Heart Information Center

Introduction
What are heart valves?
Heart valve disorders
Infection

Heart disease

Congenital

Rheumatic fever

Papillary muscle dysfunction

Bicuspid aortic valve

Endocarditis

Calcific aortic stenosis

Mitral valve prolapse

Mitral valve conditions

Aortic valve conditions
Tricuspid & Pulmonic valve conditions
Artificial (Prosthetic) valve conditions
Glossary
Other Sites
Click topics above to see more information.
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Introduction
For the heart to function properly, the four heart chambers must beat in an organized
manner. Under normal conditions, the heart valves let blood to flow in only one
direction. Problems with a heart valve (or valves) may occur because of disease,
injury or congenital factors. Two kinds of problems usually occur. If a valve is
narrowed (stenotic) the heart may have to work much harder to pump blood across
the valve. A second type of problem occurs when a valve (or valves) does not close
completely, causing some blood to be pumped backwards (regurgitation /
incompetence) instead of forwards in the heart. Both types of problems can cause the
heart to work too hard and eventually weaken over time.
Go to Animated Heart Tutorial to see how the heart and valves work.
(Use the back arrow in your browser to return to this page)

Top

What are heart valves?

Heart valves are thin flexible flaps of connective tissue. The four heart valves are:

1. the tricuspid valve, located between the right atrium and right ventricle;
2. the pulmonary or pulmonic valve, between the right ventricle and the
pulmonary artery;

3. the mitral valve, between the left atrium and left ventricle; and
4. the aortic valve, between the left ventricle and the aorta.
Blood flow occurs only when there's a difference in pressure across the valves that
causes them to open.
Each valve has a set of flaps (also called leaflets or cusps). The mitral valve has two
leaflets while the other valves have three. The mitral and tricuspid valves are
connected to small muscles (papillary) along the wall of the heart by small string like
tendons (chordeae tendineae). Papillary muscle contraction opens these valves. The
aortic and pulmonic valves are differently shaped do not have cordae tendineae nor
papillary muscles.
Top

Heart valve disorders

Valvular problems may be caused by infection, heart disease, trauma or congenital
valvular conditions and may be isolated to a single valve or effect multiple valves.
Right sided (tricuspid, pulmonary) valvular disease is much less common than left
sided (aortic, mitral) valvular disease. Roughly 90% of valvular disease is chronic,
having developed gradually over many years. Complications of rheumatic fever,
congenital disorders and aging cause the vast majority of chronic valvular disease.
The remaining 10% of valvular disease that develops acutely (over days to weeks) is
often due to complications of recent heart attack or infections.
Infection
Rheumatic fever- Most valvular heart disease is still caused by childhood rheumatic
fever (a complication of untreated streptococcal infection). During a streptococcal
infection (typically in the throat) the body makes its' own antibodies to fight the
bacterial infection. Antibodies recognize the structure of certain parts of the bacterial
surface, attach to it and destroy it. Unfortunately, the surface structure of certain
body tissues (heart valves, skin, joints, kidneys, etc..) may resemble that on certain
types of streptococcal bacteria. With rheumatic fever antibodies that normally fight
infection may attack the body's own tissues. It is important to stress that it is not
bacteria that directly cause injury.
Rheumatic fever usually occurs 2-6 weeks after untreated strep throat. Symptoms of

rheumatic fever are multiple and may include:

Fever
Arthritis (pain, swelling and warmth) that shifts from joint to joint.
Larger joints such as hips and knees tend to be more frequently
effected.
Heart failure, new heart murmurs, fast heart rate or pericardial friction
rub due to inflammation of heart muscle, valves orpericardium. This is
called carditis and occurs during rheumatic fever. Carditis is different
from delayed valvular disease that slowly develops over many years
after rheumatic fever has occurred. The latter is due to slow but
progressive thickening of effected heart valves initially injured during
rheumatic fever..
Nodules may form under the skin on the backs side of the wrist, elbow,
and knees
a temporary skin rash lasting several days may occur.
Injury to brain tissues may cause repetitive involuntary writhing
movement of the head and arms. This is called chorea.

The incidence of rheumatic fever in the USA has decreased greatly in recent years due
to the use of antibiotics to treat strep throat. Delayed symptoms of heart valve
disease may take 10-20 years to appear and gradually worsen over time. Rheumatic
fever may effect a single or multiple valves. Symptoms that occur years later is
usually from injury to the mitral and aortic valves.
Top

Infective Endocarditis is infection of heart valves directly with bacteria or fungi.

Infection may occur after certain dental /surgical procedures or with IV drug use.
Infective endocarditis can involve any heart valve but most commonly involves the
aortic or mitral valve (left sided heart disease). Infection of only the tricuspid valve
(right sided disease) is usually seen in IV drug users.
During dental or surgical procedures a small amount of bacteria may get into the
blood stream. This is almost never a problem for otherwise healthy persons with
normal heart valves- the body easily takes care of this on its own. Bacteria from these
procedures can infect previously injured heart valves (usually from rheumatic fever).
Therefore, a dose of an antibiotic (prophylactic=preventative) is always recommended
prior to dental work and certain types of surgery for people with heart valve disorders
to prevent endocarditis.
Vegetations (a mixture of bacteria and blood clots) may form on valves of the left,
right or both sides of the heart. Vegetations can embolize (break loose) and travel to
other parts of the body. Emboli from the left heart valves (mitral or aortic) will travel
via the aorta to the body; those from the right heart valves (tricuspid or pulmonic)
will travel to the lungs. Emboli lodging in the brain can cause a stroke. Emboli may
carry infection to other parts of the body. Emboli lodging in the lungs may cause
shortness of breath and cough.

Endocarditis is divided into several categories

Acute endocarditis usually occurs on previously normal valves and is most often due
to IV drug use and is due to aggressive types of bacteria associated with
contaminated needles. Rapid destruction of the heart valve(s) can happen, causing
severeheart failure.
Symptoms of acute infective endocarditis may include:

fever and chills

weakness
fast heart rate
shortness of breath and chest pain.

People are usually quite ill. Heart murmurs may be heard as well. Stroke symptoms
may occur if vegetations break loose and lodge in brain arteries. Severe heart failure
may occur if the aortic or mitral valves rupture.
Subacute endocarditis usually occurs on artificial or previously injured valves and
progresses more slowly. Bacteria associated with subacte endocarditis are not
as virulent as bacteria associated with acute endocarditis. Symptoms of subacute
infective endocarditis,often not as obvious, may include:

recurrent fever
weight loss
decreased appetite
feeling very run down

People often think they have recurrent flu or may have been treated with antibiotics
several times with antibiotics for presumed bacterial infections such as bronchitis.
As in the case of acute infective endocarditis bacterial vegetations can break loose and
go to other parts of the body. Physical signs are related to the part of the body they
lodge in:

small hemorrhages may be seen in finger and toe nail beds;

retinal hemorrhages may be seen in the eyes;
tender nodules (Osler nodes) may be felt on finger and toe tips;
nontender plaques (Janeway lesions) may occur on the palms of the
hands and soles of the feet.

Diagnosis of infective endocarditis is made if blood cultures are positive for bacteria
or fungi known to cause endocarditis and there is evidence of valvular injury or
vegetations. The heart and valves are imaged usingechocardiography.
Treatment generally requires hospitalization and intravenous antibiotic therapy for at
least 4 weeks. Infection is almost never adequately treated with oral antibiotics.
Persons with severe valvular destruction may require valve replacement.
Prevention is extremely important because infective endocarditis is so difficult to
treat and can cause severe disability or death. All persons with evidence of

valvular injury or deformity should take preventative antibiotics before

dental or surgical procedures are performed. If you have a known heart murmur
or valvular problem consult your dentist and doctor prior to dental or surgical
procedures.
Top

Heart disease
Papillary muscle dysfunction ( papillary muscles do not work properly) may occur
from a heart attack, cardiomyopathy or congestive heart failure. This can cause
regurgitation to occur across the tricuspid or mitral valves. Rupture of a papillary
muscle (usually after a heart attack) may cause sudden regurgitation of blood back
into the lungs. This may cause severe breathing problems due to excess fluid in the
lungs- this is called congestive heart failure.
Top

Calcific aortic stenosis is a degenerative condition that is the most common cause
of aortic stenosis in people over 70. Calcium deposits cause narrowing of the aortic
opening. Blood flow to the aorta is partially blocked causing the left ventricle to work
harder. This may eventually cause the left ventricle to weaken and not pump blood
efficiently.
Top

Congenital valvular conditions (present at birth)

Bicuspid aortic valve ( aortic valve has 2 cusps instead of 3 cusps) is the most
common cause of aortic stenosis in all people. Persons with a bicuspid valve often
develop symptoms in their 50's.
Top

Mitral valve prolapse (click murmur syndrome)is a condition that has caused much
debate and controversy in the medical community. Mitral valve prolapse (MVP) occurs
when one or both of the mitral valve leaflets push back (bow) into the left atrium
during contraction of the left ventricle. MVP is probably only important if a person has
both excess bowing of the mitral leaflets into the atrium and actual regurgitation of
blood from the left ventricle to the left atrium when the heart contracts.
The use of echocardiogram (ultrasound of the heart) over the past 20 years has
revolutionized examination of the heart. Using earlier ultrasound criteria it was
estimated 5-10% of the population has MVP. However, recent studies suggest that
slight bowing of the mitral valve (not accompanied by regurgitation) is normal for
many people and that MVP was likely over diagnosed because of the ability of

ultrasound to see extremely small variations in the mitral valve shape. Using revised
criteria it is believed that MVP is present in less than 1% of the general population.
People, particularly women, with heart palpitations due to anxiety often see a doctor
and have heart evaluation (including ultrasound) performed. Many persons with a
panic (anxiety) disorder were found to have mild mitral valve bowing on ultrasound- It
was believed that panic attacks were more common in people with mitral valve
prolapse. Newer studies suggest there is no correlation between panic attacks and
mitral valve prolapse. Most patients who had ultrasounds and were diagnosed with
MVP did not have true MVP but simply normal variation in the shape of their mitral
valve. For many patients and physicians it may have been easier to accept that a
physical condition was responsible for panic attacks. Most people have no symptoms
of MVP.
Persons with MVP having demonstrated regurgitation are at slightly
increased risk of developing endocarditis during dental/surgical procedures
and should receive antibiotic prophylaxis. A very small number are at increased
risk of sudden death.
Top

Mitral Valve Disorders

The mitral valve normally allows one way flow of blood from the left atrium to the left
ventricle. Disorders of the mitral valve may cause mitral valve stenosis, mitral valve
regurgitation or mitral valve prolapse (previously discussed).
Mitral Stenosis is narrowing of the mitral valve opening that usually gradually occurs
over time due chronic scarring. Rheumatic fever is still the most common cause of
mitral valve stenosis.
As the mitral opening narrows the left atrium enlarges (dilates) over time because it
must work harder to pump blood into the left ventricle. Many people (upto 50%)
eventually develop atrial fibrillation because of progressive dilatation of the left
atrium. In atrial fibrillation the left atrium quivers instead of effectively pumping blood
to the left ventricle causing a decreased amount of blood to the left ventricle.
Severe stenosis may also cause pressure to built up in the lung blood vessels
(pulmonary veins) that supply blood to the left atrium. The lung blood vessels are
normally under much lower pressure (as is the right side of the heart that pumps
blood to the lungs) than the left ventricle, aorta and its' arterial branches. Increased
blood pressure in the lungs is called pulmonary hypertension.
Symptoms may not appear for many years but are usually due to congestive heart
failure. The first ( and most common) symptom to appear is usually shortness of
breath (beyond normal) during physical activity. Any stimulus that rapidly increases
heart rate or blood flow can cause sudden increase in lung congestion and cause
shortness of breath. Other factors responsible for shortness of breath in those with
mitral stenosis (in additional to physical activity) include stress, fever, pregnancy, or

onset of atrial fibrillation. As the disease worsens shortness of breath at rest or while
lying down may occur. Severe disease is common with pulmonary hypertension.
The second most common symptom to initially appear is coughing up blood due to
rupture of a bronchial (lung) vein.
Blood clots are more likely to form in the left atrium during atrial fibrillation - these
blood clots (emboli) may dislodge and travel to other body organs including the brain,
eyes, heart and kidneys. The risk of stroke or heart attack (due to emboli traveling to
the brain or coronary arteries) is higher in persons with atrial fibrillation.
Diagnosis of mitral stenosis is suspected in a person with a history of congestive
heart failure, findings of a specific type of mitral heart murmur on physical exam, and
suggestive chest x-ray and EKG findings. Definitive diagnosis is made using
ultrasound- The entire valve can be visualized.
Cardiac catheterization ( dye is injected into a blood vessel near the heart and movielike pictures taken) is performed if surgical repair or replacement of the mitral valve is
considered. Catheterization will detect if there is narrowing of the coronary arteries.
Coronary artery disease increases the risk of heart attack during surgery and may
need to be corrected prior to surgical valve repair or replacement.
Treatment depends on the severity of symptoms, health and age of an individual,
amount of mitral valve narrowing, and whether coexisting aortic valvular disease is
present. Persons requiring treatment for this disorder must be under the care of a
physician!

Persons without symptoms and mild to moderate stenosis do not need

to restrict physical activity.
Persons with mild symptoms (shortness of breath) with physical activity
are usually started on a mild diuretic, a low salt diet, advised to avoid
vigorous exercise and extreme stress. ACE inhibitors may be used in
conjunction with diuretics.
Blood thinning agents (coumadin) are recommended with mitral
stenosis, particularly if atrial fibrillation is present, to decrease the risk
of embolization to other areas of the body.
Persons with symptoms should be evaluated by a cardiologist. Valvular
repair or replacement should not be delayed until symptoms occur at
rest or with minimal exertion. This is particularly true for younger
persons who are otherwise healthy.

Surgical treatment options include:

1. Percutaneous balloon mitral valvulotomy- a balloon tipped catheter is

2.
3.

threaded through an artery into the heart. The balloon is inflated to

expand the mitral valve. This technique has been very effective in
younger patients with valves that are not calcified (excessively stiff).
Surgical valvulotomy (commisurotomy)- the natural valve is widened by
making a cut in the mitral valve.
Total valve replacement- the mitral valve is replaced by a prosthetic
("artificial")valve. Valves may be either bioprosthetic (pig, cow, or

human) or synthetic (usually metal alloys). Valvular replacement is

usually required in older patients with heavily calcified (stiff) mitral
valves.
Prognosis
Most people have no symptoms the first 10 years, increasing shortness of breath on
exertion the next 10 years followed by worsening symptoms that may begin to occur
at rest during the next decade.
All people having mitral stenosis of any degree require antibiotic prophylaxis
to prevent infective endocarditis prior to dental or surgical procedures.
Top

Mitral Regurgitation occurs when blood flows back into the left atrium from the left
ventricle during left ventricular contraction because of a "leaky" mitral valve. Mitral
regurgitation can occur acutely (suddenly) with infective endocarditis or with a heart
attack that causes rupture of the papillary muscles or chordae tendineae. Symptoms
of severe congestive heart failure ( severe shortness of breath, fast heart rate, and
fluid in the lungs) requiring urgent surgical intervention usually occur with acute mitral
valve rupture.
Rheumatic fever is the most common cause of chronic (gradual over many years)
mitral regurgitation. Chronic regurgitation, even with large regurgitant blood flow, is
often tolerated for years due to compensatory changes in the heart. The left atrium
dilates over time to handle the increased blood volume.
Symptoms are very similar to mitral stenosis. As with mitral stenosis the most
common first symptom is shortness of breath with exertion, atrial fibrillation is
common in later stages and the risk of emboli is as high as 20%. Most emboli travel
to tissues that do not cause symptoms. However, emboli traveling to the brain may
cause stroke and emboli traveling to the coronary arteries may cause heart attack.
Diagnosis may be made by a person giving a history of shortness of breath with
exertion and the doctor hearing aheart murmur suggestive of mitral regurgitation. As
with all valvular disorders definitive diagnosis is made with ultrasonography. Persons
considered for valvular repair or replacement will have cardiac catheterization
performed.
Treatment is similar to that for mitral stenosis except balloon valvuloplasty is not
performed unless the mitral valve is also stenotic. Most cases of mitral regurgitation
do not involve significant stenosis. Valve replacement or reconstruction is indicated for
most persons with severe symptoms (shortness of breath at rest or with minimal
exertion.
Anticoagulation ( blood thinning agents) is recommended for those with mitral
regurgitation, especially persons with atrial fibrillation, due to increased risk of stroke
from emboli.

Prognosis- The time course from the presence of this disease to the first symptoms
is similar to that for mitral stenosis.
All people having mitral regurgitation require antibiotic prophylaxis to
prevent infective endocarditis prior to dental or surgical procedures.
Top

Aortic Valve Disorders

The aortic valve normally allows one way flow of blood from the left ventricle to the
aorta. Disorders of the aortic valve may cause aortic valve stenosis or aortic
valveregurgitation.
Aortic Stenosis is narrowing of the aortic valve.
Causes include:

1. congenital heart disease (bicuspid valve)- most common cause

2. rheumatic heart disease- second most common
3. degenerative heart disease (calcific aortic stenosis)- most common in
persons over 70 years of age.

What happens with aortic stenosis?

As the aortic valve narrows the left ventricle must work harder to pump the same
amount of blood through a narrower opening. The left ventricle is the largest and
strongest pumping chamber of the heart- it must pump blood to the entire body. The
left ventricular muscle increases in size (hypertrophies) over time to compensate for
the extra work it must perform. The strength and ability of the left ventricle to
compensate for increased work load may mask the symptoms of aortic stenosis for
many years until the valve becomes extremely narrow. When the aortic valve narrows
past a certain point the left ventricle can no longer fully compensate. Not as much
blood can be pumped across the aortic valve to the body, particularly during activities
requiring increased blood flow to the organs and muscles. At this point symptoms may
appear.
Symptoms include:

1. Shortness of breath with exertion. This symptom may occur earlier in

2.
3.

very physically active people. This is usually the first symptom but is
not specific for aortic stenosis.
Shortness of breath awakening a person from their sleep (second most
common symptom).
Passing out (syncope) with exertion, angina, or heart attack are also
common and indicate severe disease.

Who gets aortic stenosis?

Most people do not develop symptoms until late in the course of aortic stenosis. Age
at onset of symptoms (clinically apparent aortic stenosis) usually indicates the cause
of aortic stenosis. Symptoms in people younger than 30 years is almost always due to
congenital causes (usually bicuspid aortic valve). Symptoms in people 30-70 years
may be due to either bicuspid valve or rheumatic heart disease. Aortic stenosis caused
by rheumatic fever occurs 10-15 years later than mitral stenosis caused by rheumatic
fever. Symptoms developing in the elderly are usually due to calcific degenerative
changes of a normal aortic valve (wear and tear of aging).
How is aortic stenosis detected?
People may see their doctor concerning symptoms of aortic stenosis. Chest pain or
passing out during exertion is very concerning and may prompt a doctor into
examining the heart in detail. If aortic stenosis is present a certain type of heart
murmur may be detected when a doctor listens with a stethoscope. The doctor may
order further tests. Aortic stenosis can be definitively diagnosed
using echocardiogram (heart ultrasound).
Atrial fibrillation and traveling emboli are less common in isolated aortic stenosis.
Is aortic stenosis serious?
Once symptoms develop aortic stenosis is very serious. The presence of symptoms
almost always means that the aortic valve is extremely narrow and will not tolerate
further narrowing. Once symptoms occur with aortic stenosis, particularly angina or
shortness of breath with minimal exertion or congestive heart failure, many people die
within several years if not treated.
Sudden death, due to cardiac arrhythmias, may occur in upto 20% of people with
aortic stenosis. The cause of sudden death is speculative (unknown).
How is aortic stenosis treated?

Asymptomatic persons with mild stenosis do not have to limit physical activity.
Periodic monitoring should be done because rapid narrowing can occur over as
little as a few years.
Persons with more severe stenosis should be evaluated by a cardiologist
whether or not they have symptoms.
Persons with symptoms of passing out on exertion, angina or congestive heart
failure due to aortic stenosis require immediate evaluation by a cardiologist
and may be considered for valve repair or replacement.
Your doctor may treat symptoms of either angina or congestive heart failure
with medications as they occur. If these symptoms are caused by aortic
stenosis definitive treatment is valve repair or replacement. Very old age (80's)
is not a contraindication to valve replacement as long heart function and
overall health are reasonable.
Persons requiring treatment for this disorder must be under the care of a
physician!

Top

Pulmonary and Tricuspid Valve Disorders

Isolated valvular disorders of the right side of the heart (receiving and pumping
venous blood to the lungs for oxygenation) are much less common than left sided
valvular disease. Combined left (mitral and/or aortic) and right (tricuspid and/or
pulmonic) heart valvular disease is more common.
Tricuspid Valve Disorders - Tricuspid valve normally allows one way blood flow
from the right atrium to the right ventricle.

Isolated tricuspid disease is most commonly due to endocarditis from IV

drug use.
Right ventricular failure causing tricuspid regurgitation is usually due to
heart attack effecting the right ventricle
Tricuspid disease and left sided valvular disease due to rheumatic fever
may occur.

Pulmonary Valve Disorders - Pulmonic valve normally allows one way blood flow
from the right ventricle to the pulmonary (lung) arteries.

Pulmonary stenosis most frequently caused by a congenital defect

(Tetralogy of Fallot) that is detected and surgically corrected in infancy.
Pulmonary regurgitation (incompetence) is most commonly due
topulmonary hypertension.

Symptoms

Shortness of breath, particularly while laying flat are the most common
initial symptoms of tricuspid and pulmonary valve disorders. Symptoms
of worsening disease, in addition to shortness of breath, include
swelling of the feet, liver, abdomen or neck veins due to fluid retention.
Top

Artificial (Prosthetic) Valves

Artificial valves are placed in over 40,000 persons a year in the United States. There
are more than six dozen types of valves. Prosthetic valves can be grouped into two
main categories:

1. Mechanical (nontissue models) usually made of metal or composite alloys.

2. Tissue valves(bioprostheses) made from pig, cow or human valves.
Discussion of individual valve types is beyond the scope of this article. Readers having
questions about specific valve types or technical details must consult with their doctor,
cardiologist or cardiothoracic surgeon. Patients with prosthetic valves should always

carry a card that describes their valve.

What type of problems occur with prosthetic valves?
Are more common in patients having more advanced heart disease (cardiomyopathy,
congestive heart failure, and/or arrhythmias) at time of valve replacement.

Prosthetic valves may be slightly narrow (stenotic). A small amount

ofregurgitation, due to incomplete closing, is common.
Thrombi (blood clots) can form on prosthetic valves. If thrombi become large
enough they can interfere with blood flow or prevent the valve from closing
properly.
Thrombi can embolize. This is the most important complication of
mechanical (nontissue) valves. This occurs in about 1% of people per year with
mechanical valves. This is not as common in tissue valves. Those with
mechanical valves almost always need to take blood thinning medications
(anticoagulation). Not all tissue valves require anticoagulation.
Bioprostheses may gradually deteriorate.
Mechanical valves often cause anemia due to increased red blood cell
destruction.
Rarely, mechanical valves can suddenly fail (break). This is often fatal.
Endocarditis is more likely to occur on artificial valves.
What symptoms occur with prosthetic valve problems?
Many patients have ongoing shortness of breath and decreased exercise
tolerance after successful valve replacement. This is more likely in persons with
poorer heart function or atrial fibrillation.

Persons with a sudden decrease in normal exercise tolerance or new chest pain
should see their doctor.
In addition to these symptoms people with prosthetic valve problems may
experience symptoms of emboli. Minor episodes (temporary) are common and
can include stroke like symptoms, abdominal pain (emboli blocking intestinal
blood vessels), and arm or leg pain (emboli blocking muscle blood vessels).
Major blockages can cause stroke, heart attack, and permanent intestinal
injury.
Severe hemorrhage can occur during anticoagulation therapy. People on
anticoagulants noticing blood in the urine, feces, saliva or new skin bruising
must see their doctor.
Those with fever should see their doctor urgently. Fever could indicate infective
endocarditis.

Patients with prosthetic valves should receive antibiotic prophylaxis before

dental and surgical procedures.
Top

Glossary

Atrial fibrillation

left atrium of heart ineffectively quivers instead of normally

contracting.

Arrhythmia

irregular beating of the heart that may cause the heart to beat
too fast or slow. Certain arrhythmias may cause the heart to
stop beating.

Chorea

repetitive involuntary writhing movement of the head and

arms.

Congenital

a condition present at birth

Congestive heart
failure

the heart can't pump enough blood to meet the needs of the
body's other organs.

Echocardiography a technique that views the heart valves using sound waves
and a computer generated image. Also called a heart
ultrasound.
Heart murmur

sound caused by turbulent blood flow across a heart valve(s)

heard by a doctor using a stethoscope.

Heart valves

are thin flexible flaps of connective tissue normally permitting

one-way blood flow through the heart.

Palpitations

An uncomfortable awareness of the heart beating. May be

slow, normal or fast.

Pericardium

a tough fibrous layer of tissue normally covering the heart.

Pericardial
friction rub

a sound heard with a stethoscope due to rubbing of the heart

against the pericardium that may occur with inflammation of
the pericardium.

Pulmonary
hypertension

increased pressure in the lung veins and arteries. These

vessels are normally under lower blood pressure than arteries
arising from the aorta and its' branches. May contribute to or
be caused by chronic congestive heart failure. Often
secondary to increased left atrial pressure, due to mitral
stenosis, causing blood to back up in the lungs.

Regurgitation

backward flow of blood through a heart valve. Also called

valvular incompetence.

Stenosis

narrowing of the valve opening

Virulence

the ability of an infection to cause illness / injury to the body.

Other Sites/References

Cline, D. M., "Valvular Emergencies and Endocarditis" in Emergency Medicine

4th edition. 1996.
Liberthson, R. R.,"Management of Aquired Valvular Heart Disease" in Primary
Care Medicine- Office evaluation and Management of the Adult Patient 3rd
edition. 1995.
The American Heart Association
Dental Care and Heart Disease

Doctors Corner INternet Group, Inc. 1997-2004

Statement

Artificial heart valve

From Wikipedia, the free encyclopedia

[hide]This article has multiple issues. Please help improve it or discuss these issues on the talk page

This article needs additional citations for verification. (November 2008)

This article includes a list of references, but its sources remain unclear because it has insufficient i
This article possibly contains original research. (November 2013)
An artificial heart valve is a device implanted in the heart of a patient with valvular heart
disease.[1][2] When one of the four heart valves malfunctions, the medical choice may be to replace
the natural valve with an artificial valve. This requires open-heart surgery.
Valves are integral to the normal physiological functioning of the human heart. Natural heart
valves are evolved to forms that perform the functional requirement of inducing unidirectional
blood flow through the valve structure from one chamber of the heart to another. Natural heart
valves become dysfunctional for a variety of pathological causes. Some pathologies may require
complete surgical replacement of the natural heart valve with a heart valve prosthesis.[3]
Contents
[hide]

1 Types of heart valve prostheses

2 Mechanical valves
o 2.1 Types of mechanical heart valves

o 2.2 Durability
o 2.3 Cavitation
o 2.4 Fluid mechanics
o 2.5 Blood damage
3 Tissue (biological) valves
4 Functional requirements of heart valve prostheses
5 Design challenges of heart valve prostheses
6 Replaceable models of heart valve prostheses
7 Typical configuration of a heart valve prosthesis
8 Additional images
9 See also
10 References
11 Sources
12 External links

Types of heart valve prostheses[edit]

There are three main types of artificial heart valves: the mechanical,the biological, and the tissue
engineered valves.

Mechanical heart valve

Percutaneous implantation
Stent framed
Not framed
Sternotomy/Thoracotomy implantation
Ball and cage
Tilting disk
Bi-leaflet
Tri-leaflet
Tissue (biological) heart valves
Allograft/isograft
Xenograft
Tissue Engineered heart valves

Mechanical valves[edit]

A mechanical artificial heart valve with a pivoting disc.

Mechanical heart valves (MHV) are prosthetics designed to replicate the function of the natural
valves of the human heart. The human heart contains four valves: tricuspid valve, pulmonic
valve, mitral valve and aortic valve. Their main purpose is to maintain unimpeded forward flow
through the heart and from the heart into the major blood vessels connected to the heart,
the pulmonary artery and the aorta. As a result of a number of disease processes, both acquired and

congenital, any one of the four heart valves may malfunction and result in either stenosis (impeded
forward flow) and/or backward flow (regurgitation). Either process burdens the heart and may lead to
serious problems including heart failure. A mechanical heart valve is intended to replace a diseased
heart valve with its prosthetic equivalent.
There are two basic types of valves that can be used for valve replacement, mechanical and tissue
valves. Modern mechanical valves can last indefinitely (the equivalent of over 50,000 years in an
accelerated valve wear tester).[citation needed] However, current mechanical heart valves all require
lifelong treatment with anticoagulants (blood thinners), e.g. warfarin, which requires monthly blood
tests to monitor.[citation needed] This process of thinning the blood is called anticoagulation. Tissue heart
valves, in contrast, do not require the use of anticoagulant drugs due to the improved blood flow
dynamics resulting in less red cell damage and hence less clot formation.[citation needed] Their main
weakness however, is their limited lifespan. Traditional tissue valves, made of pig heart valves, will
last on average 15 years[citation needed] before they require replacement (but typically less in younger
patients).

Types of mechanical heart valves[edit]

Starr-Edwards-Mitral-Valve (Caged ball valve).

1. Starr-Edwards Valve
2. Starr-Edwards Valve
3. Smeloff-Cutter Valve

There are three major types of mechanical valves caged-ball, tilting-disk and bileaflet with many
modifications on these designs.
The first artificial heart valve was the caged-ball, which utilizes a metal cage to house a silicone
elastomer ball. When blood pressure in the chamber of the heart exceeds that of the pressure on the
outside of the chamber the ball is pushed against the cage and allows blood to flow. At the
completion of the heart's contraction, the pressure inside the chamber drops and is lower than
beyond the valve, so the ball moves back against the base of the valve forming a seal. In
1952, Charles A. Hufnagel implanted caged-ball heart valves in ten patients (six survived the
operation), marking the first long-term success in prosthetic heart valves.[citation needed] A similar valve
was invented by Miles "Lowell" Edwards and Albert Starr in 1960 (commonly referred to as the StarrEdwards Silastic Ball Valve).[citation needed] The first human implant was on Sept 21, 1960.[citation needed] It
consisted of a silicone ball enclosed in a cage formed by wires originating from the valve housing.
Caged ball valves have a high tendency to forming blood clots, so the patient must have a high
degree of anti-coagulation, usually with a target INR of 2.5-3.5.[citation needed] Edwards
Lifesciences discontinued production of the Starr-Edwards valve in 2007.[citation needed]
Soon after came tilting-disc valves. The first clinically available tilting disk valve was the BjorkShiley valve and has undergone several significant design changes since its introduction in
1969.[citation needed] Tilting disk valves have a single circular occluder controlled by a metal strut. They
are made of a metal ring covered by an ePTFE fabric, into which the suture threads are stitched in
order to hold the valve in place. The metal ring holds, by means of two metal supports, a disc which
opens and closes as the heart pumps blood through the valve. The disc is usually made of an

extremely hard carbon material (pyrolytic carbon), in order to allow the valve to function for years
without wearing out. The Medtronic-Hall model is the most common tilting-disc design in the US. In
some models of mechanical valves, the disc is divided into two parts, which open and close as a
door.
Bileaflet heart valves consist of two semicircular leaflets that rotate about struts attached to the
valve housing. This design was introduced in 1979[citation needed] and while they take care of some of
the issues that were seen in the other models, bileaflets are vulnerable to backflow and so they
cannot be considered as ideal. Bileaflet valves do, however, provide much more natural blood flow
than caged-ball or tilting-disc implants. One of the main advantages of these valves is that they are
well tolerated by the body. Only a small amount of blood thinner is needed to be taken by the patient
each day in order to prevent clotting of the blood when flowing through the valve.
These bileaflet valves have the advantage that they have a greater effective opening area (2.43.2
square cm c.f. 1.52.1 for the single-leaflet valves).[citation needed] Also, they are the least thrombogenic
of the artificial valves.
Mechanical heart valves are today very reliable and allow the patient to live a normal life. Most
mechanical valves last for at least 20 to 30 years.[citation needed]

Durability[edit]
Mechanical heart valves have been traditionally considered to be more durable in comparison to
their bioprosthetic counterparts. The struts and occluders are made out of either pyrolytic carbon or
titanium coated with pyrolytic carbon,[citation needed] and the sewing ring cuff is Teflon (PTFE), polyester
or dacron.[citation needed] The major load arises from transvalvular pressure generated at and after valve
closure, and in cases where structural failure does happen, it is usually as a result of occluder
impact on the components.
Impact wear and friction wear dictate the loss of material in MHV. Impact wear usually occurs in the
hinge regions of bileaflets, between the occluder and ring in tilting-discs, and between the ball and
cage in caged-ball valves. Friction wear occurs between the occluder and strut in tilting-discs, and
between the leaflet pivots and hinge cavities in bileaflets.[citation needed]
MHV, made out of metal are also susceptible to fatigue failure owing to
the polycrystalline characteristic of metals, but this is not an issue with pyrolytic carbon MHV
because this material is not crystalline in nature.[citation needed]

Cavitation[edit]
Cavitation is an event that can lead to MHV failure. While this has been a relatively rare occurrence,
in 1988 the Edwards-Duramedics bileaflet had 46 reported failures in 20,000 implants related to
cavitation damage.[citation needed] Since then, manufacturers have made cavitation testing an essential
part of the design verification process. Cavitation is the rapid formation of vaporous microbubbles in
the fluid due to a local drop of pressure below the vaporization pressure at a given temperature.
When conditions for cavitation are present bubbles will form and at the time of pressure recovery
they will collapse or implode. This event will cause pressure or thermal shockwaves and fluid
microjets which can damage a surface. These thermodynamic conditions are known to be the cause
of MHV related erosion.[citation needed]
The valvular event that causes such cavitating conditions to exist is the closing mechanics of the
MHV. Several causes of cavitation relating to valve closure have been identified. Squeeze flow is
cavitation that is said to occur as the occluder approaches the housing during closure and fluid is
squeezed between the occluder and the valve housing causing a low pressure formation. Water
hammer is cavitation caused by the sudden stop of the valve occluder as it contacts the valve
housing. This sudden retardation of the fluid retrograde inertia is said to put the fluid under tension
causing cavitation. Squeeze flow is said to form a cloud of bubbles at the circumferential lip of the

occluder whereas water hammer is said to be seen as transient bubbles at the occlude
housing.[citation needed]
For either event, cavitation occurs on the upstream side of valve. Clinically, cavitation is of primary
concern in the mitral position. This position is especially harsh due to the sudden ventricular
pressure rise which drives the valve closure against a low left atrial pressure which is said to be the
worst case condition thus position for cavitation to occur. Cavitation is also suspected as a
contributing factor in blood cell damage and increased risk of thromboembolic complications.[citation
needed]

The temporal rate of change of the left ventricular, measured as a slope of the ventricular pressure
curve (dP/dt) is regarded as the best indicator for cavitation potential. Most MHV investigated
generate cavitation only when the dP/dt is well above the physiological range. However
investigations have found that several tilting disc valves and only one bileaflet valve, the EdwardsDuromedics, generate cavitation within the physiological range. Investigations have repeatedly
demonstrated that bileaflet valves, with the exception of the Edwards Duramedics design, cavitate
only at dP/dt levels well above the physiological range.[citation needed]

Fluid mechanics[edit]
Many of the complications associated with MHV can be explained through fluid mechanics. For
example, thrombus formation is a debilitating side effect of high shear stresses created by the
design of the valves. An ideal heart valve from an engineering perspective would produce minimal
pressure drops, have small regurgitation volumes, minimize turbulence, reduce prevalence of high
stresses, and not create flow separations in the vicinity of the valve.[citation needed]
One measure of the quality of a valve is the effective orifice area (EOA), which can be calculated as
follows:

where
is the root mean square systolic/diastolic flow rate (cm/s) and
is the mean
systolic/diastolic pressure drop (mmHg). This is a measure of how much the prosthesis impedes
blood flow through the valve. A higher EOA corresponds to a smaller energy loss. The performance
index (PI) normalizes the EOA by valve size and is a size-independent measure of the valves
resistance characteristics. Bileaflet valves typically have higher PIs than tilted-disc models, which in
turn have higher PIs than caged-ball models.[citation needed]
As blood flows through a prosthetic heart valve, a sudden pressure drop occurs across the valve due
to the reduction in cross-sectional area within the valve housing. This can be quantified through the
continuity equation and Bernoullis equation:

where A represents the cross-sectional area, P is pressure, is density, and V is the velocity.[citation
needed]
As cross-sectional area decreases in the valve, velocity increases and pressure drops as a
result. This effect is more dramatic in caged-ball valves than in tilting-disc and bileaflet valves. A
larger systolic pressure is required to drive flow forward in order to compensate for a large pressure
drop, so it should be minimized.[citation needed]
Regurgitation is the sum of retrograde flow during the closing motion of the valve and leakage flow
after closure. It is directly proportional to valve size and is also dependent on valve type. Typically,
caged-ball valves have a low amount of regurgitation as there is very little leakage. Tilting-disc and

bileaflet valves are comparable, with the bileaflet valves have a slightly larger regurgitation volume.
Bioprosthetics prevail over MHV in this case, as they have virtually no regurgitation volume.[citation
needed]

Turbulence and high shear stresses are also major issues with MHV, as they can fracture the valve
housing or components, or induce blood damage. A large flow gradient can lead to these factors, so
flow separation and stagnation should be as small as possible. High stresses are created at the
edges of the annular jet in caged-ball valves, in narrow regions at the edges of the major orifice jet in
tilting-disc valves, and in regions immediately distal to the valve leaflets in bileaflet valves. The
implications of blood damage from these stresses are discussed in the next section.[citation needed]
The cavitation phenomenon can also be described using fluid mechanics. This can result from
pressure oscillations, flow deceleration, tip vortices, streamline contraction, and squeeze jets. This
last cause is the most contributive factor to cavitation. The squeeze jets are formed when the valve
is closing and the blood between the occluder and valve housing is squeezed out to create a highspeed jet. This in turn creates intense vortices with very low pressures that can lead to
cavitation.[citation needed]

Blood damage[edit]
One of the major drawbacks of mechanical heart valves is that patients with these implants require
consistent anti-coagulation therapy. Clots formed by red blood cell (RBC) and platelet damage can
block up blood vessels and lead to very serious consequences. Clotting occurs in one of three basic
pathways: tissue factor exposure, platelet activation, or contact activation by foreign materials, and
in three steps: initiation, amplification, and propagation.[citation needed]
In the tissue factor exposure path, initiation begins when cells are ruptured and expose tissue factor
(TF). Plasma Factor (f) VII binds to TF and sets off a chain reaction which activates fXa and fVa
which bind to each other to produce thrombin which in turn activates platelets and fVIII. The platelets
activate by binding to the damaged tissue in the initiation phase, and fibrin stabilizes the clot during
the propagation phase.[citation needed]
The platelet activation pathway is triggered when stresses reach a level above 6 to 8 Pa (6080
dyn/cm). The steps involved with this are less clearly understood, but initiation begins with the
binding of vWF from the plasma to GPIb on the platelet. This is followed by a large influx of
Ca2+ ions, which activates the platelets. GPIIb-IIIa facilitates platelet-platelet adhesion during
amplification. The propagation step is still under study.[citation needed]
Contact activation begins when fXII binds to a procoagulant surface. This in turn activates
prekallikrein (PK) and high-molecular-weight kininogen (HK). Eventually, HKa-PK and HKa-fXI
complexes form on the surface. In amplification, Hka-FXIa complexes activate fIX to fIXa, which in
turn forms thrombin and platelets. Proteins buildup on the surface and facilitate platelet adhesion
and tissue growth in the propagation stage.[citation needed]
All MHV models are vulnerable to thrombus formation due to high shear stress, stagnation, and flow
separation. The caged-ball designs experience high stresses at the walls that can damage cells, as
well as flow separation due to high-velocity reverse flow surrounded by stagnant flow. Tilting-disc
valves have flow separation behind the valve struts and disc as a result of a combination of high
velocity and stagnant flows. The bileaflet models have high stresses during forward and leakage
flows as well as adjacent stagnant flow in the hinge area. As it turns out, the hinge area is the most
critical part of bileaflets and is where the thrombus formation usually prevails.[citation needed]
In general, blood damage affects valves in both the mitral and aortic positions. High stresses during
leakage flow in aortal valves result from higher transvalvular pressures, and high stresses occur
during forward flow for mitral valves. Valvular thrombosis is most common in mitral prosthetics. The
caged-ball model is better than the other two models in terms of controlling this problem, because it
is at a lower risk for thrombosis and it is gradual when it does happen. The bileaflet is more

adaptable to this problem than the tilting-disc model because if one leaflet stops working, the other
can still function. However, if the hinge is blocked, both leaflets will stop functioning.[citation needed]
Because all models experience high stresses, patients with mechanical heart valve implants require
anti-coagulation therapy. Bioprosthetics are less prone to develop blood clotting, but the trade-off
concerning durability generally favors their use in patients older than age 55.[citation needed]
Mechanical heart valves can also cause mechanical hemolytic anemia with hemolysis of the red
blood cells as they pass through the valve.[citation needed]

Tissue (biological) valves[edit]

Biological valves are valves of animals, like pigs, which undergo several chemical procedures in
order to make them suitable for implantation in the human heart. The porcine (or pig) heart is most
similar to the human heart, and therefore represents the best anatomical fit for replacement.
Implantation of a porcine valve is a type of xenotransplantation, also known as a xenograft, which
means a transplant from one species (in this case a pig) to another. There are some risks
associated with a xenograft such as the human body's tendency to reject foreign material.
Medication can be used to retard this effect, but is not always successful.[citation needed]
Another type of biological valve utilizes biological tissue to make leaflets that are sewn into a metal
frame. This tissue is typically harvested from the Pericardial Sac of either Bovine (cows) or Equine
(horses). The pericardial sac is particularly well suited for a valve leaflet due to its extremely durable
physical properties. This type of biological valve is extremely effective means of valve replacement.
The tissue is sterilized so that the biological markers are removed, eliminating a response from the
host's immune system. The leaflets are flexible and durable and do not require the patient to take
blood thinners for the rest of their life.[citation needed]
The most used heart valves in the US and EU are those utilizing tissue leaflets. Mechanical valves
are more commonly used in Asia and Latin America.[citation needed] The following companies
manufacture tissue heart valves: Edwards Lifesciences, Medtronic, St. Jude Medical, Sorin,
Medtronic ATS Medical, 3F Therapeutics, CryoLife, and LifeNet Health.[citation needed]
Recently, researchers have begun working to grow heart valves in vitro. Autologous cells are seeded
on a scaffold, typically made from a biodegradable polymer such as PGA or PLA. The scaffolding
acts as an artificial extra-cellular matrix, guiding tissue growth into the correct 3D structure of the
heart valve. Mechanical stimuli must be simulated in the culture in order to condition the tissue for
physiological stress in vivo. These heart valves have not yet reached clinical trials.[4]

Functional requirements of heart valve prostheses[edit]

The functioning of natural heart valves is characterized by many advantages:

Minimal regurgitation This means that the amount of blood lost

upstream as the valve closes is small. For example, closure
regurgitation through the mitral valve would result in some blood
loss from the left ventricle to the left atrium as the mitral valve
closes. Some degree of valvular regurgitation is inevitable and
natural, up to around 5ml per beat.[5] However, several heart valve
pathologies (e.g. rheumatic endocarditis) may lead to clinically
significant valvular regurgitation. A desirable characteristic of heart
valve prostheses is that regurgitation is minimal over the full range
of physiological heart function (i.e. complete functional envelope
of cardiac output vs. heart rate).

Minimal transvalvular pressure gradient Whenever a fluid flows

through a restriction, such as a valve, a pressure gradient arises
over the restriction. This pressure gradient is a result of the
increased resistance to flow through the restriction. Natural heart
valves have a low transvalvular pressure gradient as they present
little obstruction to the flow through themselves, normally less than
16 mmHg. A desirable characteristic of heart valve prostheses is
that their transvalvular pressure gradient is as small as possible.
Non-thrombogenic As natural heart valves are lined with
an endothelium continuous with the endothelium lining the heart
chambers they are not normally thrombogenic. This is important as
should thrombi form on the heart valve leaflets and become seeded
with bacteria, so called "bacterial vegetations" will form. Such
vegetations are difficult for the body to deal with as the
normal physiological defense mechanisms are not present within
the valve leaflets because they are avascular and largely composed
ofconnective tissue (Fixme: Create article discussing the
pathgonesis of leaflet bacterial vegetations.). Should bacterial
vegetations form on the valve leafets they may continually
seed bacteria into the arterial tree which may lead
to bacteremia or septicaemia. Portions of the vegetation may also
break off forming septic emboli. Septic emboli can lodge anywhere
in the arterial tree (e.g. brain, bowel, lungs) causing local
infectious foci. Even dislodged fragments from uninfected thrombi
can be hazardous as they can lodge in, and block,
downstream arteries (e.g. coronary arteries leading to myocardial
infarction, cerebral arteries leading to stroke, see embolism). A
desirable characteristic of heart valve prostheses is that they are
non or minimally thrombogenic.
Self-repairing Although of limited extent compared to well
vascularised tissue (e.g. muscle), the valve leaflets do retain some
capacity for repair due to the presence of
regenerative cells (e.g. fibroblasts) in the connective tissue from
which the leaflets are composed. As the human heart beats
approximately 3.4x109 times during a typical human lifespan this
limited but nevertheless present repair capacity is critically
important. No heart valve prostheses can currently self-repair but
replacement tissues grown using stem cell technology may
eventually offer such capabilities.[citation needed]
Rapid dynamic response STD

Design challenges of heart valve prostheses[edit]

A replaceable model of Cardiac Biological Valve Prosthesis.

[6] [7]

Thrombogenesis / haemocompatibility
Mechanisms:
Forward and backward flow shear
Static leakage shear
Presence of foreign material (i.e. intrinsic coagulation
cascade)
Cellular maceration
Valve-tissue interaction
Wear
Blockage
Getting stuck
Dynamic responsiveness
Failure safety
Valve orifice to anatomical orifice ratio
Trans-valvular pressure gradient
Minimal leakages
Detachable And Replaceable Models Of Heart Valve Prostheses

Replaceable models of heart valve prostheses[edit]

Mechanical or biological (bioprostheses or "tissue valves"), the replaceable models of implantable
heart valve prostheses are made by two or three mechanical components. The gear attachment
mechanism usually uses the coil effect or the bayonet coupling system.[citation needed]
The replaceable models of implantable heart valve prostheses are typically supplied with a
sewing or suturing ring surrounding the valve body or stent that is to be sutured by the surgeon to
the valvar rim.[citation needed]
The biggest challenge in this type of prostheses is the difficulty in its future removal. This is due to
the formation of pannus fibrotic around the valve body and sewing ring. To separate the parts is very
laborious, keeping intact the sewing ring, which will be used in the coupling of the new valve.
To easily remove the old replaceable bioprostheses, its "stent" can be sectioned to dismount its
framework and so facilitate its removal from the sewing ring.[citation needed]

Time line of the detachable and replaceable models of heart valve prostheses:

1984 Martin, J. R [8]

1984 Martin, J. R [9]
1984 Martin, J. R [10]
1987 Fernandez J [11]
1988 Cooper DK [12]
1992 Lyra,R M [6]
1992 Lyra,R M [7]
1992 Jansen J [13]

Typical configuration of a heart valve prosthesis[edit]

Anchor
Leaflets

Additional images[edit]

3D Rendering of Mechanical Valve

3D Rendering of Mechanical Valve (St. Francis model)

See also[edit]

Artificial heart

References[edit]
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Chester, Adrian H.; Yacoub, Magdi H.; Stevens, Molly M. (2013).
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into human cardiovascular tissue calcification". Nature
Materials 12 (6): 57683. doi:10.1038/nmat3627. PMID 23603848.
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Orbicular origins". Nature Materials 12 (6): 476
8. doi:10.1038/nmat3663. PMID 23695741.
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Valves: Selection of the Optimal Prosthesis and Long-Term
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5. Jump up^ Kasegawa, H; Iwasaki, K; Kusunose, S; Tatusta, R;

Doi, T; Yasuda, H; Umezu, M (2012). "Assessment of a novel
stentless mitral valve using a pulsatile mitral valve simulator". The
Journal of heart valve disease 21 (1): 715. PMID 22474745.
a b
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Maria Alberto; Nyashida, S.; Jatene, Adib (1992). "Estudo in vitro,
de uma bioprotese recambiavel" [In vitro study of a recambiavel
bioprosthesis]. Revista da Sociedade de Cardiologia do Estado de
So Paulo (in Portuguese) 2 (2 Suppl B): 71.
a b
7. ^ Jump up to: Lyra, R. M.; Leirner, A. A.; Pomerantzeff, Pablo
Maria Alberto; Hyashida, S.; Jatene, Adib (1992). "Novo modelo de
bioprotese recambiavel" [New model of recambiavel
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8. Jump up^ Martin, J. R; Grassi, E. D; Barone, A; Milei, J; Barone,
H. D. (1984). "Protesis valvular cardiaca desmontable. Implante
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[Dismountable heart valve prosthesis. In vivo experimental implant
and delayed valvular replacement]. Revista Argentina de
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9. Jump up^ Martin, J. R; Barone, H. D; Barone, A; Milei, J; Grassi,
E. D. (1984). "Anel portador de valvulas cardiacas" [Ring porter of
cardiac valves]. Arquivos brasileiros de cardiologia (in
Portuguese) 43 (6): 41521. PMID 6399678.
10. Jump up^ Martin, J. R; Grassi, E. D; Barone, A; Barone, H. D;
Patane, A. M. (1984). "Protesis valvular cardiaca demontable
Desarrollo experimental (Prototipo I)" [Dismountable heart valve
prosthesis.Experimental development (Prototype I)]. Revista
Argentina de Ciruga (in Portuguese) 46 (6): 2724.
11. Jump up^ Fernandez, J; Gonzalez-Lavin, L; Maranhao, V; Yang,
SS (1987). "A new bioprosthesis for aortic and mitral valve
replacement: Preliminary evaluation of the Tascon valve". Texas
Heart Institute journal / from the Texas Heart Institute of St. Luke's
Episcopal Hospital, Texas Children's Hospital 14 (1): 31
8. PMC 324690. PMID 15227327.
12. Jump up^ Cooper, D.K.C.; Wicomb, W.N.; Gould, Gwyneth M.;
Boonzaier, D. (1988). "Initial Experimental Experience with a
'Replaceable' Cardiac Valve Prosthesis". The Annals of Thoracic
Surgery 45 (5): 5548. doi:10.1016/S0003-4975(10)645328. PMID 3365047.
13. Jump up^ Jansen, Josef; Willeke, Sebastian; Reul, Helmul; Rau,
Gnter (2008). "Detachable Shape-Memory Sewing Ring for Heart
Valves". Artificial Organs 16 (3): 2947. doi:10.1111/j.15251594.1992.tb00313.x. PMID 10078262.

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Exercise following mechanical heart valve replacement

1. Effects of physical training on the cardiovascular system

Physical exercise following mechanical heart valve replacement is nowadays one of the pillars of longterm therapy and should form a regular part of the patients daily or weekly routine. Long-term studies
have shown that even heart valve patients can achieve the same level of fitness following surgery as that
enjoyed by healthy persons of the same age.
Any pre-existing heart damage is a crucial factor in the fitness prognosis. As a rule of thumb one can say:
the longer the condition has pre-existed and the more complex the pre-existing damage is, the longer it
will take to restore fitness.
Cardiological sports medicine has long taken an interest in the effects of physical training on diseased
and post-surgical heart muscle.
The following effects have been scientifically proven:

reduction in the heart rate at rest and under stress,

reduction in the systolic blood pressure peak under stress,
lower rate of pressurization during the blood expulsion phase from the ventricle,
long diastolic duration,
greater elasticity of all the blood vessels,
thickening of the vascular endothelium,
lower tendency for the platelets (thrombocytes) to aggregate,
lower tendency for the red blood cells (erythrocytes) to agglutinate,
improved fibrinolysis.
This means that the bloods flow properties are improved, the heart muscle pumps with less pressure,
and resistance due to friction in the blood vessels and in the new heart valve is considerably reduced.
These primary effects are important for the heart valve patient.

2. Devising a training program

Devising an optimum training program requires the data used as the basis for the cardiological diagnosis.
The correct training program depends on:
pre-existing damage,
the surgical outcome,
healing of the heart muscle,
any secondary cardiological conditions,
the stress ECG and
echo cardiography data (the pumping action of the heart chambers).
The optimum training program is as follows:
a) It should involve endurance-type exercise (walking, hiking, running, cycling, ergometer training,
swimming, ski tours, inline skating).
b) It should be pursued daily, at least 3-4 times per week, for longer than 30 minutes each time.

c) In intensity it should not exceed 65% of maximum physical performance.

Ad a): Endurance-type exercise has the most beneficial effects on the cardiovascular system, the blood
picture and metabolism, as it involves alternate contraction and relaxation of the muscles. This
guarantees optimum blood supply with only moderate rises in blood pressure.
Ad b): A training program for the cardiovascular system and blood picture should last longer than 30
minutes, as it should allow all of the metabolic systems to be included in the energy-providing process, fat
metabolism being one of the main systems.
Ad c): The intensity should not exceed 65% of maximum physical performance. The training should be
aerobic. Up to this intensity the muscles burn fats along with carbohydrates while binding oxygen. The
lactic acid and adrenalin concentrations remain low, this being easy on the blood picture. If the muscle
becomes over-acidified through anaerobic work, a high level of adrenalin builds up owing to the presence
of lactic acid in the blood. This acidic metabolic environment makes the blood thicker and less receptive
to oxygen. Over-acidification occurs at an intensity of approximately 65% of maximum physical
performance. As the intensity of exercise increases, there is no further optimization of training effect.

3. Calculation of optimum intensity from the stress ECG

To calculate the optimum intensity, take the last wattage on the stress ECG as being 100%. Calculate
65% of this to obtain the training wattage. Then check the stress ECG records to see what heart rate was
entered for this stage. This gives the optimum training heart rate. This should not be exceeded during
exercise. Although the heart muscle will not be damaged if you briefly exceed these values, the
conditions will no longer be optimum for the blood picture.
Example: You reach 100 watts as the highest stage in the stress ECG. Your optimum training intensity
would then be 65 watts (= 65%).
If, however, there are other cardiological reasons why this training wattage cannot be maintained (e.g. too
great a rise in blood pressure, limited pumping action, stress-related arrhythmias, etc.), then the intensity
of the exercise must be reduced.

4. Rating different types of exercise

Cardiological sports medicine differentiates between volume load and pressure load when judging
different types of exercise.
Volume load is when the heart muscle is working at a high heart rate (pulse frequency) but with only a
small rise in blood pressure.
Pressure load is when the heart muscle is working at a low heart rate but with a high blood pressure. For
this reason, types of exercise with a predominantly volume load are to be preferred.
Exercise with pure volume load are rated as optimal:

walking, speed-walking,
hiking, jogging,
ski tours, inline skating,
(all on the level).
Exercise with gentle pressure load, rated as very good:
walking, speed walking, hiking, jogging, ski tours, inline skating with slight differences in altitude,
ergometer training, cycling on the level, swimming, cross-country skiing, golf.
Exercise with moderate pressure load is rated as good:
cycling with moderate differences in altitude,
ski tours with moderate differences in altitude,
rowing tours, kayak tours, canoe tours (depending on water and current conditions),
dancing.

Exercise with moderate to intense pressure load rating are considered satisfactory:
skittles, 10-pin bowling,
tennis (depending on the strength of the opponent),
sailing (depending on the class of boat and wind strength),
volleyball, badminton, family tennis,
Alpine skiing,
mountain biking with large differences in altitude.
In all these types of exercise the load depends on the skill level of the participant.

Types of exercise with a high pressure load rating are considered bad:
power sports (weightlifting, power training with heavy weights),

squash, badminton at a competitive level,

wind-surfing,
football, handball.
Looking at the last two groups in detail, it is clear how difficult it can be to give a rating. The pressure
load, for instance, depends on how good one is at a certain sport.
There must always, therefore, be in-depth individual counselling with an experienced cardiological sports
instructor and a cardiologist.
Special case swimming and diving:
These two types of sport have been very controversial over the last 20 years for heart valve patients, the
reason being that in earlier investigations cardiac arrhythmias were observed above and below water.
Furthermore, blood moves from the legs to the abdomen and chest owing to the hydrostatic pressure,
causing the pressure in the lungs to rise slightly.
Nowadays we know that the aquatic milieu does not pose any risk to the heart muscle. Patients can train
according to the same criteria (heart rate) as on land.
In addition, it has been found that patients with restricted cardiac function and/or atrial fibrillation do not
tend to have increased cardiac arrythmias in water so that, as long as the training recommendations are
followed, swimming is allowed for anyone who enjoys the sport and can reach a swimming pool without
any difficulty.
The optimum water temperature is between 24 and 32C.
Diving without equipment (holding the breath under water with simultaneous additional workload) gives
rise to extremely high pressures in the lung combined with an oxygen deficit, as regular breathing in and
out is not possible. Staying under water for less than 20 seconds does not cause any problems.
The fitness studio
Time and again the question is raised concerning the medical value of power training in a fitness studio.
Basically, it can be said that power training in order to stabilize the muscle substance and joint function is
becoming increasingly important in medical rehabilitation. More recent investigations show that power
training has a very beneficial effect in helping with everyday workloads.
Its earlier rejection by cardiologists was due to the unpredictable and poorly measurable peaks of blood
pressure that occurred, which they suspected would damage the heart muscle. Following replacement
heart valve surgery, it was feared, there would be considerable pressure at the site where the valve was
attached to the aortic arch.
Investigations in the last 7 years have shown that moderate stamina training with weights of up to 50% of
the maximum performance of the relevant muscle group pose no risk. The problematic blood pressure
peaks occur at workloads of 65% to 80% of maximum muscle power, after more than 15 repetitions, or

with a workload duration of more than 20 seconds. Short-term maximum exertion for less than 4 seconds
is unproblematic, as measured on a power machine using a right-heart catheter.
Nowadays modern fitness studios offer very good, individually tailored exercise programs. Ask the studio
about staff qualifications and their seal of quality.
Spending time at altitude
Here are a few tips on spending time at altitude, whether for a longish vacation or to enjoy winter sports.
As altitude increases, so the oxygen pressure in respired air gradually decreases, meaning that the body
is able to absorb less oxygen with each breath. The body responds with faster breathing and an increase
of up to 20% in heart rate compared to the resting value. Consequently, your usual training pulse rate is
already reached with what would appear to be only a slight workload. A further negative effect is the
increasing viscosity of the blood as, at altitude, the body also loses more fluid via the respiratory system.
You must ensure that your liquid intake is adequate.
These changes only occur at more than 2000 metres, so that time spent at this altitude under a physical
workload (skiing, ski tours, mountain hiking or cycling) is unproblematic.
Altitude acclimatization takes approximately two to three days. Do not start your training program,
therefore, until you have been at that altitude for two days.
Spending time in tropical climates
Please note that in Mediterranean or tropical regions you should not undertake intense physical training
at a temperature of more than 28C and a humidity of more than 80%, as the body can no longer keep up
the necessary heat regulation.
Here again, the resting heart rate is already raised and the training heart rate reached much sooner than
expected.
Sauna/Turkish bath
There is no risk in using a sauna. In a sauna the heat causes the heart rate to rise sharply in order to
transport the blood to the periphery. There the heat is returned to the environment. The arterial blood
pressure drops slightly. However, avoid ice-cold dips. Take a cold shower instead.

5. Taking Exercise at the onset of cardiac insufficiency or limited pump function.

Calculating the optimum training intensity when there are secondary heart conditions (e.g. hypertension,
coronary heart disease) is in itself problematic. If, in addition, cardiac insufficiency or severely limited
pump function of the left heart is present, training targets must be redefined.
If the left ventricle is unable to pump enough blood into the vascular system to cope with the workload,
then the load must not be maintained for any length of time.

Patients with these conditions were for a long time considered to be untrainable and were excluded from
sporting activities.
In recent years a new training program aimed at maintaining muscle power has been developed for this
clinical picture. The term used is interval training, i.e. the workload must not be sustained for longer than
20 to 30 seconds, and a pause of 40 to 60 seconds must follow.
Interval training is best performed on an exercise bicycle. Pedal for 20 seconds and pause for 40
seconds, or pedal for 30 seconds and pause for 60 seconds.
The wattage depends on the cardiological diagnosis.
Training targets can also be achieved with small dumb-bells or other strength-building equipment.
Devising this type of training program is extremely complicated and should only be undertaken by
clinically experienced cardiological sports instructors.

6. Are there any differences between aortic and mitral valve patients?

The same principles are applied to both groups when the training program is being worked out. The same
test results used for the cardiological diagnosis are used for the training program, irrespective of whether
the replacement heart valve is a mechanical or biological one.
Long-term results indicate that aortic valve patients without any secondary conditions who have
undergone right-heart surgery achieve the best training effect. There is practically no limitation with
regard to the exercise workload and they can achieve very high levels of fitness.
Patients who have replacement mitral valves and atrial fibrillation do not notice any rise in performance in
the first few months, as the fibrillation stops the training program being intensified. The body needs much
longer for the heart muscle to heal.

7. Summary

Replacement heart valve patients can be trained at any phase following their operation. The program of
exercise therapy is much more variable than is the case with myocardial infarction and bypass patients.
With a good surgical outcome and the exclusion of other cardiological conditions, there is virtually no limit
to the physical workload that the body can cope with.
The prescribed program of exercise is governed by the cardiological diagnosis and should nevertheless
still be properly discussed with cardiological exercise therapists in the hospital or outpatient heart clinic.
Author: Uwe Schwan, Graduate Sports Instructor, Clinic Bad Hermansborn, Bad Driburg
(Germany)