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From OpenStax, Anatomy and Physiology 2e, section 19.1 "Heart Anatomy" (CC BY 4.0). https://openstax.org/books/anatomy-andphysiology-2e/pages/19-1-heart-anatomy. Used unchanged as a test file.

Heart Anatomy
19.1 Heart Anatomy
Learning Objectives
By the end of this section, you will be able to:
Describe the location and position of the heart within the body cavity
Describe the internal and external anatomy of the heart
Identify the tissue layers of the heart
Relate the structure of the heart to its function as a pump
Compare systemic circulation to pulmonary circulation
Identify the veins and arteries of the coronary circulation system
Trace the pathway of oxygenated and deoxygenated blood thorough the chambers of the heart
The vital importance of the heart is obvious. If one assumes an average rate of contraction of 75 contractions per
minute, a human heart would contract approximately 108,000 times in one day, more than 39 million times in one
year, and nearly 3 billion times during a 75-year lifespan. Each of the major pumping chambers of the heart ejects
approximately 70 mL blood per contraction in a resting adult. This would be equal to 5.25 liters of fluid per minute
and approximately 14,000 liters per day. Over one year, that would equal 10,000,000 liters or 2.6 million gallons of
blood sent through roughly 60,000 miles of vessels. In order to understand how that happens, it is necessary to
understand the anatomy and physiology of the heart.

Location of the Heart
The human heart is located within the thoracic cavity, medially between the lungs in the space known as the
mediastinum. Figure 19.2 shows the position of the heart within the thoracic cavity. Within the mediastinum, the
heart is separated from the other mediastinal structures by a tough membrane known as the pericardium, or
pericardial sac, and sits in its own space called the pericardial cavity. The dorsal surface of the heart lies near the
bodies of the vertebrae, and its anterior surface sits deep to the sternum and costal cartilages. The great veins, the
superior and inferior venae cavae, and the great arteries, the aorta and pulmonary trunk, are attached to the superior
surface of the heart, called the base. The base of the heart is located at the level of the third costal cartilage, as seen
in Figure 19.2. The inferior tip of the heart, the apex, lies just to the left of the sternum between the junction of the
fourth and fifth ribs near their articulation with the costal cartilages. The right side of the heart is deflected anteriorly,
and the left side is deflected posteriorly. It is important to remember the position and orientation of the heart when
placing a stethoscope on the chest of a patient and listening for heart sounds, and also when looking at images taken
from a midsagittal perspective. The slight deviation of the apex to the left is reflected in a depression in the medial
surface of the superior lobe of the left lung, called the cardiac notch.

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Figure 19.2 Position of the Heart in the Thorax The heart is located within the thoracic cavity, medially between the
lungs in the mediastinum. It is about the size of a fist, is broad at the top (called the base), and tapers toward the
apex.

Everyday Connection
CPR
The position of the heart in the torso between the vertebrae and sternum (see Figure 19.2 for the position of the heart
within the thorax) allows for individuals to apply an emergency technique known as cardiopulmonary resuscitation
(CPR) if the heart of a patient should stop. By applying pressure with the flat portion of one hand on the sternum in
the area between the line at T4 and T9 (Figure 19.3), it is possible to manually compress the blood within the heart
enough to push some of the blood within it into the pulmonary and systemic circuits. This is particularly critical for
the brain, as irreversible damage and death of neurons occur within minutes of loss of blood flow. Current standards
call for compression of the chest at least 5 cm deep and at a rate of 100 compressions per minute, a rate equal to the
beat in “Staying Alive,” recorded in 1977 by the Bee Gees. If you are unfamiliar with this song, a version is
available on www.youtube.com. At this stage, the emphasis is on performing high-quality chest compressions, rather
than providing artificial respiration. CPR is generally performed until the patient regains spontaneous contraction or
is declared dead by an experienced healthcare professional.
When performed by untrained or overzealous individuals, CPR can result in broken ribs or a broken sternum, and
can inflict additional severe damage on the patient. It is also possible, if the hands are placed too low on the sternum,
to manually drive the xiphoid process into the liver, a consequence that may prove fatal for the patient. Proper
training is essential. This proven life-sustaining technique is so valuable that virtually all medical personnel as well
as concerned members of the public should be certified and routinely recertified in its application. CPR courses are

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1st rib
Trachea
Thymus
Aortic arch
Thoracic aorta
Diaphragm
Inferior vena cava
Esophagus
Sagittal view
Arch of aorta
Pulmonary trunk
Left auricle
Left lung
Left ventricle
Pericardial cavity
Apex of heart
Superior vena cava
Right lung
Right auricle
Right atrium
Right ventricle
Ribs (cut)
Diaphragm
Edge of parietal pleura (cut)
Edge of parietal pericardium (cut)

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offered at a variety of locations, including colleges, hospitals, the American Red Cross, and some commercial
companies. They normally include practice of the compression technique on a mannequin.

Figure 19.3 CPR Technique If the heart should stop, CPR can maintain the flow of blood until the heart resumes
beating. By applying pressure to the sternum, the blood within the heart will be squeezed out of the heart and into the
circulation. Proper positioning of the hands on the sternum to perform CPR would be between the lines at T4 and T9.

Interactive Link
Visit the American Heart Association website to help locate a course near your home in the United States. There are
also many other national and regional heart associations that offer the same service, depending upon the location.

Shape and Size of the Heart
The shape of the heart is similar to a pinecone, rather broad at the superior surface and tapering to the apex (see
Figure 19.2). A typical heart is approximately the size of your fist: 12 cm (5 in) in length, 8 cm (3.5 in) wide, and 6
cm (2.5 in) in thickness. Given the size difference between most members of the sexes, the weight of a female heart
is approximately 250–300 grams (9 to 11 ounces), and the weight of a male heart is approximately 300–350 grams
(11 to 12 ounces). The heart of a well-trained athlete, especially one specializing in aerobic sports, can be
considerably larger than this. Cardiac muscle responds to exercise in a manner similar to that of skeletal muscle.
That is, exercise results in the addition of protein myofilaments that increase the size of the individual cells without
increasing their numbers, a concept called hypertrophy. Hearts of athletes can pump blood more effectively at lower
rates than those of nonathletes. Enlarged hearts are not always a result of exercise; they can result from pathologies,
such as hypertrophic cardiomyopathy. The cause of an abnormally enlarged heart muscle is unknown, but the
condition is often undiagnosed and can cause sudden death in apparently otherwise healthy young people.

Chambers and Circulation through the Heart
The human heart consists of four chambers: The left side and the right side each have one atrium and one ventricle.
Each of the upper chambers, the right atrium (plural = atria) and the left atrium, acts as a receiving chamber and
contracts to push blood into the lower chambers, the right ventricle and the left ventricle. The ventricles serve as the
primary pumping chambers of the heart, propelling blood to the lungs or to the rest of the body.
There are two distinct but linked circuits in the human circulation called the pulmonary and systemic circuits.
Although both circuits transport blood and everything it carries, we can initially view the circuits from the point of
view of gases. The pulmonary circuit transports blood to and from the lungs, where it picks up oxygen and delivers

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carbon dioxide for exhalation. The systemic circuit transports oxygenated blood to virtually all of the tissues of the
body and returns relatively deoxygenated blood and carbon dioxide to the heart to be sent back to the pulmonary
circulation.
The right ventricle pumps deoxygenated blood into the pulmonary trunk, which leads toward the lungs and
bifurcates into the left and right pulmonary arteries. These vessels in turn branch many times before reaching the
pulmonary capillaries, where gas exchange occurs: Carbon dioxide exits the blood and oxygen enters. The
pulmonary trunk arteries and their branches are the only arteries in the post-natal body that carry relatively
deoxygenated blood. Highly oxygenated blood returning from the pulmonary capillaries in the lungs passes through
a series of vessels that join together to form the pulmonary veins—the only post-natal veins in the body that carry
highly oxygenated blood. The pulmonary veins conduct blood into the left atrium, which pumps the blood into the
left ventricle, which in turn pumps oxygenated blood into the aorta and on to the many branches of the systemic
circuit. Eventually, these vessels will lead to the systemic capillaries, where exchange with the tissue fluid and cells
of the body occurs. In this case, oxygen and nutrients exit the systemic capillaries to be used by the cells in their
metabolic processes, and carbon dioxide and waste products will enter the blood.
The blood exiting the systemic capillaries is lower in oxygen concentration than when it entered. The capillaries will
ultimately unite to form venules, joining to form ever-larger veins, eventually flowing into the two major systemic
veins, the superior vena cava and the inferior vena cava, which return blood to the right atrium. The blood in the
superior and inferior venae cavae flows into the right atrium, which pumps blood into the right ventricle. This
process of blood circulation continues as long as the individual remains alive. Understanding the flow of blood
through the pulmonary and systemic circuits is critical to all health professions (Figure 19.4).

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Figure 19.4 Dual System of the Human Blood Circulation Blood flows from the right atrium to the right ventricle,
where it is pumped into the pulmonary circuit. The blood in the pulmonary artery branches is low in oxygen but
relatively high in carbon dioxide. Gas exchange occurs in the pulmonary capillaries (oxygen into the blood, carbon
dioxide out), and blood high in oxygen and low in carbon dioxide is returned to the left atrium. From here, blood
enters the left ventricle, which pumps it into the systemic circuit. Following exchange in the systemic capillaries
(oxygen and nutrients out of the capillaries and carbon dioxide and wastes in), blood returns to the right atrium and
the cycle is repeated.

Membranes, Surface Features, and Layers
Our exploration of more in-depth heart structures begins by examining the membrane that surrounds the heart, the
prominent surface features of the heart, and the layers that form the wall of the heart. Each of these components
plays its own unique role in terms of function.
Membranes
The membrane that directly surrounds the heart and defines the pericardial cavity is called the pericardium or
pericardial sac. It also surrounds the “roots” of the major vessels, or the areas of closest proximity to the heart. The
pericardium, which literally translates as “around the heart,” consists of two distinct sublayers: the sturdy outer
fibrous pericardium and the inner serous pericardium. The fibrous pericardium is made of tough, dense connective
tissue that protects the heart and maintains its position in the thorax. The more delicate serous pericardium consists

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Superior vena cava
Aorta
Left pulmonary arteries
Right pulmonary arteries
Pulmonary trunk
Right pulmonary veins
Left pulmonary veins
Pulmonary semilunar valve
Aortic semilunar valve
Mitral valve
Tricuspid valve
Inferior vena cava
Systemic veins from upper body
Systemic capillaries of upper body
Pulmonary capillaries in lungs
Systemic arteries to upper body
Pulmonary trunk
Systemic veins from lower body
Systemic arteries to lower body
Systemic capillaries of lower body

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of two layers: the parietal pericardium, which is fused to the fibrous pericardium, and an inner visceral pericardium,
or epicardium, which is fused to the heart and is part of the heart wall. The pericardial cavity, filled with lubricating
serous fluid, lies between the epicardium and the pericardium.
In most organs within the body, visceral serous membranes such as the epicardium are microscopic. However, in the
case of the heart, it is not a microscopic layer but rather a macroscopic layer, consisting of a simple squamous
epithelium called a mesothelium, reinforced with loose, irregular, or areolar connective tissue that attaches to the
pericardium. This mesothelium secretes the lubricating serous fluid that fills the pericardial cavity and reduces
friction as the heart contracts. Figure 19.5 illustrates the pericardial membrane and the layers of the heart.

Figure 19.5 Pericardial Membranes and Layers of the Heart Wall The pericardial membrane that surrounds the heart
consists of three layers and the pericardial cavity. The heart wall also consists of three layers. The pericardial
membrane and the heart wall share the epicardium.

Disorders of the...
Heart: Cardiac Tamponade
If excess fluid builds within the pericardial space, it can lead to a condition called cardiac tamponade, or pericardial
tamponade. With each contraction of the heart, more fluid—in most instances, blood—accumulates within the
pericardial cavity. In order to fill with blood for the next contraction, the heart must relax. However, the excess fluid
in the pericardial cavity puts pressure on the heart and prevents full relaxation, so the chambers within the heart
contain slightly less blood as they begin each heart cycle. Over time, less and less blood is ejected from the heart. If
the fluid builds up slowly, as in hypothyroidism, the pericardial cavity may be able to expand gradually to
accommodate this extra volume. Some cases of fluid in excess of one liter within the pericardial cavity have been
reported. Rapid accumulation of as little as 100 mL of fluid following trauma may trigger cardiac tamponade. Other
common causes include myocardial rupture, pericarditis, cancer, or even cardiac surgery. Removal of this excess
fluid requires insertion of drainage tubes into the pericardial cavity. Premature removal of these drainage tubes, for
example, following cardiac surgery, or clot formation within these tubes are causes of this condition. Untreated,
cardiac tamponade can lead to death.

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[Diagram Labels]
Endocardium
Myocardium
Parietal layer of serous pericardium
Epicardium (visceral layer of serous pericardium)

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Surface Features of the Heart
Inside the pericardium, the surface features of the heart are visible, including the four chambers. There is a
superficial leaf-like extension of the atria near the superior surface of the heart, one on each side, called an auricle—
a name that means “ear like”—because its shape resembles the external ear of a human (Figure 19.6). Auricles are
relatively thin-walled structures that can fill with blood and empty into the atria or upper chambers of the heart. You
may also hear them referred to as atrial appendages. Also prominent is a series of fat-filled grooves, each of which is
known as a sulcus (plural = sulci), along the superior surfaces of the heart. Major coronary blood vessels are located
in these sulci. The deep coronary sulcus is located between the atria and ventricles. Located between the left and
right ventricles are two additional sulci that are not as deep as the coronary sulcus. The anterior interventricular
sulcus is visible on the anterior surface of the heart, whereas the posterior interventricular sulcus is visible on the
posterior surface of the heart. Figure 19.6 illustrates anterior and posterior views of the surface of the heart.

Figure 19.6 External Anatomy of the Heart Inside the pericardium, the surface features of the heart are visible.
Layers
The wall of the heart is composed of three layers of unequal thickness. From superficial to deep, these are the
epicardium, the myocardium, and the endocardium (see Figure 19.5). The outermost layer of the wall of the heart is
also the innermost layer of the pericardium, the epicardium, or the visceral pericardium discussed earlier.
The middle and thickest layer is the myocardium, made largely of cardiac muscle cells. It is built upon a framework
of collagenous fibers, plus the blood vessels that supply the myocardium and the nerve fibers that help regulate the
heart. It is the contraction of the myocardium that pumps blood through the heart and into the major arteries. The

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**Anterior view**
Brachiocephalic trunk
Superior vena cava
Right pulmonary artery
Ascending aorta
Pulmonary trunk
Right pulmonary veins
Right atrium
Right coronary artery
Anterior cardiac vein
Right marginal artery
Small cardiac vein
Inferior vena cava
Left common carotid artery
Left subclavian artery
Aortic arch
Ligamentum arteriosum
Left pulmonary artery
Left pulmonary veins
Auricle of left atrium
Circumflex artery
Left coronary artery
Left ventricle
Great cardiac vein
Anterior interventricular artery
Apex
Aorta
Left pulmonary artery
Left pulmonary veins
Auricle of left atrium
Left atrium
Circumflex branch of left coronary artery
Great cardiac vein
Posterior vein of left ventricle
Left ventricle
Superior vena cava
Right pulmonary artery
Right pulmonary veins
Right atrium
Inferior vena cava
Coronary sinus
Small cardiac vein
Right coronary artery
Posterior interventricular artery
Middle cardiac vein
Apex

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muscle pattern is elegant and complex, as the muscle cells swirl and spiral around the chambers of the heart. They
form a figure 8 pattern around the atria and around the bases of the great vessels. Deeper ventricular muscles also
form a figure 8 around the two ventricles and proceed toward the apex. More superficial layers of ventricular muscle
wrap around both ventricles. This complex swirling pattern allows the heart to pump blood more effectively than a
simple linear pattern would. Figure 19.7 illustrates the arrangement of muscle cells.

Figure 19.7 Heart Musculature The swirling pattern of cardiac muscle tissue contributes significantly to the heart’s
ability to pump blood effectively.
Although the ventricles on the right and left sides pump the same amount of blood per contraction, the muscle of the
left ventricle is much thicker and better developed than that of the right ventricle. In order to overcome the high
resistance required to pump blood into the long systemic circuit, the left ventricle must generate a great amount of
pressure. The right ventricle does not need to generate as much pressure, since the pulmonary circuit is shorter and
provides less resistance. Figure 19.8 illustrates the differences in muscular thickness needed for each of the
ventricles.

Figure 19.8 Differences in Ventricular Muscle Thickness The myocardium in the left ventricle is significantly thicker
than that of the right ventricle. Both ventricles pump the same amount of blood, but the left ventricle must generate a
much greater pressure to overcome greater resistance in the systemic circuit. The ventricles are shown in both
relaxed and contracting states. Note the differences in the relative size of the lumens, the region inside each ventricle
where the blood is contained.

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Atrial musculature
Ventricular musculature
Contracted

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The innermost layer of the heart wall, the endocardium, is joined to the myocardium with a thin layer of connective
tissue. The endocardium lines the chambers where the blood circulates and covers the heart valves. It is made of
simple squamous epithelium called endothelium, which is continuous with the endothelial lining of the blood vessels
(see Figure 19.5).
Once regarded as a simple lining layer, recent evidence indicates that the endothelium of the endocardium and the
coronary capillaries may play active roles in regulating the contraction of the muscle within the myocardium. The
endothelium may also regulate the growth patterns of the cardiac muscle cells throughout life, and the endothelins it
secretes create an environment in the surrounding tissue fluids that regulates ionic concentrations and states of
contractility. Endothelins are potent vasoconstrictors and, in a normal individual, establish a homeostatic balance
with other vasoconstrictors and vasodilators.

Internal Structure of the Heart
Recall that the heart’s contraction cycle follows a dual pattern of circulation—the pulmonary and systemic circuits—
because of the pairs of chambers that pump blood into the circulation. In order to develop a more precise
understanding of cardiac function, it is first necessary to explore the internal anatomical structures in more detail.
Septa of the Heart
The word septum is derived from the Latin for “something that encloses;” in this case, a septum (plural = septa)
refers to a wall or partition that divides the heart into chambers. The septa are physical extensions of the myocardium
lined with endocardium. Located between the two atria is the interatrial septum. Normally in an adult heart, the
interatrial septum bears an oval-shaped depression known as the fossa ovalis, a remnant of 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 pulmonary circuit. 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.
Between the two ventricles is a second septum known as the interventricular septum. Unlike the interatrial septum,
the interventricular septum is normally intact after its formation during fetal development. It is substantially thicker
than the interatrial septum, since the ventricles generate far greater pressure when they contract.
The septum between the atria and ventricles is known as the atrioventricular septum. It is marked by the presence of
four openings that allow blood to move from the atria into the ventricles and from the ventricles into the pulmonary
trunk and aorta. Located in each of these openings between the atria and ventricles is a valve, a specialized structure
that ensures one-way flow of blood. The valves between the atria and ventricles are known generically as
atrioventricular valves. The valves at the openings that lead to the pulmonary trunk and aorta are known generically
as semilunar valves. The interventricular septum is visible in Figure 19.9. In this figure, the atrioventricular septum
has been removed to better show the bicuspid and tricuspid valves; the interatrial septum is not visible, since its
location is covered by the aorta and pulmonary trunk. Since these openings and valves structurally weaken the
atrioventricular septum, the remaining tissue is heavily reinforced with dense connective tissue called the cardiac
skeleton, or skeleton of the heart. It includes four rings that surround the openings between the atria and ventricles,
and the openings to the pulmonary trunk and aorta, and serve as the point of attachment for the heart valves. The
cardiac skeleton also provides an important boundary in the heart electrical conduction system.

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Figure 19.9 Internal Structures of the Heart This anterior view of the heart shows the four chambers, the major
vessels and their early branches, as well as the valves. The presence of the pulmonary trunk and aorta covers the
interatrial septum, and the atrioventricular septum is cut away to show the atrioventricular valves.

Disorders of the...
Heart: Heart Defects
One very common form of interatrial septum pathology is patent foramen ovale, which occurs when the septum
primum does not close at birth, and the fossa ovalis is unable to fuse. The word patent is from the Latin root patens
for “open.” It may be benign or asymptomatic, perhaps never being diagnosed, or in extreme cases, it may require
surgical repair to close the opening permanently. As much as 20–25 percent of the general population may have a
patent foramen ovale, but fortunately, most have the benign, asymptomatic version. Patent foramen ovale is normally
detected by auscultation of a heart murmur (an abnormal heart sound) and confirmed by imaging with an
echocardiogram. Despite its prevalence in the general population, the causes of patent ovale are unknown, and there
are no known risk factors. In nonlife-threatening cases, it is better to monitor the condition than to risk heart surgery
to repair and seal the opening.
Coarctation of the aorta is a congenital abnormal narrowing of the aorta that is normally located at the insertion of
the ligamentum arteriosum, the remnant of the fetal shunt called the ductus arteriosus. If severe, this condition
drastically restricts blood flow through the primary systemic artery, which is life threatening. In some individuals,
the condition may be fairly benign and not detected until later in life. Detectable symptoms in an infant include
difficulty breathing, poor appetite, trouble feeding, or failure to thrive. In older individuals, symptoms include
dizziness, fainting, shortness of breath, chest pain, fatigue, headache, and nosebleeds. Treatment involves surgery to
resect (remove) the affected region or angioplasty to open the abnormally narrow passageway. Studies have shown
that the earlier the surgery is performed, the better the chance of survival.
A patent ductus arteriosus is a congenital condition in which the ductus arteriosus fails to close. The condition may
range from severe to benign. Failure of the ductus arteriosus to close results in blood flowing from the higher
pressure aorta into the lower pressure pulmonary trunk. This additional fluid moving toward the lungs increases
pulmonary pressure and makes respiration difficult. Symptoms include shortness of breath (dyspnea), tachycardia,
enlarged heart, a widened pulse pressure, and poor weight gain in infants. Treatments include surgical closure

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Superior vena cava
Right pulmonary artery
Right pulmonary veins
Right atrium
Tricuspid valve
Right ventricle
Chordae tendineae
Trabeculae carneae
Moderator band
Inferior vena cava
Left pulmonary artery
Left atrium
Left pulmonary veins
Mitral (bicuspid) valve
Aortic valve
Pulmonary valve
Left ventricle
Papillary muscle
Interventricular septum
Epicardium
Myocardium
Endocardium

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(ligation), manual closure using platinum coils or specialized mesh inserted via the femoral artery or vein, or
nonsteroidal anti-inflammatory drugs to block the synthesis of prostaglandin E2, which maintains the vessel in an
open position. If untreated, the condition can result in congestive heart failure.
Septal defects are not uncommon in individuals and may be congenital or caused by various disease processes.
Tetralogy of Fallot is a congenital condition that may also occur from exposure to unknown environmental factors; it
occurs when there is an opening in the interventricular septum caused by blockage of the pulmonary trunk, normally
at the pulmonary semilunar valve. This allows blood that is relatively low in oxygen from the right ventricle to flow
into the left ventricle and mix with the blood that is relatively high in oxygen. Symptoms include a distinct heart
murmur, low blood oxygen percent saturation, dyspnea or difficulty in breathing, polycythemia, broadening
(clubbing) of the fingers and toes, and in children, difficulty in feeding or failure to grow and develop. It is the most
common cause of cyanosis following birth. The term “tetralogy” is derived from the four components of the
condition, although only three may be present in an individual patient: pulmonary infundibular stenosis (rigidity of
the pulmonary valve), overriding aorta (the aorta is shifted above both ventricles), ventricular septal defect
(opening), and right ventricular hypertrophy (enlargement of the right ventricle). Other heart defects may also
accompany this condition, which is typically confirmed by echocardiography imaging. Tetralogy of Fallot occurs in
approximately 400 out of one million live births. Normal treatment involves extensive surgical repair, including the
use of stents to redirect blood flow and replacement of valves and patches to repair the septal defect, but the
condition has a relatively high mortality. Survival rates are currently 75 percent during the first year of life; 60
percent by 4 years of age; 30 percent by 10 years; and 5 percent by 40 years.
In the case of severe septal defects, including both tetralogy of Fallot and patent foramen ovale, failure of the heart to
develop properly can lead to a condition commonly known as a “blue baby.” Regardless of normal skin
pigmentation, individuals with this condition have an insufficient supply of oxygenated blood, which leads to
cyanosis, a blue or purple coloration of the skin, especially when active.
Septal defects are commonly first detected through auscultation, listening to the chest using a stethoscope. In this
case, instead of hearing normal heart sounds attributed to the flow of blood and closing of heart valves, unusual heart
sounds may be detected. This is often followed by medical imaging to confirm or rule out a diagnosis. In many
cases, treatment may not be needed. Some common congenital heart defects are illustrated in Figure 19.10.

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Figure 19.10 Congenital Heart Defects (a) A patent foramen ovale defect is an abnormal opening in the interatrial
septum, or more commonly, a failure of the foramen ovale to close. (b) Coarctation of the aorta is an abnormal
narrowing of the aorta. (c) A patent ductus arteriosus is the failure of the ductus arteriosus to close. (d) Tetralogy of
Fallot includes an abnormal opening in the interventricular septum.
Right Atrium
The right atrium serves as the receiving chamber for blood returning to the heart from the systemic circulation. The
two major systemic veins, the superior and inferior venae cavae, and the large coronary vein called the coronary
sinus that drains the heart myocardium empty into the right atrium. The superior vena cava drains blood from
regions superior to the diaphragm: the head, neck, upper limbs, and the thoracic region. It empties into the superior
and posterior portions of the right atrium. The inferior vena cava drains blood from areas inferior to the diaphragm:
the lower limbs and abdominopelvic region of the body. It, too, empties into the posterior portion of the atria, but
inferior to the opening of the superior vena cava. Immediately superior and slightly medial to the opening of the
inferior vena cava on the posterior surface of the atrium is the opening of the coronary sinus. This thin-walled vessel
drains most of the coronary veins that return systemic blood from the heart. The majority of the internal heart
structures discussed in this and subsequent sections are illustrated in Figure 19.9.
While the bulk of the internal surface of the right atrium is smooth, the depression of the fossa ovalis is medial, and
the anterior surface demonstrates prominent ridges of muscle called the pectinate muscles. The right auricle also has
pectinate muscles. The left atrium does not have pectinate muscles except in the auricle.
The atria receive venous blood on a nearly continuous basis, preventing venous flow from stopping while the
ventricles are contracting. While most ventricular filling occurs while the atria are relaxed, they do demonstrate a
contractile phase and actively pump blood into the ventricles just prior to ventricular contraction. The opening
between the atrium and ventricle is guarded by the tricuspid valve.
Right Ventricle
The right ventricle receives blood from the right atrium through the tricuspid valve. Each flap of the valve is attached
to strong strands of connective tissue, the chordae tendineae, literally “tendinous cords,” or sometimes more
poetically referred to as “heart strings.” There are several chordae tendineae associated with each of the flaps. They
are composed of approximately 80 percent collagenous fibers with the remainder consisting of elastic fibers and
endothelium. They connect each of the flaps to a papillary muscle that extends from the inferior ventricular surface.

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fails to close
Narrow segment
of aorta
remains open
Stenosed
pulmonary
semilunar valve
Aorta emerges
from both
septal defect
Enlarged right
(c) Patent ductus arteriosus

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There are three papillary muscles in the right ventricle, called the anterior, posterior, and septal muscles, which
correspond to the three sections of the valves.
When the myocardium of the ventricle contracts, pressure within the ventricular chamber rises. Blood, like any fluid,
flows from higher pressure to lower pressure areas, in this case, toward the pulmonary trunk and the atrium. To
prevent any potential backflow, the papillary muscles also contract, generating tension on the chordae tendineae.
This prevents the flaps of the valves from being forced into the atria and regurgitation of the blood back into the atria
during ventricular contraction. Figure 19.11 shows papillary muscles and chordae tendineae attached to the tricuspid
valve.

Figure 19.11 Chordae Tendineae and Papillary Muscles In this frontal section, you can see papillary muscles
attached to the tricuspid valve on the right as well as the mitral valve on the left via chordae tendineae. (credit:
modification of work by “PV KS”/flickr.com)
The walls of the 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 (see Figure 19.9) reinforces the thin walls of the right ventricle and plays a crucial role in cardiac conduction. It
arises from the inferior portion of the interventricular septum and crosses the interior space of the right ventricle to
connect with the inferior papillary muscle.
When the right ventricle contracts, it ejects blood into the pulmonary trunk, which branches into the left and right
pulmonary arteries that carry it to each lung. The superior surface of the right ventricle begins to taper as it
approaches the pulmonary trunk. At the base of the pulmonary trunk is the pulmonary semilunar valve that prevents
backflow from the pulmonary trunk.
Left Atrium
After exchange of gases in the pulmonary capillaries, blood returns to the left atrium high in oxygen via one of the
four pulmonary veins. While the left atrium does not contain pectinate muscles, it does have an auricle that includes
these pectinate ridges. Blood flows nearly continuously from the pulmonary veins back into the atrium, which acts as
the receiving chamber, and from here through an opening into the left ventricle. Most blood flows passively into the
heart while both the atria and ventricles are relaxed, but toward the end of the ventricular relaxation period, the left
atrium will contract, pumping blood into the ventricle. This atrial contraction accounts for approximately 20 percent
of ventricular filling. The opening between the left atrium and ventricle is guarded by the mitral valve.

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Left Ventricle
Recall that, although both sides of the heart will pump the same amount of blood, the muscular layer is much thicker
in the left ventricle compared to the right (see Figure 19.8). Like the right ventricle, the left also has trabeculae
carneae, but there is no moderator band. The mitral valve is connected to papillary muscles via chordae tendineae.
There are two papillary muscles on the left—the anterior and posterior—as opposed to three on the right.
The left ventricle is the major pumping chamber for the systemic circuit; it ejects blood into the aorta through the
aortic semilunar valve.
Heart Valve Structure and Function
A transverse section through the heart slightly above the level of the atrioventricular septum reveals all four heart
valves along the same plane (Figure 19.12). The valves ensure unidirectional blood flow through the heart. Between
the right atrium and the right ventricle is the right atrioventricular valve, or tricuspid valve. It typically consists of
three flaps, or leaflets, made of endocardium reinforced with additional connective tissue. The flaps are connected by
chordae tendineae to the papillary muscles, which control the opening and closing of the valves.

Figure 19.12 Heart Valves With the atria and major vessels removed, all four valves are clearly visible, although it is
difficult to distinguish the three separate cusps of the tricuspid valve.
Emerging from the right ventricle at the base of the pulmonary trunk is the pulmonary semilunar valve, or the
pulmonary valve; it is also known as the pulmonic valve or the right semilunar valve. The pulmonary valve is
comprised of three small flaps of endothelium reinforced with connective tissue. When the ventricle relaxes, the
pressure differential causes blood to flow back into the ventricle from the pulmonary trunk. This flow of blood fills
the pocket-like flaps of the pulmonary valve, causing the valve to close and producing an audible sound. Unlike the
atrioventricular valves, there are no papillary muscles or chordae tendineae associated with the pulmonary valve.
Located at the opening between the left atrium and left ventricle is the mitral valve, also called the bicuspid valve or
the left atrioventricular valve. Structurally, this valve consists of two cusps, compared to the three cusps of the
tricuspid valve. In a clinical setting, the valve is referred to as the mitral valve, rather than the bicuspid valve. The
two cusps of the mitral valve are attached by chordae tendineae to two papillary muscles that project from the wall of
the ventricle.

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[Diagram Labels]
Bicuspid (mitral) valve
Right side of heart
Left side of heart
Aortic valve

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At the base of the aorta is the aortic semilunar valve, or the aortic valve, which prevents backflow from the aorta. It
normally is composed of three flaps. When the ventricle relaxes and blood attempts to flow back into the ventricle
from the aorta, blood will fill the cusps of the valve, causing it to close and producing an audible sound.
In Figure 19.13a, the two atrioventricular valves are open and the two semilunar valves are closed. This occurs when
both atria and ventricles are relaxed and when the atria contract to pump blood into the ventricles. Figure 19.13b
shows a frontal view. Although only the left side of the heart is illustrated, the process is virtually identical on the
right.

Figure 19.13 Blood Flow from the Left Atrium to the Left Ventricle (a) A transverse section through the heart
illustrates the four heart valves. The two atrioventricular valves are open; the two semilunar valves are closed. The
atria and vessels have been removed. (b) A frontal section through the heart illustrates blood flow through the mitral
valve. When the mitral valve is open, it allows blood to move from the left atrium to the left ventricle. The aortic
semilunar valve is closed to prevent backflow of blood from the aorta to the left ventricle.
Figure 19.14a shows the atrioventricular valves closed while the two semilunar valves are open. This occurs when
the ventricles contract to eject blood into the pulmonary trunk and aorta. Closure of the two atrioventricular valves
prevents blood from being forced back into the atria. This stage can be seen from a frontal view in Figure 19.14b.

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[Diagram Labels]
Posterior
Tricuspid valve (open)
Bicuspide (mitral) valve (open)
Right side of heart
Left side of heart
Aortic valve (closed)
Pulmonary valve (closed)
Anterior
Aortic valve (Closed)
Chordae tendineae (loose)
Papillary muscle (relaxed)
Mitral valve (open)

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Figure 19.14 Blood Flow from the Left Ventricle into the Great Vessels (a) A transverse section through the heart
illustrates the four heart valves during ventricular contraction. The two atrioventricular valves are closed, but the two
semilunar valves are open. The atria and vessels have been removed. (b) A frontal view shows the closed mitral
(bicuspid) valve that prevents backflow of blood into the left atrium. The aortic semilunar valve is open to allow
blood to be ejected into the aorta.
When the ventricles begin to contract, pressure within the ventricles rises and blood flows toward the area of lowest
pressure, which is initially in the atria. This backflow causes the cusps of the tricuspid and mitral (bicuspid) valves to
close. These valves are tied down to the papillary muscles by chordae tendineae. During the relaxation phase of the
cardiac cycle, the papillary muscles are also relaxed and the tension on the chordae tendineae is slight (see Figure
19.13b). However, as the myocardium of the ventricle contracts, so do the papillary muscles. This creates tension on
the chordae tendineae (see Figure 19.14b), helping to hold the cusps of the atrioventricular valves in place and
preventing them from being blown back into the atria.
The aortic and pulmonary semilunar valves lack the chordae tendineae and papillary muscles associated with the
atrioventricular valves. Instead, they consist of pocket-like folds of endocardium reinforced with additional
connective tissue. When the ventricles relax and the change in pressure forces the blood toward the ventricles, the
blood presses against these cusps and seals the openings.

Interactive Link
Visit this site to observe an echocardiogram of actual heart valves opening and closing. Although much of the heart
has been “removed” from this gif loop so the chordae tendineae are not visible, why is their presence more critical
for the atrioventricular valves (tricuspid and mitral) than the semilunar (aortic and pulmonary) valves?

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Posterior
Tricuspid valve (closed)
Bicuspid (mitral) valve (closed)
Right side of heart
Left side of heart
Aortic valve (open)
Pulmonary valve (open)
Anterior
Aortic valve (open)
Chordae tendineae (tight)
Papillary muscle (contracted)
Mitral valve (closed)

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Disorders of the...
Heart Valves
When heart valves do not function properly, they are often described as incompetent and result in valvular heart
disease, which can range from benign to lethal. Some of these conditions are congenital, that is, the individual was
born with the defect, whereas others may be attributed to disease processes or trauma. Some malfunctions are treated
with medications, others require surgery, and still others may be mild enough that the condition is merely monitored
since treatment might trigger more serious consequences.
Valvular disorders are often caused by carditis, or inflammation of the heart. One common trigger for this
inflammation is rheumatic fever, or scarlet fever, an autoimmune response to the presence of a bacterium,
Streptococcus pyogenes, normally a disease of childhood.
While any of the heart valves may be involved in valve disorders, mitral regurgitation is the most common, detected
in approximately 2 percent of the population, and the pulmonary semilunar valve is the least frequently involved.
When a valve malfunctions, the flow of blood to a region will often be disrupted. The resulting inadequate flow of
blood to this region will be described in general terms as an insufficiency. The specific type of insufficiency is
named for the valve involved: aortic insufficiency, mitral insufficiency, tricuspid insufficiency, or pulmonary
insufficiency.
If one of the cusps of the valve is forced backward by the force of the blood, the condition is referred to as a
prolapsed valve. Prolapse may occur if the chordae tendineae are damaged or broken, causing the closure mechanism
to fail. The failure of the valve to close properly disrupts the normal one-way flow of blood and results in
regurgitation, when the blood flows backward from its normal path. Using a stethoscope, the disruption to the
normal flow of blood produces a heart murmur.
Stenosis is a condition in which the heart valves become rigid and may calcify over time. The loss of flexibility of
the valve interferes with normal function and may cause the heart to work harder to propel blood through the valve,
which eventually weakens the heart. Aortic stenosis affects approximately 2 percent of the population over 65 years
of age, and the percentage increases to approximately 4 percent in individuals over 85 years. Occasionally, one or
more of the chordae tendineae will tear or the papillary muscle itself may die as a component of a myocardial
infarction (heart attack). In this case, the patient’s condition will deteriorate dramatically and rapidly, and immediate
surgical intervention may be required.
Auscultation, or listening to a patient’s heart sounds, is one of the most useful diagnostic tools, since it is proven,
safe, and inexpensive. The term auscultation is derived from the Latin for “to listen,” and the technique has been
used for diagnostic purposes as far back as the ancient Egyptians. Valve and septal disorders will trigger abnormal
heart sounds. If a valvular disorder is detected or suspected, a test called an echocardiogram, or simply an “echo,”
may be ordered. Echocardiograms are sonograms of the heart and can help in the diagnosis of valve disorders as well
as a wide variety of heart pathologies.

Interactive Link
Visit this site for audio examples of heart sounds.

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Career Connection
Cardiologist
Cardiologists are medical doctors that specialize in the diagnosis and treatment of diseases of the heart. After
completing 4 years of medical school, cardiologists complete a three-year residency in internal medicine followed by
an additional three or more years in cardiology. Following this 10-year period of medical training and clinical
experience, they qualify for a rigorous two-day examination administered by the Board of Internal Medicine that
tests their academic training and clinical abilities, including diagnostics and treatment. After successful completion
of this examination, a physician becomes a board-certified cardiologist. Some board-certified cardiologists may be
invited to become a Fellow of the American College of Cardiology (FACC). This professional recognition is
awarded to outstanding physicians based upon merit, including outstanding credentials, achievements, and
community contributions to cardiovascular medicine.

Interactive Link
Visit this site to learn more about cardiologists.

Career Connection
Cardiovascular Technologist/Technician
Cardiovascular technologists/technicians are trained professionals who perform a variety of imaging techniques,
such as sonograms or echocardiograms, used by physicians to diagnose and treat diseases of the heart. Nearly all of
these positions require an associate degree. Growth within the field is fast, projected at 29 percent from 2010 to
2020.
There is a considerable overlap and complementary skills between cardiac technicians and vascular technicians, and
so the term cardiovascular technician is often used. Special certifications within the field require documenting
appropriate experience and completing additional and often expensive certification examinations. These
subspecialties include Certified Rhythm Analysis Technician (CRAT), Certified Cardiographic Technician (CCT),
Registered Congenital Cardiac Sonographer (RCCS), Registered Cardiac Electrophysiology Specialist (RCES),
Registered Cardiovascular Invasive Specialist (RCIS), Registered Cardiac Sonographer (RCS), Registered Vascular
Specialist (RVS), and Registered Phlebology Sonographer (RPhS).

Interactive Link
Visit this site for more information on cardiovascular technologists/technicians.

Coronary Circulation
You will recall that the heart is a remarkable pump composed largely of cardiac muscle cells that are incredibly
active throughout life. Like all other cells, a cardiomyocyte requires a reliable supply of oxygen and nutrients, and a
way to remove wastes, so it needs a dedicated, complex, and extensive coronary circulation. And because of the
critical and nearly ceaseless activity of the heart throughout life, this need for a blood supply is even greater than for
a typical cell. However, coronary circulation is not continuous; rather, it cycles, reaching a peak when the heart
muscle is relaxed and nearly ceasing while it is contracting.

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Coronary Arteries
Coronary arteries supply blood to the myocardium and other components of the heart. The first portion of the aorta
after it arises from the left ventricle gives rise to the coronary arteries. There are three dilations in the wall of the
aorta just superior to the aortic semilunar valve. Two of these, the left posterior aortic sinus and anterior aortic sinus,
give rise to the left and right coronary arteries, respectively. The third sinus, the right posterior aortic sinus, typically
does not give rise to a vessel. Coronary vessel branches that remain on the surface of the artery and follow the sulci
are called epicardial coronary arteries.
The left coronary artery distributes blood to the left side of the heart, the left atrium and ventricle, and the
interventricular septum. The circumflex artery arises from the left coronary artery and follows the coronary sulcus to
the left. Eventually, it will fuse with the small branches of the right coronary artery. The larger anterior
interventricular artery, also known as the left anterior descending artery (LAD), is the second major branch arising
from the left coronary artery. It follows the anterior interventricular sulcus around the pulmonary trunk. Along the
way it gives rise to numerous smaller branches that interconnect with the branches of the posterior interventricular
artery, forming anastomoses. An anastomosis is an area where vessels unite to form interconnections that normally
allow blood to circulate to a region even if there may be partial blockage in another branch. The anastomoses in the
heart are very small. Therefore, this ability is somewhat restricted in the heart so a coronary artery blockage often
results in death of the cells (myocardial infarction) supplied by the particular vessel.
The right coronary artery proceeds along the coronary sulcus and distributes blood to the right atrium, portions of
both ventricles, and the heart conduction system. Normally, one or more marginal arteries arise from the right
coronary artery inferior to the right atrium. The marginal arteries supply blood to the superficial portions of the right
ventricle. On the posterior surface of the heart, the right coronary artery gives rise to the posterior interventricular
artery, also known as the posterior descending artery. It runs along the posterior portion of the interventricular sulcus
toward the apex of the heart, giving rise to branches that supply the interventricular septum and portions of both
ventricles. Figure 19.15 presents views of the coronary circulation from both the anterior and posterior views.

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Figure 19.15 Coronary Circulation The anterior view of the heart shows the prominent coronary surface vessels. The
posterior view of the heart shows the prominent coronary surface vessels.

Diseases of the...
Heart: Myocardial Infarction
Myocardial infarction (MI) is the formal term for what is commonly referred to as a heart attack. It normally results
from a lack of blood flow (ischemia) and oxygen (hypoxia) to a region of the heart, resulting in death of the cardiac
muscle cells. An MI often occurs when a coronary artery is blocked by the buildup of atherosclerotic plaque
consisting of lipids, cholesterol and fatty acids, and white blood cells, primarily macrophages. It can also occur when
a portion of an unstable atherosclerotic plaque travels through the coronary arterial system and lodges in one of the
smaller vessels. The resulting blockage restricts the flow of blood and oxygen to the myocardium and causes death
of the tissue. MIs may be triggered by excessive exercise, in which the partially occluded artery is no longer able to
pump sufficient quantities of blood, or severe stress, which may induce spasm of the smooth muscle in the walls of
the vessel.
In the case of acute MI, there is often sudden pain beneath the sternum (retrosternal pain) called angina pectoris,
often radiating down the left arm in males but not in female patients. Until this anomaly between the sexes was
discovered, many female patients suffering MIs were misdiagnosed and sent home. In addition, patients typically
present with difficulty breathing and shortness of breath (dyspnea), irregular heartbeat (palpations), nausea and
vomiting, sweating (diaphoresis), anxiety, and fainting (syncope), although not all of these symptoms may be
present. Many of the symptoms are shared with other medical conditions, including anxiety attacks and simple

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Aortic arch
Ascending aorta
Right coronary artery
Right atrium
Atrial arteries
Anterior cardiac veins
Small cardiac vein
Marginal artery
Left coronary artery
Pulmonary trunk
Circumflex artery
Anterior interventricular artery
Great cardiac vein
Coronary sinus
Small cardiac vein
Circumflex artery
Great cardiac vein
Marginal artery
Posterior interventricular artery
Posterior cardiac vein
Left ventricle
Middle cardiac vein
Marginal artery
Right coronary artery
In the case of acute MI, there is often sudden pain beneath the sternum (retrosternal pain) called angina pectoris, often radiating down the left arm in males but not in female patients. Until this anomaly between the sexes was discovered, many female patients suffering MIs were misdiagnosed and sent home. In addition, patients typically present with difficulty breathing and shortness of breath (dyspnea), irregular heartbeat (palpitations), nausea and vomiting, sweating (diaphoresis), anxiety, and fainting (syncope), although not all of these symptoms may be present. Many of the symptoms are shared with other medical conditions, including anxiety attacks and simple

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indigestion, so differential diagnosis is critical. It is estimated that between 22 and 64 percent of MIs present without
any symptoms.
An MI can be confirmed by examining the patient’s ECG, which frequently reveals alterations in the ST and Q
components. Some classification schemes of MI are referred to as ST-elevated MI (STEMI) and non-elevated MI
(non-STEMI). In addition, echocardiography or cardiac magnetic resonance imaging may be employed. Common
blood tests indicating an MI include elevated levels of creatine kinase MB (an enzyme that catalyzes the conversion
of creatine to phosphocreatine, consuming ATP) and cardiac troponin (the regulatory protein for muscle contraction),
both of which are released by damaged cardiac muscle cells.
Immediate treatments for MI are essential and include administering supplemental oxygen, aspirin that helps to
break up clots, and nitroglycerine administered sublingually (under the tongue) to facilitate its absorption. Despite its
unquestioned success in treatments and use since the 1880s, the mechanism of nitroglycerine is still incompletely
understood but is believed to involve the release of nitric oxide, a known vasodilator, and endothelium-derived
releasing factor, which also relaxes the smooth muscle in the tunica media of coronary vessels. Longer-term
treatments include injections of thrombolytic agents such as streptokinase that dissolve the clot, the anticoagulant
heparin, balloon angioplasty and stents to open blocked vessels, and bypass surgery to allow blood to pass around
the site of blockage. If the damage is extensive, coronary replacement with a donor heart or coronary assist device, a
sophisticated mechanical device that supplements the pumping activity of the heart, may be employed. Despite the
attention, development of artificial hearts to augment the severely limited supply of heart donors has proven less
than satisfactory but will likely improve in the future.
MIs may trigger cardiac arrest, but the two are not synonymous. Important risk factors for MI include cardiovascular
disease, age, smoking, high blood levels of the low-density lipoprotein (LDL, often referred to as “bad” cholesterol),
low levels of high-density lipoprotein (HDL, or “good” cholesterol), hypertension, diabetes mellitus, obesity, lack of
physical exercise, chronic kidney disease, excessive alcohol consumption, and use of illegal drugs.
Coronary Veins
Coronary veins drain the heart and generally parallel the large surface arteries (see Figure 19.15). The great cardiac
vein can be seen initially on the surface of the heart following the interventricular sulcus, but it eventually flows
along the coronary sulcus into the coronary sinus on the posterior surface. The great cardiac vein initially parallels
the anterior interventricular artery and drains the areas supplied by this vessel. It receives several major branches,
including the posterior cardiac vein, the middle cardiac vein, and the small cardiac vein. The posterior cardiac vein
parallels and drains the areas supplied by the marginal artery branch of the circumflex artery. The middle cardiac
vein parallels and drains the areas supplied by the posterior interventricular artery. The small cardiac vein parallels
the right coronary artery and drains the blood from the posterior surfaces of the right atrium and ventricle. The
coronary sinus is a large, thin-walled vein on the posterior surface of the heart lying within the atrioventricular
sulcus and emptying directly into the right atrium. The anterior cardiac veins parallel the small cardiac arteries and
drain the anterior surface of the right ventricle. Unlike these other cardiac veins, it bypasses the coronary sinus and
drains directly into the right atrium.

Disorders of the...
Heart: Coronary Artery Disease
Coronary artery disease is the leading cause of death worldwide. It occurs when the buildup of plaque—a fatty
material including cholesterol, connective tissue, white blood cells, and some smooth muscle cells—within the walls
of the arteries obstructs the flow of blood and decreases the flexibility or compliance of the vessels. This condition is
called atherosclerosis, a hardening of the arteries that involves the accumulation of plaque. As the coronary blood

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vessels become occluded, the flow of blood to the tissues will be restricted, a condition called ischemia that causes
the cells to receive insufficient amounts of oxygen, called hypoxia. Figure 19.16 shows the blockage of coronary
arteries highlighted by the injection of dye. Some individuals with coronary artery disease report pain radiating from
the chest called angina pectoris, but others remain asymptomatic. If untreated, coronary artery disease can lead to MI
or a heart attack.

Figure 19.16 Atherosclerotic Coronary Arteries In this coronary angiogram (X-ray), the dye makes visible two
occluded coronary arteries. Such blockages can lead to decreased blood flow (ischemia) and insufficient oxygen
(hypoxia) delivered to the cardiac tissues. If uncorrected, this can lead to cardiac muscle death (myocardial
infarction).
The disease progresses slowly and often begins in children and can be seen as fatty “streaks” in the vessels. It then
gradually progresses throughout life. Well-documented risk factors include smoking, family history, hypertension,
obesity, diabetes, high alcohol consumption, lack of exercise, stress, and hyperlipidemia or high circulating levels of
lipids in the blood. Treatments may include medication, changes to diet and exercise, angioplasty with a balloon
catheter, insertion of a stent, or coronary bypass procedure.
Angioplasty is a procedure in which the occlusion is mechanically widened with a balloon. A specialized catheter
with an expandable tip is inserted into a superficial vessel, normally in the leg, and then directed to the site of the
occlusion. At this point, the balloon is inflated to compress the plaque material and to open the vessel to increase
blood flow. Then, the balloon is deflated and retracted. A stent consisting of a specialized mesh is typically inserted
at the site of occlusion to reinforce the weakened and damaged walls. Stent insertions have been routine in
cardiology for more than 40 years.
Coronary bypass surgery may also be performed. This surgical procedure grafts a replacement vessel obtained from
another, less vital portion of the body to bypass the occluded area. This procedure is clearly effective in treating
patients experiencing a MI, but overall does not increase longevity. Nor does it seem advisable in patients with stable
although diminished cardiac capacity since frequently loss of mental acuity occurs following the procedure. Longterm changes to behavior, emphasizing diet and exercise plus a medicine regime tailored to lower blood pressure,
lower cholesterol and lipids, and reduce clotting are equally as effective.

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[Image Labels]
Blockage of common trunk
of left coronary artery
circumflex artery