anterior descending and the left circumflex artery. The left anterior descending artery supplies heart tissue and the front, outer side, and the septum of the left ventricle. It does this by smaller branching arteries - diagonal and septal branches. The left circumflex supplies the back and underneath of the left ventricle. The right coronary artery supplies the right atrium, right ventricle, and lower posterior sections of the left ventricle. The right coronary artery also supplies blood to the atrioventricular node (in about 90% of people) and the sinoatrial node (in about 60% of people). The right coronary artery runs in a groove at the back of the heart and the left anterior descending artery runs in a groove at the front. There is significant variation between people in the anatomy of the arteries that supply the heart  The arteries divide at their furtherst reaches into smaller branches that join together at the edges of each arterial distribution.

The coronary sinus is a large vein that drains into the right atrium, and receives most of the venous drainage of the heart. It receives blood from the great cardiac vein (receiving the left atrium and both ventricles), the posterior cardiac vein (draining the back of the left ventricle), the middle cardiac vein (draining the bottom of the left and right ventricles), and small cardiac veins. The anterior cardiac veins drain the front of the right ventricle and drain directly into the right atrium.

Small lymphatic networks called plexuses exist beneath each of the three layers of the heart. These networks collect into a main left and a main right trunk, which travel up the groove between the ventricles that exists on the heart's surface, receiving smaller vessels as they travel up. These vessels then travel into the atrioventricular groove, and receive a third vessel which drains the section of the left ventricle sitting on the diaphragm. The left vessel joins with this third vessel, and travels along the pulmonary artery and left atrium, ending in the inferior tracheobronchial node. The right vessel travels along the right atrium and the part of the right ventricle sitting on the diaphragm. It usually then travels in front of the ascending aorta and then ends in a brachiocephalic node.

Development

The heart is the first functional organ to develop and starts to beat and pump blood at about three weeks into embryogenesis. This early start is crucial for subsequent embryonic and prenatal development.

The heart derives from splanchnopleuric mesenchyme in the neural plate which forms the cardiogenic region. Two endocardial tubes form here that fuse to form a primitive heart tube known as the tubular heart.  Between the third and fourth week, the heart tube lengthens, and begins to fold to form an S-shape within the pericardium. This places the chambers and major vessels into the correct alignment for the developed heart. Further development will include the septa and valves formation and remodelling of the heart chambers. By the end of the fifth week the septa are complete and the heart valves are completed by the ninth week.

Before the fifth week, there is an opening in the fetal heart known as the foramen ovale. The foramen ovale allowed blood in the fetal heart to pass directly from the right atrium to the left atrium, allowing some blood to bypass the lungs. Within seconds after birth, a flap of tissue known as the septum primum that previously acted as a valve closes the foramen ovale and establishes the typical cardiac circulation pattern. A depression in the surface of the right atrium remains where the foramen ovale once walls, called the fossa ovalis. 

The embryonic heart begins beating at around 22 days after conception (5 weeks after the last normal menstrual period, LMP). It starts to beat at a rate near to the mother's which is about 75–80 beats per minute (bpm). The embryonic heart rate then accelerates and reaches a peak rate of 165–185 bpm early in the early 7th week (early 9th week after the LMP).   After 9 weeks (start of the fetal stage) it starts to decelerate, slowing to around 145 (±25) bpm at birth. There is no difference in female and male heart rates before birth. 

Physiology

Blood flow

The heart functions as a pump in the circulatory system to provide a continuous flow of blood throughout the body. This circulation consists of the systemic circulation to and from the body and the pulmonary circulation to and from the lungs. Blood in the pulmonary circulation exchanges carbon dioxide for oxygen in the lungs through the process of respiration. The systemic circulation then transports oxygen to the body and returns carbon dioxide and relatively deoxygenated blood to the heart for transfer to the lungs. 

The right heart collects deoxygenated blood from two large veins, the superior and inferior venae cavae. Blood collects in the right and left atrium continuously. The superior vena cava drains blood from above the diaphragm and empties into the upper back part of the right atrium. The inferior vena cava drains the blood from below the diaphragm and empties into the back part of the atrium below the opening for the superior vena cava. Immediately above and to the middle of the opening of the inferior vena cava is the opening of the thin-walled coronary sinus. Additionally, the coronary sinus returns deoxygenated blood from the myocardium to the right atrium. The blood collects in the right atrium. When the right atrium contracts, the blood is pumped through the tricuspid valve into the right ventricle. As the right ventricle contracts, the tricuspid valve closes and the blood is pumped into the pulmonary trunk through the pulmonary valve. The pulmonary trunk divides into pulmonary arteries and progressively smaller arteries throughout the lungs, until it reaches capillaries. As these pass by alveoli carbon dioxide is exchanged for oxygen. This happens through the passive process of diffusion.

In the left heart, oxygenated blood is returned to the left atrium via the pulmonary veins. It is then pumped into the left ventricle through the mitral valve and into the aorta through the aortic valve for systemic circulation. The aorta is a large artery that branches into many smaller arteries, arterioles, and ultimately capillaries. In the capillaries, oxygen and nutrients from blood are supplied to body cells for metabolism, and exchanged for carbon dioxide and waste products. Capillary blood, now deoxygenated, travels into venules and veins that ultimately collect in the superior and inferior vena cavae, and into the right heart.

Cardiac cycle

The cardiac cycle refers to a complete heartbeat which includes systole and diastole and the intervening pause. The cycle begins with contraction of the atria and ends with relaxation of the ventricles.  Systole refers to contraction of the atria or ventricles of the heart contract. Diastole is when the atria or ventricles relax and fill with blood. The atria and ventricles work in concert, so in systole when the ventricles are contracting, the atria are relaxed and collecting blood. When the ventricles are relaxed in diastole, the atria contract to pump blood to the ventricles. This coordination ensures blood is pumped efficiently to the body.

At the beginning of the cardiac cycle, in early diastole, both the atria and ventricles are relaxed. Since blood moves from areas of high pressure to areas of low pressure, when the chambers are relaxed, blood will flow into the atria (through the coronary sinus and the pulmonary veins). As the atria begin to fill, the pressure will rise so that the blood will move from the atria into the ventricles. In late diastole the atria contract, pumping more blood into the ventricles. This causes a rise in pressure in the ventricles. As the ventricles reach systole, blood will be pumped into the pulmonary artery (right ventricle) or aorta (left ventricle).

When the atrioventricular valves (tricuspid and mitral) are open, during blood flow to the ventricles, the aortic and pulmonary valves are closed to prevent backflow into the ventricles. When the ventricular pressure is greater than the atrial pressure the tricuspid and mitral valves will shut. When the ventricles contract the pressure forces the aortic and pulmonary valves open. As the ventricles relax, the aortic and pulmonary valves will close in response to decreased pressure.

Cardiac output

Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle (stroke volume) in one minute. This is calculated by multiplying the stroke volume (SV) by the beats per minute of the heart rate (HR). So that:  CO SV x HR.
The cardiac output is normalized to body size through body surface area and is called the cardiac index.

The average cardiac output, using an average stroke volume of about 70mL, is 5.25 L/min, with a normal range of 4.0–8.0 L/min. The stroke volume is normally measured using an echocardiogram and can be influenced by the size of the heart, physical and mental condition of the individual, sex, contractility, duration of contraction, preload and afterload.

Preload refers to the filling pressure of the atria at the end of diastole, when they are at their fullest. A main factor is how long it takes the ventricles to fill—if the ventricles contract faster, then there is less time to fill and the preload will be less. Preload can also be affected by a person's blood volume. The force of each contraction of the heart muscle is proportional to the preload, described as the Frank-Starling mechanism. This states that the force of contraction is directly proportional to the initial length of muscle fiber, meaning a ventricle will contract more forcefully, the more it is stretched.

Afterload, or how much pressure the heart must generate to eject blood at systole, is influenced by vascular resistance. It can be influenced by narrowing of the heart valves (stenosis) or contraction or relaxation of the peripheral blood vessels.

The strength of heart muscle contractions controls the stroke volume. This can be influenced positively or negatively by agents termed inotropes. These can be either conditions or drugs. Positive inotropes that cause stronger contractions include high blood calcium and drugs such as Digoxin, which will act to stimulate the sympathetic nerves in the fight-or-flight response. Negative inotropes causing weaker contractions include high blood potassium, hypoxia, acidosis, and drugs such as beta blockers and calcium channel blockers.

Electrical conduction

The normal rhythmical heart beat, called sinus rhythm, is established by the sinoatrial node, the heart's pacemaker. Here an electrical signal is created that travels through the heart, causing the heart muscle to contract.

The sinoatrial node is found in the upper part of the right atrium near to the junction with the superior vena cava.  The electrical signal generated by the sinoatrial node travels through the right atrium in a radial way that is not completely understood. It travels to the left atrium via Bachmann's bundle, such that both left and right atria contract together.    The signal then travels to the atrioventricular node. This is found at the bottom of the right atrium in the atrioventricular septum—the boundary between the right atrium and the left ventricle. The septum is part of the cardiac skeleton, tissue within the heart that the electrical signal cannot pass through, which forces the signal to pass through the atrioventricular node only. The signal then travels along the bundle of His to left and right bundle branches through to the ventricles of the heart. In the ventricles the signal is carried by specialized tissue called the Purkinje fibers which then transmit the electric charge to the cardiac muscle. 

Conduction system of the heart

Heart rate

The normal resting heart rate is called the sinus rhythm, created and sustained by the sinoatrial node, a group of pacemaking cells found in the wall of the right atrium. Cells in the sinoatrial node do this by creating an action potential. The cardiac action potential is created by the movement of specific electrolytes into and out of the pacemaker cells. The action potential then spreads to nearby cells.

When the sinoatrial cells are resting, they have a negative charge on their membranes. However a rapid influx of sodium ions causes the membrane's charge to become positive. This is called depolarisation and occurs spontaneously. Once the cell has a sufficiently high charge, the sodium channels close and calcium ions then begin to enter the cell, shortly after which potassium begins to leave it. All the ions travel through ion channels in the membrane of the sinoatrial cells. The potassium and calcium only start to move out of and into the cell once it has a sufficiently high charge, and so are called voltage-gated. Shortly after this, the calcium channels close and potassium channels open, allowing potassium to leave the cell. This causes the cell to have a negative resting charge and is called repolarization. When the membrane potential reaches approximately −60 mV, the potassium channels close and the process may begin again.

The ions move from areas where they are concentrated to where they are not. For this reason sodium moves into the cell from outside, and potassium moves from within the cell to outside the cell. Calcium also plays a critical role. Their influx through slow channels means that the sinoatrial cells have a prolonged "plateau" phase when they have a positive charge. A part of this is called the absolute refractory period. Calcium ions also combine with the regulatory protein troponin C in the troponin complex to enable contraction of the cardiac muscle, and separate from the protein to allow relaxation.

Influences

The normal sinus rhythm of the heart, giving the resting heart rate, is influenced by the autonomic nervous system through sympathetic and parasympathetic nerves. These arise from two paired cardiovascular centres in the medulla oblongata.The vagus nerve of the parasympathetic nervous system acts to decrease the heart rate, and nerves from the sympathetic trunk act to increase the heart rate. These come together in the cardiac plexus near the base of the heart. Without parasympathetic input which normally predominates, the sinoatrial node would generate a heart rate of about 100 bpm.

The nerves from the sympathetic trunk emerge through the T1-T4 thoracic ganglia and travel to both the sinoatrial and atrioventricular nodes, as well as to the atria and ventricles. The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (also known as noradrenaline) at the neuromuscular junction of the cardiac nerves. This shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increased heart rate. It opens chemical or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. Norepinephrine binds to the beta–1 receptor. High blood pressure medications are used to block these receptors and so reduce the heart rate.

The cardiovascular centres receive input from a series of receptors including proprioreceptors, baroreceptors, and chemoreceptors, plus stimuli from the limbic system.  Through a series of reflexes these help regulate and sustain blood flow. For example, increased physical activity results in increased rates of firing by various proprioreceptors located in muscles, joint capsules, and tendons. With increased rates of firing, the parasympathetic stimulation may decrease or sympathetic stimulation may increase as needed in order to increase blood flow.

Similarly, baroreceptors are stretch receptors located in the aortic sinus, carotid bodies, the venae cavae, and other locations, including pulmonary vessels and the right side of the heart itself. Rates of firing from the baroreceptors represent blood pressure, level of physical activity, and the relative distribution of blood. The cardiac centers monitor baroreceptor firing to maintain cardiac homeostasis, a mechanism called the baroreceptor reflex. With increased pressure and stretch, the rate of baroreceptor firing increases, and the cardiac centers decrease sympathetic stimulation and increase parasympathetic stimulation. As pressure and stretch decrease, the rate of baroreceptor firing decreases, and the cardiac centers increase sympathetic stimulation and decrease parasympathetic stimulation.

There is a similar reflex, called the atrial reflex or Bainbridge reflex, associated with varying rates of blood flow to the atria. Increased venous return stretches the walls of the atria where specialized baroreceptors are located. However, as the atrial baroreceptors increase their rate of firing and as they stretch due to the increased blood pressure, the cardiac center responds by increasing sympathetic stimulation and inhibiting parasympathetic stimulation to increase heart rate. The opposite is also true.

In addition to the autonomic nervous system, other factors can impact on this. These include epinephrine, norepinephrine, and thyroid hormones; levels of various ions including calcium, potassium, and sodium; body temperature; hypoxia; and pH balance. Factors that increase the heart rate can include release of norepinephrine, hypoxemia, low blood pressure and dehydration, a strong emotional response, a higher body temperature, and metabolic and hormonal factors such as a low potassium or sodium level or stimulus from thyroid hormones. Decreased body temperature, relaxation, and metabolic factors can also contribute to a decrease in heart rate.

The resting heart rate of a newborn can be 129 beats per minute (bpm) and this gradually decreases until maturity.  The adult resting heart rate ranges from 60 to 100 bpm. Exercise and fitness levels, age and basal metabolic rate can all affect the heart rate. An athlete's heart rate can be lower than 60 bpm. During exercise the rate can be 150 bpm with maximum rates reaching from 200 to 220 bpm.

Heart sounds

One of the simplest methods of assessing the heart's condition is to listen to it using a stethoscope. Typically, healthy hearts have only two audible heart sounds, called S1 and S2. The first heart sound S1, is the sound created by the closing of the atrioventricular valves during ventricular contraction and is normally described as "lub". The second heart sound, S2, is the sound of the semilunar valves closing during ventricular diastole and is described as "dub". Each sound consists of two components, reflecting the slight difference in time as the two valves close. S2 may split into two distinct sounds, either as a result of inspiration or different valvular or cardiac problems. Additional heart sounds may also be present and these give rise to gallop rhythms. A third heart sound, S3 usually indicates an increase in ventricular blood volume. A fourth heart sound S4 is referred to as an atrial gallop and is produced by the sound of blood being forced into a stiff ventricle. The combined presence of S3 and S4 give a quadruple gallop.

Heart murmurs are abnormal heart sounds which can be either pathological or benign.  One example of a murmur is Still's murmur, which presents a musical sound in children, has no symptoms and disappears in adolescence.

A different type of sound, a pericardial friction rub can be heard in cases of pericarditis where the inflamed membranes can rub together. 

Clinical significance

Disease

Cardiovascular diseases, which include diseases of the heart, are the leading cause of death worldwide.  The majority of cardiovascular disease is noncommunicable and related to lifestyle and other factors, becoming more prevalent with ageing. Heart disease is a major cause of death, accounting for an average of 30% of all deaths in 2008, globally. This rate varies from a lower 28% to a high 40% in high-income countries. Doctors that specialise in the heart are called cardiologists. Many other medical professionals are involved in treating diseases of the heart, including doctors such as general practitioners, cardiothoracic surgeons and intensivists, and allied health practitioners including physiotherapists and dieticians. 

Coronary artery disease is also known as ischemic heart disease, is caused by atherosclerosis – a build-up of plaque along the inner walls of the arteries which narrows them, reducing the blood flow to the heart.  A stable plaque may cause chest pain (angina) or breathlessness during exercise or at rest, or no symptoms at all. A ruptured plaque can block a blood vessel and lead to ischaemia of the heart muscle, causing unstable angina or a heart attack. In the worst case this may cause cardiac arrest, a sudden and utter loss of output from the heart. Obesity, high blood pressure, uncontrolled diabetes, smoking and high cholesterol can all increase the risk of developing atherosclerosis and coronary artery disease.

Heart failure is where the heart can't beat enough blood to meet the needs of the body. It is generally a chronic condition, associated with age, that progresses gradually.Each side of the heart can fail independently of the other, resulting in heart failure of the right heart or the left heart. Left heart failure can also lead to right heart failure (cor pulmonale) by increasing strain on the right heart. If the heart is unable to pump sufficient blood, it may accumulate throughout the body, causing breathlessness in the lungs (pulmonary congestion; pulmonary edema), swelling (edema) of the feet or other gravity-dependent areas, decrease exercise tolerance, or cause other clinical signs such as an enlarged liver, cardiac murmurs, or a raised jugular venous pressure. Common causes of heart failure include coronary artery disease, valve disorders and diseases of cardiac muscle.

Cardiomyopathy is a noticeable deterioration of the heart muscle's ability to contract, which can lead to heart failure. The causes of many types of cardiomyopathy are poorly understood; some identified causes include alcohol, toxins, systemic disease such as sarcoidosis, and congenital conditions such as HOCM. The types of cardiomyopathy are described according to how they affect heart muscle. Cardiomyopathy can cause the heart to become enlarged (hypertrophic cardiomyopathy), constrict the outflow tracts of the heart (restrictive cardiomyopathy), or cause the heart to dilate and impact on the effiency of its beating (dilated cardiomyopathy). HOCM is often undiagnosed and can cause sudden death in young athletes.

Heart murmurs are abnormal heart sounds which can be either related to disease or benign, and there are several kinds. There are normally two heart sounds, and abnormal heart sounds can either be extra sounds, or "murmurs" related to the flow of blood between the sounds. Murmurs are graded by volume, from 1) the quietest, to 6) the loudest, and evaluated by their relationship to the heart sounds, position in the cardiac cycle, and additional features such as their radiation to other sites, changes with a person's position, the frequency of the sound as determined by the side of the stethoscope by which they are heard, and site at which they are heard loudest.Phonocardiograms can record these sounds, and echocardiograms are generally required for their diagnosis. Murmurs can result from valvular heart diseases due to narrowing (stenosis), or regurgitation of any of the main heart valves, such as aortic stenosis, mitral regurgitation or mitral valve prolapse. They can also result from a number of other disorders, including atrial and ventricular septal defects. Two common and infective causes of heart murmurs, are infective endocarditis and rheumatic fever, particularly in developing countries. Infective endocarditis involves colonisation of a heart valve, and rheumatic fever involves an initial bacterial infection by Group A streptococcus followed by a reaction against heart tissue that resembles the streptococcal antigen.

Abnormalities in the normal sinus rhythm of the heart can prevent the heart from effectively pumping blood, and are generally identified by ECG. These cardiac arrhythmias can cause an abnormal but regular heart rhythm, such as a rapid heart rate (tachycardia, classified as arising from above the ventricles or from the ventricles) or a slow heart rate (bradycardia); or may result in irregular rhythms. Tachycardia is generally defined as a heart rate faster than 100 beats per minute, and bradycardia as a heart rate slower than 60. Asystole is the cessation of heart rhythm. A random and varying rhythm is classified as atrial or ventricular fibrillation depending if the electrical activity originates in the atria or the ventricles. Abnormal conduction can cause a delay or unusual order of contraction of the heart muscle. This can be a result of a disease process, such as heart block, or congenital, such as Wolff-Parkinson-White syndrome.

Diseases may also affect the pericardium which surrounds the heart, which when inflammed is called pericarditis. This may result from infective causes (such as glandular fever, cytomegalovirus, coxsackievirus, tuberculosis or Q fever), systemic disorders such as amyloidosis or sarcoidosis, tumours, high uric acid levels, and other causes. This inflammation affects the ability of the heart to pump effectively. When fluid builds up in the pericardium this is called pericardial effusion, which when it causes acute heart failure is called cardiac tamponade. This may be blood from a traumatic injury or fluid from an effusion. This can compress the heart and adversely affect the function of the heart. The fluid can be removed from the pericardial sac using a syringe in a procedure called pericardiocentesis.

The heart can be affected by congenital diseases. These include failure of the developmental foramen ovale to close, present in up to 25% of people;  ventricular or atrial septal defects, congenital diseases of the heart valves (e.g. congenital aortic stenosis) or disease relating to blood vessels or blood flow from the heart (such as a patent ductus arteriosus or aortic coarctation).; Harrisons 1458–1465 These may cause symptoms at a variety of ages. If unoxygenated blood travels directly from the right to the left side of the heart, it may be noticed at birth, as it may cause a baby to become blue (cyanotic) such as Tetralogy of Fallot. A heart problem may impact a child's ability to grow. Some causes rectify with time and are regarded as benign. Other causes may be incidentally detected on a cardiac examination. These disorders are often diagnosed on an echocardiogram.

Diagnosis

Heart disease is diagnosed by the taking of a medical history, a cardiac examination, and further investigations, including blood tests, echocardiograms, ECGs and imaging. Other invasive procedures such as cardiac catheterisation can also play a role.

Examination

The cardiac examination includes inspection, feeling the chest with the hands (palpation) and listening with a stethoscope (auscultation).  It involves assessment of signs that may be visible on a person's hands (such as splinter haemorrhages), joints and other areas. A person's pulse is taken, usually at the radial artery near the wrist, in order to assess for the rhythm and strength of the pulse. The blood pressure is taken, using either a manual or automatic sphygmomanometer or using a more invasive measurement from within the artery. Any elevation of the jugular venous pulse is noted. A person's chest is felt for any transmitted vibrations from the heart, and then listened to with a stethoscope. A normal heart has two hearts sounds - additional heart sounds or heart murmurs may also be able to be heard and may point to disease. Additional tests may be conducted to assess a person's heart murmurs if they are present, and peripheral signs of heart disease such as swollen feet or fluid in the lungs may be assessed.

Electrocardiogram

Using surface electrodes on the body, it is possible to record the electrical activity of the heart. This tracing of the electrical signal is the electrocardiogram (ECG) or (EKG). An ECG is a bedside test and usually requires the placement of ten leads on the body. This produces a "12 lead" ECG (three extra leads are calculated mathematically, and one lead is a ground).

There are five prominent features on the ECG: the P wave (atrial depolarisation), the QRS complex (atrial repolarisation and ventricular depolarisation) and the T wave (ventricular repolarisation). These reflect the summed action potential of the heart's muscle cells as they contract. A downward deflection on the ECG implies cells are becoming more negative in charge ("depolarising"), whereas an upward inflection implies cells are becoming more positive ("repolarising"). The ECG is a useful tool in detecting rhythm disturbances and in detecting insufficient blood supply to the heart. Sometimes abnormalities are not immediately visible on the ECG. Testing when exercising can be used to provoke an abnormality, or an ECG can be worn for a longer period such as a 24-hour Holter monitor if a suspected rhythm abnormality is not present at the time of assessment.

Imaging

Several imaging methods can be used to assess the anatomy and function of the heart, including ultrasound (echocardiography), angiography, CT scans, MRI and PET. An echocardiogram is an ultrasound of the heart used to measure the heart's function, assess for valve disease, and look for any abnormalities. Echocardiography can be conducted by a probe on the chest ("transthoracic") or by a probe in the esophagus ("transoesophageal"). A typical echocardiography report will include information about the width of the valves noting any stenosis, whether there is any backflow of blood (regurgitation) and information about the blood volumes at the end of systole and diastole, including an ejection fraction, which describes how much blood is ejected from the left and right ventricles after systole. Ejection fraction can then be obtained by dividing the volume ejected by the heart (stroke volume) by the volume of the filled heart (end-diastolic volume).  Echocardiograms can also be conducted under circumstances when the body is more stressed, in order to examine for signs of lack of blood supply. This cardiac stress test involves either direct exercise, or where this is not possible, injection of a drug such as dobutamine.

CT scans, chest X-rays and other forms of imaging can help evaluate the heart's size, evaluate for signs of pulmonary oedema, and indicate whether there is fluid around the heart. They are also useful for evaluating the aorta, the major blood vessel which leaves the heart.

Treatment

A number of medications are used to treat diseases of the heart, or ameliorate symptoms.

For diseases of the heart rate or rhythm, a number of different antiarrhythmic agents are used. These may interfere with electrolyte channels and thus the cardiac action potential (such as calcium channel blockers, sodium channel blockers), interfere with stimulation of the heart by the sympathetic nervous system (beta blockers), or interfere with the movement of sodium and potassium across the cell membrane, such as digoxin.  Other examples include atropine for slow rhythms, and amiodarone for irregular rhythms. Such medications are not the only way of treating diseases of heart rate or rhythm. In the context of a new-onset irregular heart rhythm (atrial fibrillation), immediate electrical cardioversion may be attempted. For a slow heartbeat or heart block, a pacemaker or defibrillator may be inserted. The acuity of onset often affects how a rhythm disturbance is managed, as does whether a rhythm causes hemodynamic instability, such as low blood pressure or symptoms. An instigating cause is investigated for, such as a heart attack, medication, or metabolic problem.

For ischaemic heart disease, treatment also includes amelioration of symptoms. This includes GTN, beta blockers and, in the context of an acute event, stronger pain relief such as morphine and other opiates. Many of these drugs have additional protective benefits, by decreasing the sympathetic tone on the heart that occurs with the pain, or by dilating blood vessels (GTN).

Treatment of heart disease includes primary and secondary prevention to prevent the occurrence or worsening of symptoms and atherosclerosis. This includes recommendations to cease smoking, decrease alcohol consumption, increase exercise, and make modifications to their diet to decrease the consumption of fats and sugars. Medications may also be given to help better control concurrent diabetes. Statins or other drugs such as fibrates may also be given to decrease a person's cholesterol levels. Blood pressure medication may also be commenced or modified.

For many diseases of the heart, including atrial fibrillation and valvular disease, and after a heart operation, anticoagulation in the form of aspirin, warfarin, clopidogrel or novel oral anticoagulants is often given simultaneously, because of an increased risk of stroke or, in the context of a clotted heart vessel, rethrombosis.

Surgery

Surgery, when considered necessary for diseases of the heart, can take place via an open operation or via small guidewires inserted via peripheral arteries ("percutaneous coronary intervention"). Percutaneous coronary intervention is usually used in the context of an acute coronary syndrome, and may be used to insert a stent.

Coronary artery bypass surgery is one such operation. In this operation, one or more arteries surrounding the heart that have become narrowed are bypassed. This is done by taking blood vessels harvested from another part of the body. Commonly harvested veins include the saphenous veins or the internal mammary artery. Because this operation involves the heart tissue, a machine is used so that blood can bypass the heart during the operation.

Heart valve repair or valve replacement are options for diseases of the heart valves.

History 

Ancient 

Humans have known about the heart since ancient times, although its precise function and anatomy were not clearly understood.  From the primarily religious views of earlier societies towards the heart, ancient Greeks are considered to have been the primary seat of scientific understanding of the heart in the ancient world.     Aristotle considered the heart to be organ responsible for creating blood; Plato considered the heart as the source of circulating blood and Hippocrates noted blood circulating cyclically from the body through the heart to the lungs. Erasistratos (304-250 BC) noted the heart as a pump, causing dilation of blood vessels, and noted that arteries and veins both radiate from the heart, becoming progressively smaller with distance, although he believed they were filled with air and not blood. He also discovered the heart valves.

The Greek physician Galen (2nd century AD) knew blood vessels carried blood and identified venous (dark red) and arterial (brighter and thinner) blood, each with distinct and separate functions. Galen, noting the heart as the hottest organ in the body, concluded that it provided heat to the body. The heart did not pump blood around, the heart's motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves.  Galen believed the arterial blood was created by venous blood passing from the left ventricle to the right through 'pores' between the ventricles. Air from the lungs passed from the lungs via the pulmonary artery to the left side of the heart and created arterial blood. 

These ideas went unchallenged for almost a thousand years.

Pre-modern 

The earliest descriptions of the coronary and pulmonary circulation systems can  be found in the Commentary on Anatomy in Avicenna's Canon, published in 1242 by Ibn al-Nafis.  In his manuscript, al-Nafis wrote that blood passes through the pulmonary circulation instead of moving from the right to the left ventricle as previously believed by Galen. His work was later translated into Latin by Andrea Alpago. 

In Europe, the teachings of Galen continued to dominate the academic community and his doctrines were adopted as the official canon of the Church. Andreas Vesalius questioned some of Galen's beliefs of the heart in De humani corporis fabrica (1543), but his magnum opus was interpreted as a challenge to the authorities and he was subjected to a number of attacks.  Michael Servetus wrote in Christianismi Restitutio (1553) that blood flows from one side of the heart to the other via the lungs.

Modern 

The breakthrough came with the publication of De Motu Cordis (1628) by the English physician William Harvey. Harvey's book completely describes the systemic circulation and the mechanical force of the heart, leading to an overhaul of the Galenic doctrines.   Otto Frank (1865–1944) was a German physiologist; among his many published works are detailed studies of this important heart relationship. Ernest Starling (1866–1927) was an important English physiologist who also studied the heart. Although they worked largely independently, their combined efforts and similar conclusions have been recognized in the name "Frank–Starling mechanism".

Although Purkinje fibers and the bundle of His were discovered as early as the 19th century, their specific role in the electrical conduction system of the heart remained unknown until Sunao Tawara published his monograph, titled Das Reizleitungssystem des Säugetierherzens, in 1906. Tawara's discovery of the atrioventricular node prompted Arthur Keith and Martin Flack to look for similar structures in the heart, leading to their discovery of 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. 

The first successful heart transplantation was performed in 1967 by the South African surgeon Christiaan Barnard at Groote Schuur Hospital in Cape Town. This marked an important milestone in cardiac surgery, capturing the attention of both the medical profession and the world at large. However, long-term survival rates of patients were initially very low. Louis Washkansky, the first recipient of a donated heart, died 18 days after the operation while other patients did not survive for more than a few weeks.  The American surgeon Norman Shumway has been credited for his efforts to improve transplantation techniques, along with pioneers Richard Lower, Vladimir Demikhov and Adrian Kantrowitz. As of March 2000, more than 55,000 heart transplantations have been performed worldwide. 

By the middle of the 20th century, heart disease had surpassed infectious disease as the leading cause of death in the United States, and it is currently the leading cause of deaths worldwide. Since 1948, the ongoing Framingham Heart Study has shed light on the effects of various influences on the heart, including diet, exercise, and common medications such as aspirin. Although the introduction of ACE inhibitors and beta blockers has improved the management of chronic heart failure, the disease continues to be an enormous medical and societal burden, with 30 to 40% of patients dying within a year of receiving the diagnosis. 

Society and culture

Symbolism

As one of the vital organs, the heart was long identified as the center of the entire body, the seat of life, or emotion, or reason, will, intellect, purpose or the mind. The heart is an emblematic symbol in many religions, signifying "truth, consience or moral courage in many religions - the temple or throne of God in Islamic and Judeo-Christian thought; the divine centre, or atman, and the third eye of transcendent wisdom in Hinduism; the diamond of purity and essence of the Buddha; the Taoist centre of understanding."

In the Hebrew Bible, the word for heart, lev, is used in these meanings, as the seat of emotion, the mind, and referring to the anatomical organ. It is also connected in function and symbolism to the stomach. 

An important part of the concept of the soul in Ancient Egyptian religion was thought to be the heart, or ib. The ib or metaphysical heart was believed to be formed from one drop of blood from the child's mother's heart, taken at conception.  To ancient Egyptians, the heart was the seat of emotion, thought, will, and intention. This is evidenced by Egyptian expressions which incorporate the word ib, such as Awi-ib for  "happy" (literally, "long of heart"), Xak-ib for  "estranged" (literally, "truncated of heart").  In Egyptian religion, the heart was the key to the afterlife. It was conceived as surviving death in the nether world, where it gave evidence for, or against, its possessor. It was thought that the heart was examined by Anubis and a variety of deities during the Weighing of the Heart ceremony. If the heart weighed more than the feather of Maat, which symbolized the ideal standard of behavior. If the scales balanced, it meant the heart's possessor had lived a just life and could enter the afterlife; if the heart was heavier, it would be devoured by the monster Ammit. 

The Chinese character for "heart", 心, derives from a comparatively realistic depiction of a heart (indicating the heart chambers) in seal script.  The Chinese word xīn also takes the metaphorical meanings of "mind", "intention", or "core".  In Chinese medicine, the heart is seen as the center of 神 shén "spirit, consciousness".  The heart is associated with the small intestine, tongue, governs the six organs and five viscera, and belongs to fire in the five elements. 

The Sanskrit word for heart is hṛd or hṛdaya, found in the oldest surviving Sanskrit text, the Rigveda.  In Sanskrit, it may mean both the anatomical object and "mind" or "soul", representing the seat of emotion. Hrd may be a cognate of the word for heart in Greek, Latin, and English.  

Many classical philosophers and scientists, including Aristotle, considered the heart the seat of thought, reason, or emotion, often disregarding the brain as contributing to those functions. The identification of the heart as the seat of emotions in particular is due to the Roman physician Galen, who also located the seat of the passions in the liver, and the seat of reason in the brain. 

The heart also played a role in the Aztec system of belief. The most common form of human sacrifice practiced by the Aztecs was heart-extraction.  The Aztec believed that the heart (tona) was both the seat of the individual and a fragment of the Sun's heat (istli). To this day, the Nahua consider the Sun to be a heart-soul (tona-tiuh): "round, hot, pulsating". 

In Catholicism, there has been a long tradition of worship of the heart, stemming from worship of the wounds of Jesus Christ which gained prominence from the mid sixteenth century.  This tradition influenced the development of the medieval Christian devotion to the Sacred Heart of Jesus and the parallel worship of Immaculate Heart of Mary, made popular by John Eudes. 

The expression of a broken heart is a cross-cultural reference to grief for a lost one or to unfulfilled romantic love.

The notion of "Cupid's arrows" is ancient, due to Ovid, but while Ovid describes Cupid as wounding his victims with his arrows, it is not made explicit that it is the heart that is wounded. The familiar iconography of Cupid shooting little heart symbols is a Renaissance theme that became tied to Valentine's day.

Food

Animal hearts are widely consumed as food. As they are almost entirely muscle, they are high in protein. They are often included in dishes with other offal, for example in the pan-Ottoman kokoretsi.

Chicken hearts are considered to be giblets, and are often grilled on skewers: Japanese hāto yakitori, Brazilian churrasco de coração, Indonesian chicken heart satay.  They can also be pan-fried, as in Jerusalem mixed grill. In Egyptian cuisine, they can be used, finely chopped, as part of stuffing for chicken.  Many recipes combined them with other giblets, such as the Mexican pollo en menudencias  and the Russian ragu iz kurinyikh potrokhov. 

The hearts of beef, pork, and mutton can generally be interchanged in recipes. As heart is a hard-working muscle, it makes for "firm and rather dry" meat,  so is generally slow-cooked. Another way of dealing with toughness is to julienne the meat, as in Chinese stir-fried heart. 

Beef heart may be grilled or braised. In the Peruvian anticuchos de corazón, barbecued beef hearts are grilled after being tenderized through long marination in a spice and vinegar mixture. An Australian recipe for "mock goose" is actually braised stuffed beef heart. 

Pig heart is stewed, poached, braised,  or made into sausage. The Balinese oret is a sort of blood sausage made with pig heart and blood. A French recipe for cœur de porc à l'orange is made of braised heart with an orange sauce.

Other animals

The structure of the heart varies among the different animal groups. Cephalopods have two "gill hearts" also known as branchial hearts and one "systemic heart". The vertebrate heart lies in the front (ventral) part of the body cavity, dorsal to the gut. It is always surrounded by a pericardium, which is usually a distinct structure, but may be continuous with the peritoneum in jawless and cartilaginous fish.

The SA node is found in all amniotes but not in more primitive vertebrates. In these animals, the muscles of the heart are relatively continuous and the sinus venosus coordinates the beat which passes in a wave through the remaining chambers. Indeed, since the sinus venosus is incorporated into the right atrium in amniotes, it is likely homologous with the SA node. In teleosts, with their vestigial sinus venosus, the main centre of coordination is, instead, in the atrium. The rate of heartbeat varies enormously between different species, ranging from around 20 beats per minute in codfish to around 600 in hummingbirds and up to 1200 bpm in the ruby-throated hummingbird. 

Double circulatory systems 

In the heart of lungfish, the septum extends part-way into the ventricle. This allows for some degree of separation between the de-oxygenated bloodstream destined for the lungs and the oxygenated stream that is delivered to the rest of the body. The absence of such a division in living amphibian species may be partly due to the amount of respiration that occurs through the skin; thus, the blood returned to the heart through the venae cavae is already partially oxygenated. As a result, there may be less need for a finer division between the two bloodstreams than in lungfish or other tetrapods. Nonetheless, in at least some species of amphibian, the spongy nature of the ventricle does seem to maintain more of a separation between the bloodstreams. Also, the original valves of the conus arteriosus have been replaced by a spiral valve that divides it into two parallel parts, thereby helping to keep the two bloodstreams separate.

Adult amphibians and most reptiles have a double circulatory system but the heart is not separated into two pumps. The development of the double system is necessitated by the presence of lungs which deliver oxygenated blood directly to the heart.

In amphibians, the atrium is divided into two chambers by a muscular septum but there is only one ventricle. The sinus venosus, which remains large, connects only to the right atrium and receives blood from the venae cavae, with the pulmonary vein by-passing it to enter the left atrium.

The heart of most reptiles is similar in structure to that of lungfish but the septum is generally much larger. This divides the ventricle into two halves but the septum does not reach the whole length of the heart and there is a considerable gap near the pulmonary artery and aorta openings. In most reptilian species, there appears to be little, if any, mixing between the bloodstreams, so the aorta receives, essentially, only oxygenated blood.

The fully divided heart 

Archosaurs (crocodilians and birds) and mammals show complete separation of the heart into two pumps for a total of four heart chambers; it is thought that the four-chambered heart of archosaurs evolved independently from that of mammals. In crocodilians, there is a small opening, the foramen of Panizza, at the base of the arterial trunks and there is some degree of mixing between the blood in each side of the heart, during a dive underwater; thus, only in birds and mammals are the two streams of blood – those to the pulmonary and systemic circulations – permanently kept entirely separate by a physical barrier.

Fish 

Primitive fish have a four-chambered heart, but the chambers are arranged sequentially so that this primitive heart is quite unlike the four-chambered hearts of mammals and birds. The first chamber is the sinus venosus, which collects deoxygenated blood, from the body, through the hepatic and cardinal veins. From here, blood flows into the atrium and then to the powerful muscular ventricle where the main pumping action will take place. The fourth and final chamber is the conus arteriosus which contains several valves and sends blood to the ventral aorta. The ventral aorta delivers blood to the gills where it is oxygenated and flows, through the dorsal aorta, into the rest of the body. (In tetrapods, the ventral aorta has divided in two; one half forms the ascending aorta, while the other forms the pulmonary artery).

In the adult fish, the four chambers are not arranged in a straight row but, instead form an S-shape with the latter two chambers lying above the former two. This relatively simpler pattern is found in cartilaginous fish and in the ray-finned fish. In teleosts, the conus arteriosus is very small and can more accurately be described as part of the aorta rather than of the heart proper. The conus arteriosus is not present in any amniotes, presumably having been absorbed into the ventricles over the course of evolution. Similarly, while the sinus venosus is present as a vestigial structure in some reptiles and birds, it is otherwise absorbed into the right atrium and is no longer distinguishable.

Invertebrates

Arthropods have an open circulatory system, and often some short open-ended arteries.The arthropod heart is typically a muscular tube that runs the length of the body, under the back and from the base of the head. Instead of blood the circulatory fluid is haemolymph which carries the most commonly used respiratory pigment, copper-based haemocyanin as the oxygen transporter; iron-based haemoglobin is used by only a few arthropods. The heart contracts in ripples from the rear to the front of the animal transporting water and nutrients. Pairs of valves run alongside the heart, allowing fluid to enter whilst preventing backflow.

In insects, the circulatory system is not used to transport oxygen and so is much reduced, having no veins or arteries and consisting of a single perforated tube running dorsally which pumps peristaltically. The simpler unsegmented invertebrates have no body cavity, and oxygen and nutrients pass through their bodies by diffusion.

Additional images 

File:Blausen 0451 Heart Anterior.png|The human heart viewed from the front
File:Blausen 0456 Heart Posterior.png|The human heart viewed from behind
File:Blausen 0260 CoronaryVessels Anterior.png|The coronary circulation
File:Slide2aaaaaa.JPG|An anatomical specimen of the heart
File:Human_Heart_and_Circulatory_System.png|Heart Illustration with circulatory system

Notes Cardiovascular disease (CVD) is a class of diseases that involve the heart or blood vessels.  Cardiovascular disease includes coronary artery diseases (CAD) such as angina and myocardial infarction (commonly known as a heart attack). Other CVDs are stroke, hypertensive heart disease, rheumatic heart disease, cardiomyopathy, heart arrhythmia, congenital heart disease, valvular heart disease, carditis, aortic aneurysms, peripheral artery disease, and venous thrombosis.

The underlying mechanisms vary depending on the disease in question. Coronary artery disease, stroke, and peripheral artery disease involve atherosclerosis. This may be caused by high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, and excessive alcohol consumption, among others. High blood pressure results in 13% of CVD deaths, while tobacco results in 9%, diabetes 6%, lack of exercise 6% and obesity 5%. Rheumatic heart disease may follow untreated strep throat.

It is estimated that 90% of CVD is preventable. Prevention of atherosclerosis is by decreasing risk factors through: healthy eating, exercise, avoidance of tobacco smoke and limiting alcohol intake. Treating high blood pressure and diabetes is also beneficial. Treating people who have strep throat with antibiotics can decrease the risk of rheumatic heart disease.  The effect of the use of aspirin in people who are otherwise healthy is of unclear benefit.   The United States Preventive Services Task Force recommends against its use for prevention in women less than 55 and men less than 45 years old; however, in those who are older it is recommends in some individuals.  Treatment of those who have CVD improves outcomes.

Cardiovascular diseases are the leading cause of death globally. This is true in all areas of the world except Africa. Together they resulted in 17.3 million deaths (31.5%) in 2013 up from 12.3 million (25.8%) in 1990. Deaths, at a given age, from CVD are more common and have been increasing in much of the developing world, while rates have declined in most of the developed world since the 1970s.  Coronary artery disease and stroke account for 80% of CVD deaths in males and 75% of CVD deaths in females. Most cardiovascular disease affects older adults. In the United States 11% of people between 20 and 40 have CVD, while 37% between 40 and 60, 71% of people between 60 and 80, and 85% of people over 80 have CVD.  The average age of death from coronary artery disease in the developed world is around 80 while it is around 68 in the developing world. Disease onset is typically seven to ten years earlier in men as compared to women.

Types

There are many cardiovascular diseases involving the blood vessels. They are known as vascular diseases:
*Coronary artery disease (also known as coronary heart disease and ischemic heart disease)
*Peripheral arterial disease – disease of blood vessels that supply blood to the arms and legs
*Cerebrovascular disease – disease of blood vessels that supply blood to the brain (includes stroke)
*Renal artery stenosis
*Aortic aneurysm

There are also many cadiovascular diseases that involve the heart.
*Cardiomyopathy – diseases of cardiac muscle
*Hypertensive heart disease – diseases of the heart secondary to high blood pressure or hypertension
* Heart failure
* Pulmonary heart disease – a failure at the right side of the heart with respiratory system involvement
* Cardiac dysrhythmias – abnormalities of heart rhythm
*Inflammatory heart disease
** Endocarditis – inflammation of the inner layer of the heart, the endocardium. The structures most commonly involved are the heart valves.
** Inflammatory cardiomegaly
** Myocarditis – inflammation of the myocardium, the muscular part of the heart.
*Valvular heart disease
*Congenital heart disease – heart structure malformations existing at birth
*Rheumatic heart disease – heart muscles and valves damage due to rheumatic fever caused by  Streptococcus pyogenes a group A streptococcal infection.

Risk factors

There are several risk factors for heart diseases: age, gender, tobacco use, physical inactivity, excessive alcohol consumption, unhealthy diet, obesity, family history of cardiovascular disease, raised blood pressure (hypertension), raised blood sugar (diabetes mellitus), raised blood cholesterol (hyperlipidemia), psychosocial factors, poverty and low educational status, and air pollution.     While the individual contribution of each risk factor varies between different communities or ethnic groups the overall contribution of these risk factors is very consistent. Some of these risk factors, such as age, gender or family history, genetic, are immutable; however, many important cardiovascular risk factors are modifiable by lifestyle change, social change, drug treatment and prevention of hypertension, hyperlipidemia, and diabetes.

Genetics

Cardiovascular disease in a person's parents increases their risk by 3 fold. 

Age

Age is by far the most important risk factor in developing cardiovascular or heart diseases, with approximately a tripling of risk with each decade of life.  Coronary fatty streaks can begin to form in adolescence.  It is estimated that 82 percent of people who die of coronary heart disease are 65 and older.  At the same time, the risk of stroke doubles every decade after age 55. 

Multiple explanations have been proposed to explain why age increases the risk of cardiovascular/heart diseases. One of them is related to serum cholesterol level. In most populations, the serum total cholesterol level increases as age increases. In men, this increase levels off around age 45 to 50 years. In women, the increase continues sharply until age 60 to 65 years.

Aging is also associated with changes in the mechanical and structural properties of the vascular wall, which leads to the loss of arterial elasticity and reduced arterial compliance and may subsequently lead to coronary artery disease. 

Sex

Men are at greater risk of heart disease than pre-menopausal women.http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors Once past menopause, it has been argued that a woman's risk is similar to a man's although more recent data from the WHO and UN disputes this. If a female has diabetes, she is more likely to develop heart disease than a male with diabetes. 

Coronary heart diseases are 2 to 5 times more common among middle-aged men than women.  In a study done by the World Health Organization, sex contributes to approximately 40% of the variation in sex ratios of coronary heart disease mortality.  Another study reports similar results finding that gender differences explains nearly half the risk associated with cardiovascular diseases One of the proposed explanations for gender differences in cardiovascular diseases is hormonal difference.  Among women, estrogen is the predominant sex hormone. Estrogen may have protective effects through glucose metabolism and hemostatic system, and may have direct effect in improving endothelial cell function.  The production of estrogen decreases after menopause, and this may change the female lipid metabolism toward a more atherogenic form by decreasing the HDL cholesterol level while increasing LDL and total cholesterol levels.

Among men and women, there are notable differences in body weight, height, body fat distribution, heart rate, stroke volume, and arterial compliance. In the very elderly, age-related large artery pulsatility and stiffness is more pronounced among women than men. This may be caused by the women's smaller body size and arterial dimensions which are independent of menopause.

Tobacco

Cigarettes are the major form of smoked tobacco. Risks to health from tobacco use result not only from direct consumption of tobacco, but also from exposure to second-hand smoke. Approximately 10% of cardiovascular disease is attributed to smoking; however, people who quit smoking by age 30 have almost as low a risk of death as never smokers. 

Physical inactivity

Insufficient physical activity (defined as less than 5 x 30 minutes of moderate activity per week, or less than 3 x 20 minutes of vigorous activity per week) is currently the fourth leading risk factor for mortality worldwide.  In 2008, 31.3% of adults aged 15 or older (28.2% men and 34.4% women) were insufficiently physically active.  
The risk of ischemic heart disease and diabetes mellitus is reduced by almost a third in adults who participate in 150 minutes of moderate physical activity each week (or equivalent).  In addition, physical activity assists weight loss and improves blood glucose control, blood pressure, lipid profile and insulin sensitivity. These effects may, at least in part, explain its cardiovascular benefits.

Diet

High dietary intakes of saturated fat, trans-fats and salt, and low intake of fruits, vegetables and fish are linked to cardiovascular risk, although whether all these associations are a cause is disputed. The World Health Organization attributes approximately 1.7 million deaths worldwide to low fruit and vegetable consumption. The amount of dietary salt consumed is also an important determinant of blood pressure levels and overall cardiovascular risk. Frequent consumption of high-energy foods, such as processed foods that are high in fats and sugars, promotes obesity and may increase cardiovascular risk.  High trans-fat intake has adverse effects on blood lipids and circulating inflammatory markers,  and elimination of trans-fat from diets has been widely advocated.  
There is evidence that higher consumption of sugar is associated with higher blood pressure and unfavorable blood lipids,  and sugar intake also increases the risk of diabetes mellitus.  High consumption of processed meats is associated with an increased risk of cardiovascular disease, possibly in part due to increased dietary salt intake. 

The relationship between alcohol consumption and cardiovascular disease is complex, and may depend on the amount of alcohol consumed. There is a direct relationship between high levels of alcohol consumption and risk of cardiovascular disease.  Drinking at low levels without episodes of heavy drinking may be associated with a reduced risk of cardiovascular disease. 
Overall alcohol consumption at the population level is associated with multiple health risks that exceed any potential benefits. 

Socioeconomic disadvantage

Cardiovascular disease affects low- and middle-income countries even more than high-income countries. There is relatively little information regarding social patterns of cardiovascular disease within low- and middle-income countries, but within high-income countries low income and low educational status are consistently associated with greater risk of cardiovascular disease.  Policies that have resulted in increased socio-economic inequalities have been associated with greater subsequent socio-economic differences in cardiovascular disease implying a cause and effect relationship. Psychosocial factors, environmental exposures, health behaviours, and health-care access and quality contribute to socio-economic differentials in cardiovascular disease. 
  The Commission on Social Determinants of Health recommended that more equal distributions of power, wealth, education, housing, environmental factors, nutrition, and health care were needed to address inequalities in cardiovascular disease and non-communicable diseases. 

Air pollution

Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, PM2.5 is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m3 of PM2.5 long-term exposure, there was an estimated 8–18% CVD mortality risk. Women had a higher relative risk (RR) (1.42) for PM2.5 induced coronary artery disease than men (0.90) did.  Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m3 of PM2.5 resulted in a 48% increase of CVD mortality risk. In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m3 of PM2.5.   Other research has implicated PM2.5 in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure.   PM2.5 is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

Cardiovascular risk assessment

Existing cardiovascular disease or a previous cardiovascular event, such as a heart attack or stroke, is the strongest predictor of a future cardiovascular event.  Age, sex, smoking, blood pressure, blood lipids and diabetes are important predictors of future cardiovascular disease in people who are not known to have cardiovascular disease.  These measures, and sometimes others, may be combined into composite risk scores to estimate an individual's future risk of cardiovascular disease. Numerous risk scores exist although their respective merits are debated.  Other diagnostic tests and biomarkers remain under evaluation but currently these lack clear-cut evidence to support their routine use. They include family history, coronary artery calcification score, high sensitivity C-reactive protein (hs-CRP), ankle brachial index, lipoprotein subclasses and particle concentration, lipoprotein(a), apolipoproteins A-I and B, fibrinogen, white blood cell count, homocysteine, N-terminal pro B-type natriuretic peptide  (NT-proBNP), and markers of kidney function.  

Work 

Little is known about the relationship between work and cardiovascular disease, but links have been established between certain toxins, extreme heat and cold, exposure to tobacco smoke, and mental health concerns such as stress and depression. 

Pathophysiology

Population-based studies show that atherosclerosis, the major precursor of cardiovascular disease, begins in childhood. The Pathobiological Determinants of Atherosclerosis in Youth Study demonstrated that intimal lesions appear in all the aortas and more than half of the right coronary arteries of youths aged 7–9 years. 

This is extremely important considering that 1 in 3 people die from complications attributable to atherosclerosis. In order to stem the tide, education and awareness that cardiovascular disease poses the greatest threat, and measures to prevent or reverse this disease must be taken.

Obesity and diabetes mellitus are often linked to cardiovascular disease,  as are a history of chronic kidney disease and hypercholesterolaemia.   In fact, cardiovascular disease is the most life-threatening of the diabetic complications and diabetics are two- to four-fold more likely to die of cardiovascular-related causes than nondiabetics.   

Screening

Screening ECGs (either at rest or with exercise) are not recommended in those without symptoms who are at low risk. This includes those who are young without risk factors.  In those at higher risk the evidence for screening with ECGs is inconclusive.

Additionally echocardiography, myocardial perfusion imaging, and cardiac stress testing is not recommended in those at low risk who do not have symptoms. 

Some biomarkers may add to conventional cardiovascular risk factors in predicting the risk of future cardiovascular disease; however, the clinical value of some biomarkers is questionable.  

The NIH recommends lipid testing in children beginning at the age of 2 if there is a family history of heart disease or lipid problems.  It is hoped that early testing will improve lifestyle factors in those at risk such as diet and exercise. 

Prevention

Up to 90% of cardiovascular disease may be preventable if established risk factors are avoided.   Currently practiced measures to prevent cardiovascular disease include:
* A low-fat, high-fiber diet including whole grains and fruit and vegetables.   Five portions a day reduces risk by about 25%. 
* Tobacco cessation and avoidance of second-hand smoke
* Limit alcohol consumption to the recommended daily limits; consumption of 1–2 standard alcoholic drinks per day may reduce risk by 30%.   However, excessive alcohol intake increases the risk of cardiovascular disease. 
* Lower blood pressures, if elevated
* Decrease non-HDL cholesterol.  
* Decrease body fat if overweight or obese 
* Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week (multiply by three if horizontal);
* Reduce sugar consumptions
* Decrease psychosocial stress.  This measure may be complicated by imprecise definitions of what constitute psychosocial interventions.  Mental stress–induced myocardial ischemia is associated with an increased risk of heart problems in those with previous heart disease.  Severe emotional and physical stress leads to a form of heart dysfunction known as Takotsubo syndrome in some people.  Stress, however, plays a relatively minor role in hypertension.  Specific relaxation therapies are of unclear benefit. 

For adults without a known diagnosis of hypertension, diabetes, hyperlipidemia, or cardiovascular disease, routine counseling to advise them to improve their diet and increase their physical activity has not been found to significantly alter behavior, and thus is not recommended.  It is unclear whether or not dental care in those with periodontitis affects the risk of cardiovascular disease.  Exercise in those who are at high risk of heart disease has not been well studied as of 2014. 

Diet

A diet high in fruits and vegetables decreases the risk of cardiovascular disease and death. Evidence suggests that the Mediterranean diet may improve cardiovascular outcomes.  There is also evidence that a Mediterranean diet may be more effective than a low-fat diet in bringing about long-term changes to cardiovascular risk factors (e.g., lower cholesterol level and blood pressure).  The DASH diet (high in nuts, fish, fruits and vegetables, and low in sweets, red meat and fat) has been shown to reduce blood pressure,  lower total and low density lipoprotein cholesterol   and improve metabolic syndrome;  but the long-term benefits outside the context of a clinical trial have been questioned.  A high fiber diet appears to lower the risk. 

Total fat intake does not appear to be an important risk factor.  A diet high in trans fatty acids, however, does appear to increase rates of cardiovascular disease. Worldwide, dietary guidelines recommend a reduction in saturated fat. However, there are some questions around the effect of saturated fat on cardiovascular disease in the medical literature. Reviews from 2014 and 2015 did not find evidence of harm from saturated fats. A 2012 Cochrane review found suggestive evidence of a small benefit from replacing dietary saturated fat by unsaturated fat.  A 2013 meta analysis concludes that substitution with omega 6 linoleic acid (a type of unsaturated fat) may increase cardiovascular risk. Replacement of saturated fats with carbohydrates does not change or may increase risk.   Benefits from replacement with polyunsaturated fat appears greatest;  however, supplementation with omega-3 fatty acids (a type of polysaturated fat) does not appear to have an effect. 

The effect of a low-salt diet is unclear. A Cochrane review concluded that any benefit in either hypertensive or normal-tensive people is small if present. In addition, the review suggested that a low-salt diet may be harmful in those with congestive heart failure. However, the review was criticized in particular for not excluding a trial in heart failure where people had low-salt and -water levels due to diuretics. When this study is left out, the rest of the trials show a trend to benefit. Another review of dietary salt concluded that there is strong evidence that high dietary salt intake increases blood pressure and worsens hypertension, and that it increases the number of cardiovascular disease events; the latter happen both through the increased blood pressure and, quite likely, through other mechanisms. Moderate evidence was found that high salt intake increases cardiovascular mortality; and some evidence was found for an increase in overall mortality, strokes, and left ventricular hypertrophy.

Medication

Aspirin has been found to be of only modest benefit in those at low risk of heart disease as the risk of serious bleeding is almost equal to the benefit with respect to cardiovascular problems.  In those at very low risk it is not recommended. 

Statins are effective in preventing further cardiovascular disease in people with a history of cardiovascular disease. As the event rate is higher in men than in women, the decrease in events is more easily seen in men than women. In those without cardiovascular disease but risk factors statins appear to also be beneficial with a decrease in the risk of death and further heart disease.  A United States guideline recommends statins in those who have a 12% or greater risk of cardiovascular disease over the next ten years. 

The time course over which statins provide prevention against death appears to be long, of the order of one year, which is much longer than the duration of their effect on lipids.  The medications niacin, fibrates and CETP Inhibitors, while they may increase HDL cholesterol do not affect the risk of cardiovascular disease in those who are already on statins. 

The use of vasoactive agents for people with pulmonary hypertension with left heart disease or hypoxemic lung diseases may cause harm and unnecessary expense. 

Supplements

While a healthy diet is beneficial, in general the effect of antioxidant supplementation (vitamin E, vitamin C, etc.) or vitamins has not been shown to protection against cardiovascular disease and in some cases may possibly result in harm.   Mineral supplements have also not been found to be useful.  Niacin, a type of vitamin B3, may be an exception with a modest decrease in the risk of cardiovascular events in those at high risk.   Magnesium supplementation lowers high blood pressure in a dose dependent manner. Magnesium therapy is recommended for patients with ventricular arrhythmia associated with torsades de pointes who present with long QT syndrome as well as for the treatment of patients with digoxin intoxication-induced arrhythmias. Evidence to support omega-3 fatty acid supplementation is lacking. 

Management

Cardiovascular disease is treatable with initial treatment primarily focused on diet and lifestyle interventions.

Epidemiology

Cardiovascular diseases are the leading cause of death. In 2008, 30% of all global death is attributed to cardiovascular diseases. Death caused by cardiovascular diseases are also higher in low- and middle-income countries as over 80% of all global death caused by cardiovascular diseases occurred in those countries. It is also estimated that by 2030, over 23 million people will die from cardiovascular diseases each year.

It is estimated that 60% of the world's cardiovascular disease burden will occur in the South Asian subcontinent despite only accounting for 20% of the world's population. This may be secondary to a combination of genetic predisposition and environmental factors. Organizations such as the Indian Heart Association are working with the World Heart Federation to raise awareness about this issue.Indian Heart Association Why South Asians Facts Web. 29 April 2015. 

Research

The first studies on cardiovascular health were performed in year 1949 by Jerry Morris using occupational health data and were published in year 1958.  The causes, prevention, and/or treatment of all forms of cardiovascular disease remain active fields of biomedical research, with hundreds of scientific studies being published on a weekly basis.

A fairly recent emphasis is on the link between low-grade inflammation that hallmarks atherosclerosis and its possible interventions. C-reactive protein is a common inflammatory marker that has been found to be present in increased levels in patients who are at risk for cardiovascular disease.   Also osteoprotegerin, which is involved with regulation of a key inflammatory transcription factor called NF-κB, has been found to be a risk factor of cardiovascular disease and mortality.  

Some areas currently being researched include the possible links between infection with Chlamydophila pneumoniae (a major cause of pneumonia) and coronary artery disease. The Chlamydia link has become less plausible with the absence of improvement after antibiotic use. 

Several research also investigated the benefits of melatonin on cardiovascular diseases prevention and cure. Melatonin is a pineal gland secretion and it is shown to be able to lower total cholesterol, very-low-density and low-density lipoprotein cholesterol levels in the blood plasma of rats. Reduction of blood pressure is also observed when pharmacological doses are applied. Thus, it is deemed to be a plausible treatment for hypertension. However, further research needs to be conducted to investigate the side-effects, optimal dosage, etc. before it can be licensed for use.
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