Acquired Heart Dx

8/4/2019 Acquired Heart Dx

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Your heart has four chambers and four valves that regulate blood flow:

Anatomy Function

Left and right atriaChambers that receive blood returning from your body through your

veins

Left and right ventriclesChambers where blood is pumped to your body through your

arteries

Mitral valveThe mitral valve controls the flow of oxygen-rich blood from the left

atrium to the left ventricle

Tricuspid valve

The tricuspid valve controls the flow of oxygen-poor blood from the

right atrium to the right ventricle

Aortic valveThe aortic valve controls flow of oxygen-rich blood from the left

ventricle to the body

Pulmonary valveThe pulmonary valve controls flow of oxygen-poor blood from the

right ventricle to the lungs

The four heart valves can be grouped by their job:

Atrioventricular valves control blood flow between your heart's upper and lower chambers. The valve

between the right atrium and the right ventricle is called the tricuspid valve. The valve between the left

atrium and the left ventricle is called the mitral valve.

Semilunar valves control blood flow out of your heart. Blood flows out of the right ventricle to the lungs

through the pulmonary valve. Blood flows out of the left ventricle to your body through the aortic valve.


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Diagram shows heart during

systole (ventricles contracting)

The valve is made of strong, thin pieces or flaps of tissue called leaflets.

The leaflets are attached to and supported by a ring of tough fibrous tissue called the annulus. The annulus

helps to provide support and maintain the proper shape of the valve.

The valve leaflets can be compared to doors opening and closing. While the annulus functions as the door

frame.

The leaflets of the mitral and tricuspid valve are also supported by tough, fibrous strings called chordae

tendineae. These are similar to the strings supporting a parachute. The chordae tendineae extend from the

valve leaflets to small muscles, called papillary muscles, which are part of the inside walls of the ventricles.

The chordae tendineae and papillary muscles keep the leaflets stable against any backward flow of blood.

How Valves WorkThe right and left sides of the heart work together to pump blood throughout the whole body. The four heart

valves make sure that blood always flows freely in a forward direction and that there is no backward leakage.

1. Blood flows from your right and left atria into your ventricles through the open mitral and tricuspid valves.


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2. When the ventricles are full, the mitral and tricuspid valves shut. This prevents blood from flowing

backward into the atria while the ventricles contract (squeeze).

3. As the ventricles begin to contract, the pulmonic and aortic valves are forced open and blood is pumped out

of the ventricles through the open valves into the pulmonary artery toward the lungs, and the aorta, to the

body.

4. When the ventricles finish contracting and begin to relax, the aortic and pulmonic valves snap shut. These

valves prevent blood from flowing back into the ventricles.

This pattern is repeated, causing blood to flow continuously to the heart, lungs and body.

What is heart valve disease?Valvular heart disease occurs when your heart's valves do not work correctly. Valvular heart disease can be

caused by valvular stenosis or valvular insufficiency.

In the valvular heart disease condition valvular stenosis , the tissues forming the valve leaflets become

stiffer, narrowing the valve opening and reducing the amount of blood that can flow through it. If the

narrowing is mild, the overall functioning of the heart may not be reduced. However, the valve can become


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so narrow (stenotic) that heart function is reduced, and the rest of the body may not receive adequate blood

flow.

Another valvular heart disease condition, called valvular insufficiency (or regurgitation, incompetence, "leaky

valve"), occurs when the leaflets do not close completely, letting blood leak backward across the valve. This

backward flow is referred to as regurgitant flow.

Stenotic Valve Regurgitant Valve

A narrowed or stenotic valve requires the heart to pump harder, which can strain the heart and reduce blood

flow to the body. A regurgitant (incompetent, insufficient, or leaky) valve does not close completely, letting

blood move backward through the valve.

Some patients may have both valvular stenosis and valvular insufficiency in one or more valves. Valve disease

causes the heart muscle to work harder to circulate the right amount of blood through the body.

What causes heart valve disease?

There are many types of valve disease. Valve disease can becongenital(present at birth) or may

be acquired later in life. Sometimes the cause of valve disease may be unknown.

Congenital valve diseaseis an abnormality that develops before birth. It may be related to improper valve

size, malformed leaflets, or an irregularity in the way the leaflets are attached. This most often affects the

aortic or pulmonic valve.

Bicuspid aortic valve disease is a congenital valve disease that affects the aortic valve. Instead of the normal

three leaflets or cusps, the bicuspid aortic valve has only two. Without the third leaflet, the valve may be:

stenotic - stiff valve leaflets that can not open or close properly leaky - not able close tightly

Normal aortic valve Bicuspid aortic valve
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This occurs more frequently in some family members. About 1/4 of patients may have some enlargement of

the aorta above the valve. Bicuspid aortic valve disease affects about 2 percent of the population.

Acquired valve disease includes problems that develop with valves that were once normal. These mayinvolve changes in the structure of your valve or infection.

Infection

Infective endocarditis and rheumatic fever are the two common infections that cause valve disease.

Rheumatic heart disease

Rheumatic fever

Rheumatic fever causes a common type of valve disease, rheumatic heart disease

It causes:

the heart valve leaflets to become inflamed may cause the leaflets to stick together and become scarred, rigid, thickened and shortened may cause one or more of the valves (most commonly the mitral valve) to become stenotic

(narrowed) or leaky

Rheumatic fever is usually caused by an untreated streptococcal infection, such as strep throat. The use of

penicillin to treat strep throat can prevent this disease. Rheumatic fever occurs most often in children aged

five to fifteen, but symptoms of valve disease may not be seen for years. The valve itself is not infected in

rheumatic fever. Antibodies developed by the body to fight the infection react with the heart valves, causing

inflammation and eventual scarring.

EndocarditisEndocarditis is a major infection and can be life-threatening. It occurs when germs (especially bacteria) enter

your blood stream and attach to the surface of your heart valves. With endocarditis:


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Endocarditis

germs attack the heart valve, causing growths on the valve, holes in the valve or scarring of the valvetissue

may cause the valve to leak or become stenotic (narrowed)The germs can enter your blood stream during:

dental procedures surgery intravenous (IV) drug use severe infections

If you have valve disease (unless you have mild forms of mitral valve prolapse) or have had valve surgery, you

are at increased risk for getting this life-threatening infection.Learn More.

Other causes of valve disease include:

coronary artery disease heart attacks cardiomyopathy(heart muscle disease) syphilis hypertension aortic aneurysms connective tissue diseases and less commonly, tumors some types of drugs and radiation
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Stretching or tearing of chordae tendineae or papillary muscles

Changes in your valve structure can occur due to both acquired and congenital causes:

Stretching or Tearing of Chordae Tendineae or Papillary MusclesStretching or tearing of chordae tendineae or papillary muscles most commonly occurs to the mitral valve.

This can be a result of:

heart attack heart valve infection trauma

If the chordae become torn or papillary muscles become stretched, the leaflets may flop backward when the

ventricles contract (flail leaflet), causing a leaky valve.

Mitral Valve Prolapse (MVP)

Mitral valve prolapse (MVP) is a type of myxomatous valve disease. MVP causes the leaflets of the mitralvalve to flop back into the left atrium during the heart's contraction. MVP also causes the tissues of the valve

to become abnormal and stretchy, causing the valve to leak.

Normal mitral valve Mitral valve prolapse


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MVP occurs in about 1 to 2 percent of the population and equally in men and women. Most often it is not a

cause for concern. Only 1 in 10 patients with MVP eventually require surgery. If the prolapse becomes severe

or is associated with torn chordae or flail (floppy, lacking support) leaflets, the leak may be greater, and

surgery may be needed.

All patients with MVP should ask their doctor if they require measures to preventendocarditis.

Fibro-calcific Degeneration

Fibro-calcific degeneration most commonly affects the aortic valve. It most often occurs in adults over the

age of 65. This condition can be compared to atheroma in coronary artery disease. The valve leaflets become

fibrotic (thickened) and calcified (hardened), producing a narrowed valve opening. Risk factors for this type of

valve disease include:

increased age low body weight

high blood pressure

Dilation of the Valve Annulus

Dilatation of the valve annulus is a widening or stretching of the annulus. This causes the leaflets to lack

support and not close tightly.

Dilatation may occur when the heart muscle is damaged due to:

a heart attack (heart muscle injury) cardiomyopathy (weakened heart muscle) heart failure advanced stages of high blood pressure syphilis inherited disorders (such as Marfan syndrome)

Dilatation of the valve annulus causes the valve to leak
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MITRAL REGURGITATION

Mitral valve prolapse is a disorder in which,

during the contraction phase of the heart, the

mitral valve does not close properly. When the

valve does not close properly it allows blood to

backflow into the left atrium. Some symptoms

can include palpitations, chest pain, difficulty

breathing after exertion, fatigue, cough, and

shortness of breath while lying down.

The mitral valve separates the left atrium from the left ventricle. It should be considered as the sum of its

three components: the leaflets, the annulus to which the leaflets attach, and the subvalvar apparatus,consisting of the cords and papillary muscles. The mitral valve has two leaflets, anterior and posterior \The

anterior leaflet is larger in surface area, but its attachment to the annulus represents only one third of the

circumference. The anterior portion of the mitral valve annulus is in direct continuity with the annulus of the

left and noncoronary cusps of the aortic valve, also known as the aortomitral continuity. The posterior leaflet

is shorter, but its annular attachments cover two thirds of the circumference. The posterior leaflet often can

be separated into three distinct scallops, although the prominence of these separations varies among

individuals. The anterior and posterior leaflets are separated from each other by the anterolateral and

posteromedial commissures, which mark the location of the right and left fibrous trigones respectively. The

trigones are dense collagenous structures within the annulus representing a portion of the fibrous skeleton of

the heart. The mitral annulus is elliptical in shape, and its dimensions change dynamically during cardiac

contraction, reducing its cross-sectional area by as much as 40%. The anterolateral and posteromedial

papillary muscles are vertically oriented bundles of cardiac myocytes. Chordae tendineae originate from theheads of the papillary muscles and span the distance to both the anterior and posterior mitral valve leaflets.

Chords are designated as primary if they attach to the leading edge of the leaflet, secondary if they attach to

the ventricular surface of the leaflets, or tertiary if they attach to the ventricular surface of the mitral

annulus. The chords play an important role in preventing leaflet prolapse. The posteromedial papillary muscle

is prone to ischemic injury, since it relies on a single right coronary artery for circulation. In contrast, the

anterolateral papillary muscle gains its blood supply from the LAD and circumflex branches and tends to be

more resistant to ischemic injury.

Classification of Mitral Regurgitation

Table 192. Carpentier Classification of Mitral Regurgitation.

I Normal leaflet motion

Annular dilation, leaflet perforation

II Excessive leaflet motion

Prolapsed or myxomatous leaflet, ruptured chord

III Restricted leaflet motion

Rheumatic disease, ischemic mitral regurgitation


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Mitral regurgitation is always pathologic but can be tolerated surprisingly well when the onset is gradual,

allowing for a series of physiologic adaptations. On the other hand, acute mitral regurgitation, as can be

associated with infective endocarditis or ischemic papillary muscle rupture, results in immediate pulmonary

congestion because the unprepared left atrium is incapable of handling the additional volume load. Several

compensatory mechanisms occur as mitral regurgitation develops and progressively worsens. The left atrium

and pulmonary venous system gradually dilates, thus increasing compliance to better accommodate the

excess volume. The backwards flow of mitral regurgitation reduces ventricular afterload, reducing myocardial

wall tension. The reduction in forward flow is accounted for by increased diastolic filling, increasing preload.

This maintains cardiac output and can delay onset of symptoms for significant time. Gradually, left ventricular

end diastolic volume continues to rise, resulting in pathologic remodeling, creating a dilated and more

spherical ventricular cavity. Systolic function is progressively and inexorably impaired as a result of both

mechanical considerations owing to the altered shape and molecular mechanisms both intracellular and

extracellular. A vicious cycle ensues, with deteriorating systolic function and rising end diastolic volume

promoting further ventricular remodeling and dilation and worsening mitral regurgitation. Longstanding

mitral regurgitation will result in sustained elevation in left atrial pressure and volume, resulting in pulmonary

vascular changes, pulmonary hypertension, and eventually, right ventricular dysfunction.

Symptoms

Acute mitral regurgitation is poorly tolerated and is typically associated with pulmonary congestion and low

cardiac output. Patients describe dyspnea, poor exercise tolerance, and fatigue. Often, the etiology of the

mitral regurgitation is more dominant in the clinical presentation. Patients with acute endocarditis patients

may have fever, shaking chills, and manifestations of septic embolization such as stroke and intestinal or

extremity ischemia. Patients suffering from acute myocardial infarction with a ruptured papillary muscle

complain of chest pain and diaphoresis.

Chronic mitral regurgitation can be asymptomatic for many years as a result of progressive atrial and

ventricular adaptation. Eventually, patients develop symptoms of heart failure, including dyspnea, fatigue,

and lower extremity edema. When left atrial dilation results in atrial fibrillation, patients may describe heart

palpitations. Often, the onset of atrial fibrillation is the initial presentation of symptoms, as rapid ventricularresponse decreases diastolic filling time and creates a sudden reduction in cardiac output. As ventricular

function deteriorates and pulmonary vascular changes occur, signs of right sided heart failure develop, such

as lower extremity edema and ascites.

Diagnostic Testing

1. Thephysical findings of mitral regurgitation vary depending on the duration and the degree ofcompensation. For patients with longstanding mitral regurgitation, ventricular dilation displaces the

point of maximal impulse (PMI) laterally. On auscultation, an S3 gallop is often heard, resulting from

increased diastolic flow. The systolic murmur is characteristically described as blowing, best heard

over the cardiac apex and radiating to the axilla. In acute mitral regurgitation, the murmur tends to

be limited to early in systole. With more chronicity, the murmur is progressively holosystolic.

2. The chest radiograph often demonstrates cardiomegaly from ventricular dilation. With severeuncompensated heart failure, pulmonary edema may be evident; however, this is more commonlyseen with acute mitral regurgitation. The electrocardiogram is often nonspecific but may

demonstrate evidence of previous myocardial infarction and will confirm the presence of atrial

fibrillation.

3. Echocardiographyis the mainstay in the diagnosis of mitral regurgitation; it provides informationabout the mechanism of the disease, which is essential in planning surgical intervention. Images of

the leaflets can determine if the leaflet motion is normal, restricted, or excessive. Information about

annular size and mobility can be obtained. Using color, the size and direction of the regurgitant jet


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can quantify the severity and give clues as to the mechanism. The severity of the regurgitation is

determined by the width and length of the regurgitant jet or the presence of reversed flow within

the pulmonary veins. Echocardiography also provides information about the chronicity of the disease

and can document progressive adaptation such as left atrial and ventricular dilation. This information

is often used in determining timing of surgical intervention, particularly in asymptomatic patients.

Echocardiography is usually performed transthoracic. However, in some patients, the views are

obscured by body habitus or emphysema, limiting the image quality. Transesophagealechocardiography (TEE) can improve the resolution of images and better clarify the severity and

mechanism of the mitral valve pathology.

4. Cardiac catheterization is an important adjunctive tool, helping to identify additional cardiacpathology, and can determine the adequacy of preoperative medical optimization. Coronary

angiography is performed preoperatively to identify coronary arterial occlusive lesions that may

require bypass grafting at the time of mitral valve repair or replacement. Although contrast

ventriculography can demonstrate the regurgitant jet, it is no longer necessarily used to quantify the

regurgitant volume, since echocardiography has become the standard technique. Right heart

catheterization will demonstrate intravascular volume overload and low cardiac output. It may also

be helpful in diagnosing pulmonary vascular changes in patients who deny symptoms.

Management

Management strategy for patients with chronic severe mitral regurgitation. *Mitral valve (MV) repair may be

performed in asymptomatic patients with normal left ventricular (LV) function if performed by an experienced


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surgical team and if the likelihood of successful MV repair is >90%. AF, atrial fibrillation; Echo, echocardiography;

EF, ejection fraction; ESD, end-systolic dimension; eval, evaluation; HT, hypertension; MVR, mitral valve

replacement. (From Bonow et al.)

Surgical Treatment

Indications

The indications for operation on the mitral valve depend on the specific pathology as well as clinicalsymptoms. In addition, the indications have evolved in recent years owing to improved outcomes related to

better surgical techniques, anesthetic considerations, myocardial protection, and postoperative care.

Furthermore, intervention on the mitral valve may be performed for less severe disease if operation is

indicated for coronary artery disease or aortic valve pathology.

Certainly, among patients who represent reasonable operative risks, those with severe mitral regurgitation

and heart failure symptoms should be offered an operation. In addition, those with severe mitral

regurgitation and signs of left ventricular dysfunction should undergo operation because myocardial

decompensation can progress rapidly without corrective action. There is insufficient evidence that operative

intervention for asymptomatic severe mitral regurgitation and normal ventricular function improves survival.

Historically, these patients were observed with close clinical follow-up and serial echocardiography. Signs of

left ventricular dilation, dysfunction, or new-onset symptoms prompted surgical referral. Some have arguedthat the presence of pulmonary hypertension should indicate maladaptive changes and suggests surgical

correction.

Surgical indications for operation in endocarditis of the mitral valve are different than for other pathologies.

Certainly, valvular destruction with severe mitral regurgitation, heart failure, and ventricular dilation requires

operative intervention. However, there are other specific indications for valve replacement. A history of

systemic embolization or the presence of large, highly mobile vegetations at risk of embolization necessitates

urgent surgical intervention. In addition, ongoing bacteremia despite appropriate antibiotic treatment

coverage mandates early operation. The presence of certain organisms, such as highly resistant bacteria or

fungal endocarditis warrants surgical treatment. Surgery is required for the presence of mitral annular

abscess with incipient cardiac conduction abnormalities or creation of an intracardiac fistula. Prior to surgery,

attempts at controlling the original source of infection should be made, including dental extractions and

drainage of abscesses.

Techniques

Approach to the mitral valve is best accomplished via a median sternotomy. Although the mitral valve can be

exposed via a right or left thoracotomy, the median sternotomy offers the best access for initiation of CPB as

well as the ability to perform other cardiac procedures if necessary, such as coronary bypass grafting or aortic

valve replacement. CPB is initiated, typically draining the superior and inferior vena cavae separately, and

infusing into the ascending aorta. The heart is arrested using cold cardioplegia delivered into the aortic root.

The left ventricle is vented, typically using the right superior pulmonary vein.


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A variety of incisions can be used to expose the mitral valve, and the quality of exposure is essential inobtaining a good surgical result. The most frequent approach is by an incision directly into the left atrium.

The interatrial groove of Sondergaard can be developed using sharp technique, lifting the right atrium

anteriorly off of the left atrium. A vertical incision is made in the left atrium, just medial to the confluence of

the right-sided pulmonary veins. Self-retaining retractors are available to elevate the atriotomy and provide

visualization. Often, rotation of the table to the left away from the surgeon improves the exposure.

Alternatively, an approach across the interatrial septum can be chosen. The superior and inferior vena cavae

are controlled with snares, and the right atrium is opened. The fossa ovalis is identified and incised vertically.

This incision is extended superiorly toward the superior vena cava through the muscular portion of the

interatrial septum. The septal incision can also be extended medially along the dome of the left atrium, the

so-called superior septal approach.

Once the valve has been exposed, assessment of the mitral valve is performed to determine the mechanismof mitral regurgitation and the technique for repair or replacement. Injection of cold saline into the left

ventricle will identify the location of regurgitation and the presence of flail or significantly prolapsed leaflets.

The leaflets are inspected for their mobility and the presence of calcifications or perforations. The annulus is

inspected for dilation and calcium. Once the mechanism of regurgitation is clear, a plan is made for repair or

replacement. The strategy used depends on the pathologic mechanism.

When the mitral regurgitation is purely a result of annular dilation or posterior leaflet restriction from a

previous myocardial infarction, mitral annuloplasty alone often adequately alleviates the leak. Horizontal


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sutures are placed along the mitral annulus, including the fibrous trigones. Care must be taken to avoid injury

to underlying structures, such as the circumflex coronary artery, the coronary sinus, and the atrioventricular

node. Annuloplasty is typically performed with the assistance of prosthetic rings or bands of varying degrees

of rigidity. Some of the rings completely encircle the entire annulus, and some are incomplete, designed to

extend posteriorly from trigone to trigone (Figure 199). The annular mattress sutures are brought up

through the sewing cuff of the ring and tied down. The size of the ring is selected to match the area of the

anterior leaflet and the distance between the trigones. Competence is tested with saline injection, and thecardiac chambers are closed. After weaning from CPB, the valve is inspected using transesophageal

echocardiography. An adequate repair must demonstrate both competence and low resistance, as evidenced

by low pressure gradients across the valve.

Myxomatous degeneration of the mitral valve typically involves the posterior leaflet, particularly the P2

scallop. This lesion can be reproducibly repaired using techniques with the potential for indefinite durability.

After exposure of the mitral valve, the point of prolapse is identified. A quadrangular portion of the

prolapsing section is excised to the annulus. The gap is bridged by undercutting the annular attachments of

the adjacent portion of the posterior leaflet. The mobilized edge of the posterior leaflet is sewn back to the

annulus with running suture (Figure 1910), reducing its effective height. An annuloplasty can be performed

to address any annular dilation as well as to provide reinforcement to the posterior annular reconstruction.

.Quadrangular resection

Probably the most common situation seen in mitral regurgitation secondary to myxomatous degeneration is

prolapse of the middle scallop of the posterior leaflet. This may result from chordal rupture or chordal

elongation. Quadrangular resection of the involved middle scallop of the posterior leaflet combined with a

posterior mitral annuloplasty is the best way to handle this situation (Figure 7,8).


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This quadrangular resection is accomplished by first locating the margins of the involved portion where the

chordae are of normal length and structure. A heavy silk tie is passed around these chords to identify and

gently retract the section of the posterior leaflet that is not going to be excised. The involved or prolapsed

segment is then excised. Advancement flaps are generally then created by cutting along the annulus of

remaining posterior leaflet. This creates a sliding plasty of the posterior annulus. The annulus may then beselectively plicated at areas of severe dilatation. Ring annuloplasty sutures are then placed along the

posterior annulus. The posterior leaflet is then reconstructed. First, the free edges along the margin of

coaptation are identified. A 5-0 polypropylene suture is used to reapproximates these two points. From here,

the same suture is run along the body of the leaflet halves back towards the base in a two-layer fashion. The

two ends of the suture are then placed through the plicated posterior annulus. The same suture, again, is

used to attach the leaflet to the posterior annulus in running two-layer stitch.


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Chordae Tendinae repair

SHORTENING: We discourage the use of chordal shortening techniques in which a trench is created in the

papillary muscle a segment of the elongated chord is buried within the muscle. There are two alternative

approaches that we believe are significantly more reliable.

REPLACEMENT: Polytetrafluoroethylene (Gore-Tex) CV-5 can be used to create chordae tendinae in

circumstances of elongated or broken chords or when additional chords are required to support the free

edge of a leaflet after repair techniques are employed. In particular, when removing a large segment of the

posterior leaflet, the remaining chordae form acute angles after sliding annuloplasty (Figures 8 and 9,Movie

Clip 5).

CV-5 suture is used to create new chords at the central portion of the posterior leaflet. These chords are

constructed by passing one of the needles on a double-armed suture twice through the tendinous portion of

the papillary muscle that is closest to the free margin of the desired leaflet. Several knots are placed in the

suture and then each arm of the suture is passed through the free edge of the leaflet twice. These are placed

from the ventricular surface to the atrial side. The sutures are then tied with the knot on the leaflet surface

so that the Gore-Tex is the same length as the normal reference chordae.

TRANSFER: If a medial or paramedial chord is torn or elongated from the anterior leaflet, a corresponding

opposing chord from the posterior leaflet is transferred to the anterior leaflet and the defect in the posterior

leaflet closed.Chordae of proper length are borrowed from the posterior leaflet and are transposed to theanterior leaflet. The affected chord is excised close to the anterior leaflet contact area. The body of the

anterior leaflet is undisturbed. The chosen chords from the posterior leaflet are left attached and a square

piece of the leaflet is cut out (Figure 10.)
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This cutout is then flipped over onto the anterior leaflet so that the two atrial surfaces of the valve leaflets

are opposed. A running 5-0 polypropylene suture is then used to approximate these surfaces (Figure 11.)

For the posterior leaflet, a focal annuloplasty is performed and the leaflet defect repaired with a running 5-0

polypropylene suture as well.

Valve transplantation

Often, the regurgitant mitral valve cannot be repaired, such as when there is severe valvular destruction from

infective endocarditis or extensive calcifications as can be seen with rheumatic mitral valve disease. The

mitral valve is exposed, and the leaflets are excised. Attempts are made to preserve chordal attachments to

the annulus, and portions of the posterior leaflet can be plicated to the annulus to preserve secondary

chords. This is typically not possible with rheumatic disease because the calcified annulus will require

extensive debridement. Annular mattress sutures with felt or Teflon pledgets are placed circumferentially.

For mechanical prostheses, the pledgets are oriented on the atrial side to avoid interference with theactuation of the disk. For bioprosthetic implants, the pledgets can be placed on the ventricular side, which

allows for a slightly larger prosthetic (Figure 1911). After sutures are placed, the annulus is sized and an

appropriate prosthetic is chosen. The sutures are driven through the sewing ring of the valve and tied down.

After weaning from CPB, the valve is carefully inspected using transesophageal echocardiography for signs of

paravalvular leak, normal motion of the leaflets or disks, and a low pressure gradient across the valve.


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Annuloplasty Ring Tissue Valve Mechanical Valve

Results

Repair or replacement of the mitral valve for regurgitation preserves ventricular function and allows some

remodeling by eliminating the volume overload and its associated incipient changes. However, loss of

myocardial contractility, as a result of longstanding mitral regurgitation or otherwise, typically does not

recover. Only its progressive decline can be halted. This reinforces the need to intervene before severe

ventricular dilation has occurred, even in asymptomatic patients.

Mitral regurgitation associated with prolapsing myxomatous leaflets carries low perioperative mortality, and

the freedom from degeneration of a repaired valve is greater than 90% at 10 years. Some of the low

periprocedural mortality is related to the young age and low incidence of comorbidities in this patient

population. Mitral valve repair associated with coronary bypass grafting carries a perioperative mortality of

approximately 5%, with ejection fraction, renal function, and age being independent predictors of death.

Although mortality after coronary bypass grafting is associated with the severity of preoperative mitral

regurgitation, there is no evidence that mitral repair reduces this mortality. Repairing the mitral valve,

however, is associated with improved long-term survival, as compared to replacing the valve.

Table 3 Mortality Rates after Valve Surgerya

Operation Number Operative Mortality (%)

AVR (isolated) 12,501 2.8

MVR (isolated) 3788 5.3

AVR + CAB 12,748 5.2


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MVR + CAB 2683 10.3

AVR + MVR 1018 8.8

MVP 3982 1.0

MVP + CAB 4293 7.0

TV surgery 4358 9.6

PV surgery 432 5.2aData are for calendar year 2004, in which 594 sites reported a total of 232,050 procedures. Data are

available from the Society of Thoracic Surgeons

athttp://www.sts.org/sections/stsnationaldatabase/publications/executive/article.html.

MITRAL STENOSIS

The characteristic features of rheumatic mitral valve disease include leaflet and chordal thickening and

retraction (Figure 1912). Commissural fusion is also apparent, and a late feature is dense calcification of the

annulus and leaflets. Turbulence created by impaired leaflet mobility exacerbates the valve destruction,

accelerating further fibrosis and calcification.

Mitral valve stenosis can also be caused by mitral annular calcification, which can become quite bulky,

protruding into the valve orifice. The posterior leaflet can become contracted and fixed, while the anterior

leaflet thickens and becomes less mobile. Structural valvular degeneration of bioprosthetic mitral valves can

cause mitral valve stenosis as well as thrombosis or pannus formation in mechanical prostheses. Advanced

endocarditis can result in effective mitral valve stenosis, as bulky vegetations obstruct the inflow path.

Congenital abnormalities, such as the parachute mitral valve with a single papillary muscle, can become

stenotic, requiring intervention.

The stenotic mitral valve results in a pressure gradient between the left atrium and ventricle. This fixed

resistance increases the left atrial pressure even further during exercise, as cardiac output increases, but

resistance across the valve is unchanged. Severe mitral valve stenosis is associated with a mean transvalvular

gradient of 1015 mm Hg at rest. Cardiac output is dependent on ventricular filling, and left ventricular end

diastolic pressure and volume are typically low. Exercise-induced tachycardia decreases diastolic filling time,

producing a paradoxical reduction in cardiac output. Left ventricular function is typically normal or
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hyperdynamic, but some patients have combined mitral valve stenosis and mitral regurgitation, as well as

significant aortic valve insufficiency, and will develop chronic left ventricular volume overload and

dysfunction. Thus, the hemodynamic consequences of mitral valve stenosis depend to a certain degree on

the presence of mitral regurgitation and other associated valvular pathology.

As the mitral transvalvular gradient worsens, the left atrial wall hypertrophies. The a-wave on the atrial

pressure tracing is accentuated during atrial contraction. Progressively, the left atrium dilates, creating

disorganized electrical conduction pathways. Reentry pathways lead to frequent premature atrial

contractions and eventually to atrial fibrillation. The onset of atrial fibrillation often is the inciting clinical

event, with the reduced diastolic filling time from rapid ventricular response and the loss of atrial contraction

both resulting in reduced left ventricular filling and a drop in cardiac output. The sustained elevation in left

atrial pressure results in pulmonary vascular changes producing pulmonary hypertension. These changes can

lead to right ventricular pressure overload with tricuspid valve insufficiency and to right ventricular volume

overload.

Symptoms

Symptoms of mitral valve stenosis often do not develop until the disease is advanced, owing to ventricularand atrial adaptive responses. Patients describe dyspnea from pulmonary congestion or reduced cardiac

output, initially limited to exertion. Onset of atrial fibrillation often prompts urgent evaluation, as the loss of

atrial contraction and tachycardia cause a precipitous drop in cardiac output and pulmonary congestion. Late

findings include signs of right-sided heart failure such as ascites and lower extremity edema. Cerebrovascular

events or other thromboembolic complications from an intracardiac thrombus are not uncommon with

longstanding mitral valve stenosis, as the dilated left atrium and left atrial appendage have regions of

stagnation and thrombus formation, particularly in the setting of atrial fibrillation. Since two thirds of the

patients with mitral valve stenosis are women, symptoms often present during later stages of pregnancy as

the increased cardiac output results in higher left atrial pressures and pulmonary congestion.

Diagnostic Evaluation

1. Becausepresentation tends to be late, many patients present with signs of longstanding heartfailure, including cachexia, ascites, and lower extremity edema. On auscultation, the low diastolic

rumble is best heard over the cardiac apex. An opening snap can be heard in the early stages of the

disease, and the systolic murmur of tricuspid regurgitation is a late finding, as is a parasternal heave

from right ventricular hypertrophy.

2. The electrocardiogram will diagnose atrial fibrillation, and right axis deviation may be present,suggesting advanced pulmonary hypertension. Otherwise, the electrocardiogram can be nonspecific

or normal. The chest radiograph is often normal but may demonstrate straightening of the left heart

border caused by dilation of the pulmonary arteries. Pulmonary edema may be present on initial


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evaluation when atrial fibrillation is the inciting event. Cardiac catheterization is important in

identifying associated coronary arterial pathology and can confirm the severity of the mitral stenosis

using simultaneous left and right heart catheterization with pressure measurements. The degree of

pulmonary hypertension and its reversibility with provocative agents may be assistive in determining

surgical candidacy in advanced cases.

3. Echocardiographyis the mainstay in diagnosis of mitral valve stenosis. Surface, or transthoracicechocardiography is preferred because it is noninvasive, and can usually provide imagesdemonstrating the characteristic thickening and restricted mobility of the mitral leaflets. If images

are obscured by patient body habitus or obstructive lung disease, a transesophageal echocardiogram

can be performed. The proximity of the esophagus with the left atrium provides excellent

visualization and can easily demonstrate the thickened mitral subvalvar apparatus typical of

rheumatic disease. Color Doppler can be used to show turbulent flow across the valve orifice, and

the pressure gradients can be estimated by measuring the peak and mean velocity of blood through

the valve.

Treatment

Medical treatment is limited to control of symptoms. Recurrent episodes of infection must be prevented, as

accelerated progression of the disease can be seen. Prompt initiation of antibiotics for suspected infections is

prudent. Complications of mitral valve stenosis should be addressed and controlled. Rapid ventricular

response to atrial fibrillation can be treated with a number of pharmacologic agents, and attempts at

cardioversion should be made once the presence of intracardiac thrombus has been excluded. It is often

difficult to maintain sinus rhythm in the mitral valve stenosis patient with a significantly dilated left atrium in

whom rate control alone may be acceptable. Systemic anticoagulation with warfarin should be initiated if

there has been a history of atrial fibrillation. Once the patient describes symptoms of heart failure,

intervention on the mitral valve should be considered. For symptomatic patients not candidates for catheter-

based or surgical intervention, diuretics and oral sodium restriction to control heart failure symptoms is all

that is available.

Table 2 Medical Therapy of Valvular Heart Disease

Lesion Symptom Control Natural History

Mitral stenosis Beta blockers, nondihydropyridine calcium channel

blockers, or digoxin for rate control of AF; cardioversion

for new-onset AF and HF; diuretics for HF

Warfarin for AF or

thromboembolism; PCN for RF

prophylaxis

Mitral

regurgitation

Diuretics for HF Warfarin for AF or

thromboembolism

Vasodilators for acute MR Vasodilators for HTN

Aortic stenosis Diuretics for HF No proven therapy

Aortic

regurgitation

Diuretics and vasodilators for HF Vasodilators for HTN

Note: Antibiotic prophylaxis is recommended according to current American Heart Association guidelines.

For patients with these forms of valvular heart disease, prophylaxis is indicated for a prior history of

endocarditis. HF is an indication for surgical or percutaneous treatment, and the recommendations here

pertain to short-term therapy prior to definitive correction of the valve lesion. For patients whose

comorbidities prohibit surgery, the medical therapies listed can be continued according to available

guidelines for the management of HF. See text.


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Management strategy for patients with mitral stenosis (MS) and mild symptoms. There is controversy as to

whether patients with severe MS (MVA 2) and severe pulmonary hypertension(PH) (PASP >60 mmHg)

should undergo percutaneous mitral balloon valvotomy (PMBV) or mitral valve replacement (MVR) to

prevent right ventricular failure. CXR, chest x-ray; ECG, electrocardiogram; echo, echocardiography; LA, left

atrial; MR, mitral regurgitation; MVA, mitral valve area; MVG, mean mitral valve pressure gradient; NYHA,

New York Heart Association; PASP, pulmonary artery systolic pressure; PAWP, pulmonary artery wedge

pressure; 2D, 2-dimensional. (From Bonow et al.)


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Catheter-based balloon mitral valvotomycan reduce the obstructing pressure gradient and improve

symptoms in selected patients. Patients with severe mitral valve stenosis and symptoms and asymptomatic

patients with severe mitral valve stenosis and pulmonary hypertension are eligible if there is no mitral

regurgitation, no left atrial thrombus, and favorable valve morphology, such as absence of extensive

subvalvular fibrosis and calcification. The procedure is performed by femoral venous puncture and transeptal

access to the mitral valve across the interatrial septum. A 25-mm hourglass Inoue balloon is advanced across

the valve orifice and inflated. Significant improvement in hemodynamics is seen immediately, with reduction

in transvalvular pressure gradients by as much as 15 mm Hg. The incidence of restenosis in selected patients

is approximately 25% at 4 years.

Indications for surgical treatment are the same as for balloon valvuloplasty, including symptomatic patients

with moderate or severe mitral valve stenosis and asymptomatic patients with pulmonary hypertension.

Valve repair can be performed in carefully selected patients with reasonable long-term results. CPB is

initiated in the same manner as for mitral repair for mitral regurgitation. After cardioplegic arrest, the mitral

valve is exposed. Any thrombus within the atrium or atrial appendage is removed. The left atrial appendage

can be transected and oversewn at its base to remove its future embolic potential. The areas of commissural

fusion are cut, and the leaflets are decalcified. Occasionally, fused chords are divided to increase leaflet

mobility. In carefully selected patients, recurrent mitral valve stenosis is less than 20% in up to 15 years.

Open Commissurotomy

This perhaps may be the best-known technique of mitral reconstruction. With rheumatic valvular disease,


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mitral stenosis is caused by restricted leaflet mobility. Partial fusion of the commissures with a well-defined

border between the anterior and posterior leaflets is ideal (Figure 6).

If there is no delineation between the anterior and posterior leaflets or the subvalvular apparatus is fused to

the leaflets, there is little long-term success and the valve should be replaced. Of note, in this circumstance,

we find that there is little benefit to saving this abnormal subvalvular apparatus during valve replacement.

The repair technique requires continued observance of the chordal support mechanism. With traction

applied to the major chords of the anterior leaflet near the commisure, a furrow or dimple is created where

the leaflets should be incised and separated. This is usually carried out with a No. 15 blade and extends themitral orifice to within 2mm to 3 mm of the annulus.

In most cases, however, severe leaflet and subvalvular calcification has made the valve unreconstructable,

requiring valve replacement. Overaggressive debridement of the posterior mitral annulus can result in

perforation and atrioventricular separation and should be avoided. The selection of valve prosthetic depends

on the unique clinical circumstances. Bioprosthetic valves are minimally thrombogenic and do not require


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lifelong anticoagulation with warfarin. However, they are prone to structural valvular degeneration resulting

in recurrent mitral valve stenosis or mitral regurgitation. Valve prosthetics are improving, and freedom from

structural valvular degeneration is as high as 85% at 10 years. Mechanical valves are thrombogenic and

require lifelong anticoagulation, such as warfarin, which is associated with a 12% annual incidence of major

bleeding complications. They are more durable and reduce the need for reoperation. In general, patients

younger than 60 years of age or those already requiring warfarin for atrial fibrillation should be considered

for a mechanical valve.

Aortic Valve Disease

The aortic valve separates the outflow tract of the left ventricle with the ascending aorta. It is a trileaflet

structure, with three semilunar cusps named for the coronary arteries that arise within the underlying

sinuses. The left and right coronary arteries originate within these respective sinuses, with no coronary artery

arising within the noncoronary sinus. The free edges of the cusps are thickened at regions called the nodules

of Arantius. The valve leaflets attach to the wall of the aorta at the annulus, and the locations where two

adjacent cusps meet are the commissures. Important structures can be identified under these triangular-

shaped zones (Figure 1913). The commissure between the right and noncoronary cusp serves as the

superior border to the membranous interventricular septum and the atrioventricular conduction center. The

nonleft commissure guards the aortomitral curtain and the center of the anterior leaflet of the mitral valve.

The left-right commissure overlies the muscular interventricular septum and the medial border of the right

ventricular outflow tract. These intimate intracardiac relationships are no more apparent than within the left

ventricular outflow tract.

The thin-walled aortic valve leaflets easily open and close during the cardiac cycle, purely following the

pressure changes and blood flow path. Under normal circumstances, opening offers very little resistance to

flow. The aortic sinuses have an important role during valve closure, as the volume of blood within the space

between the opened valve cusp and the aortic wall develop vortices as blood velocity falls. These vortices

exert central pressure and initiates valve closure. The sudden reversal of flow from deceleration completes

the diastolic closure.

Aortic Stenosis

The photograph above shows the aortic valve with a short segment of the aorta around it. The valve clearly

has only two cusps (bicuspid aortic valve), and is narrowed and densely calcified.
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The most common cause of aortic stenosis is senile calcific aortic stenosis. It is believed to represent

degenerative changes at the cellular level, including lipid accumulation and inflammatory infiltrates, similar

to atherosclerotic changes seen in the medium-sized arterial tree. Not surprisingly, it is associated with

elevated cholesterol, hypertension, cigarette smoking, diabetes, and other risk factors for atherosclerosis. It

is most common in the seventh and eighth decades of life and occurs in patients whose valves previously

appeared normal. The cusps become progressively immobilized and calcified, starting at the flexion points

and extending both along the leaflets and into the wall of the aortic root.

Congenital bicuspid aortic valve represents the most common congenital cardiac lesion, occurring in 2% of

the general population. Turbulent flow across the valve causes trauma, leading to fibrosis and calcium

deposition, further increasing turbulence, and accelerating the process. Significant stenosis typically occurs in

the fifth and sixth decades of life, although they can present earlier. Patients with congenital bicuspid aortic

valves often have dilation or aneurysmal degeneration of the ascending aorta. Some evidence suggests a

genetic etiology, with presence of abnormal microfibrils causing premature cystic medial necrosis.

Rheumatic heart disease can affect the aortic valve, although it is unusual for the disease to be limited to the

aorta, with mitral involvement far more common. As with rheumatic mitral stenosis, fusion of the

commissures tends to be the initial feature, followed by progressive thickening and retraction of the leaflets.

The reduced leaflet mobility results in a clinical picture of combined aortic valve stenosis and insufficiency.

Aortic stenosis develops gradually, allowing adaptive changes to maintain cardiac output. The left ventricle

gradually hypertrophies in response to the severity of the outflow tract obstruction, often resulting in

pressure gradients exceeding 100 mm Hg. As a result, patients can remain asymptomatic until severely

advanced disease is present. While concentric left ventricular hypertrophy maintains systolic function in the

face of severe outflow obstruction, diastolic function of the thickened and noncompliant ventricle is

progressively impaired. Diastolic dysfunction can be overcome to a certain degree with atrial hypertrophy

and enhanced atrial kick. In addition, as left ventricular end diastolic pressure rises, intravascular volume

status and peripheral vascular resistance adjust to maintain the required preload. Certain triggers can disrupt

this delicate balance, including loss of atrial contribution from atrial fibrillation or reduced diastolic fillingtime from increased heart rate, as might be seen during exercise. These triggers can create sudden clinical

decompensation, producing markedly reduced cardiac output and pulmonary edema, even in a previously

asymptomatic patient.

The most common clinical presentation in a patient with aortic stenosis is gradual decrease in exercise

tolerance. The fixed outflow obstruction prevents an increase in stroke volume typically seen in exercise with

elevated circulating catecholamines. Any change in cardiac output is limited to an increase in heart rate,


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decreasing diastolic filling time for the stiff and noncompliant ventricle. As a result, there is limited boost in

cardiac output during exercise, producing premature exertional fatigue and dyspnea. Some patients describe

angina, as myocardial oxygen demand exceeds supply. The hypertrophied heart consumes more oxygen

without reciprocal increase in epicardial delivery. In addition, the outflow obstruction prolongs systole,

further increasing oxygen demand. Symptoms are typically exertional, as the increased heart rate reduces

diastolic coronary perfusion time. Syncope or presyncope is occasionally described in patients with aortic

stenosis, presumable related to systemic vasodilation during exercise without a reciprocal increase in cardiacoutput. Advanced heart failure with symptoms at rest or with minimal activity suggest a decrease in systolic

function, likely a result of longstanding disease with alterations within the myocardium at the cellular level.

Diagnostic Evaluation

1. Physical examination of the patient reveals several findings specific for aortic stenosis. There is acharacteristic systolic crescendo/decrescendo murmur heard best over the base of the heart and

radiating up the carotid arteries. The murmur becomes harsher and peaks later in systole as the

severity worsens. Palpation of the carotid pulses reveals parvus and tardus, or a late peaking and

low-amplitude pulse. A palpable thrill may be felt over the right second intercostal space.

2. The electrocardiogram demonstrates left ventricular hypertrophy in the majority of patients.Conduction or rhythm abnormalities is identified in some patients. The chest radiograph typically is

normal but may demonstrate dilation of the ascending aorta in patients with congenital bicuspid

valve. Cardiac catheterization provides important information about associated cardiac pathology,

particularly coronary occlusive disease. In addition, hemodynamic assessment can confirm the

severity of the aortic valve stenosis and quantify the degree of pulmonary hypertension.

3. The standard evaluation of patients with suspected aortic stenosis is echocardiography. Images ofthe valve reveal the severity of the stiffness and calcifications. Images also differentiate bicuspid

from tricuspid anatomy and identify associated dilation of the ascending aorta. Ventricular function

and additional valvular pathology, particularly in patients with rheumatic heart disease, is essential.

Doppler echocardiography can measure the velocity of the aortic jet, allowing reliable estimates of

the pressure gradients using the modified Bernoulli equation.

Treatment

Medical Therapy

Because aortic stenosis can progress over 1015 years, patients with mild to moderate disease and without

symptoms can be followed without intervention. Serial echocardiography should be performed annually or

every other year to assess for disease progression. The most important aspect of medical therapy is

education of the patient about potential symptoms. Since symptoms can develop gradually, many patients

will unconsciously alter their lifestyles and activity levels without recognizing the presence of limitations.

Although there is some suggestion that cholesterol reduction with statins can reduce the calcifications, there

is little evidence that medications can adequately palliate the symptomatic patient or can alter the timing of

surgical intervention in asymptomatic patients.

Indications for SurgeryThe indications for surgery on the stenotic aortic valve have been largely determined by the presence of

symptoms. Numerous studies have demonstrated reasonably good prognosis in asymptomatic patients

managed without surgery. However, symptoms may be equivocal, particularly in the elderly population.

Exercise stress testing under the observation of a physician can help elucidate significant limitations that may

not be apparent by merely questioning the patient. Surgery is also indicated for patients with moderate to

severe aortic stenosis who are undergoing cardiac surgery for other indications, such as coronary bypass

grafting or mitral valve replacement.


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Handling of the asymptomatic patient with severe aortic stenosis is under some controversy. The severity of

aortic stenosis can be quantified using Doppler echocardiography to estimate the pressure gradient across

the aortic valve using the velocity of the outflow jet and the modified Bernoulli equation. Severe aortic

stenosis is present when the mean gradient exceeds 40 mm Hg in the normal ventricle. Although some have

described an increase in the rate of sudden death in patients with severe aortic stenosis, there remains no

evidence to justify aortic valve replacement in the absence of symptoms.

Management strategy for patients with severe aortic stenosis. Preoperative coronary angiography should be

performed routinely as determined by age, symptoms, and coronary risk factors. Cardiac catheterization and

angiography may also be helpful when there is discordance between clinical findings and echocardiography. AVA,

aortic valve area; BP, blood pressure; CABG, coronary artery bypass graft surgery; echo, echocardiography; LV, left

ventricle; Vmax, maximal velocity across aortic valve by Doppler echocardiography.

Valvuloplasty

According to St. Jude Medical, Valvuloplasty is a technique aimed at making sure the flaps of the valves (or

leaflets) close properly, preventing blood from backing up into the atrium. In the healthy heart, blood flows

from the upper chamber (atrium) to the lower chamber (ventricle), and from the ventricle to the body.


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Commissurotomy is a special form of valvuloplasty. It is used when the leaflets of the valve become stiff and

actually fuse together at the base, which is the ring portion (or annulus) of the valve. Sometimes a scalpel is

used to cut the fused leaflets (commissures) near the ring, which may help them open and close better. In

other cases, a balloon catheter, similar to a catheter used during angioplasty, is inserted into the valve. The

balloon is inflated, splitting the commissures and freeing the leaflets to open and shut fully

AORTIC INSUFFICIENCY

Several conditions can cause incompetence of the aortic valve. Any of the disease processes that cause aortic

stenosis can also cause some degree of aortic valve insufficiency, including senile calcific aortic stenosis,

degenerated bicuspid aortic valve, and rheumatic aortic valve disease. Aortic valve endocarditis is another

common cause of aortic valve insufficiency. The most common cause of incompetence of the aortic valve is

related to pathology within the aortic root and ascending aorta. Aneurysmal dilation of the ascending aorta,

either from congenital conditions such as Marfan disease, from degenerative age-related changes, or from

changes associated with a bicuspid aortic valve, can cause aortic valve insufficiency. As the wall of the aorta

enlarges, the aortic valve annulus dilates and the leaflets separate, causing incompetence.

As with mitral valve regurgitation, aortic valve insufficiency is best tolerated when it occurs gradually. As the

volume of regurgitation worsens, the ventricle adapts by dilating to accommodate the increased preload, and

it hypertrophies to maintain the same level of systolic pressure at larger volumes. Despite progressive

dilation, ventricular output and systolic function are maintained for long periods of time, leaving many

patients asymptomatic for years. While end diastolic volume is elevated, end systolic volume is normal. With

severe degrees of chronic aortic insufficiency, the heart can require ejecting as much as two to three times

the circulating cardiac output, resulting in longstanding volume overload. Eventually, systolic function

declines, resulting in a rapid and progressive rise in end diastolic volume, and heart failure symptoms ensue.

Most patients with chronic aortic insufficiency do not develop symptoms of heart failure until there is severe

left ventricular dilation. Some patients describe palpitations or the sensation of ventricular heave, particularlywhen lying down. Acute aortic valve insufficiency, as can occur with aortic valve endocarditis, can present

with cardiogenic shock because the relatively noncompliant ventricle is unprepared for the excess volume

during both systole and diastole. There is a combination of high intracardiac filling pressures and low cardiac

output. Patients are tachycardic and hypotensive as well as acutely dyspneic at rest. The patient with

endocarditis may also be febrile with signs of embolization of vegetations, causing stroke or extremity or

intestinal ischemia.

Diagnostic Testing


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1. Certain characteristic physical examination findings are pathognomonic for chronic aortic valveinsufficiency. The water-hammer pulse can be appreciated, with accentuated systole and abrupt

collapse. Patients may have a head bob with each heart beat, or a pulse may be seen in the uvula. A

systolic thrill is also described over the femoral artery from the augmented forward flow. The apical

impulse is displaced laterally and inferiorly from cardiomegaly, and diastolic blood pressure is low.

Auscultation will reveal a high-pitched diastolic murmur heard immediately after the second heart

sound. The severity of the valvular lesion usually correlates with the duration of the murmur, not theintensity. The murmur is best heard with the patient leaning forward during a breath hold.

2. Echocardiography will establish the etiology of the aortic valve insufficiency, visualizing the motion ofthe leaflets and dilation of the aorta or the presence of vegetations or leaflet perforations. In

addition, the ventricular size can be followed, as elevated end systolic volumes or reduced ejection

fraction are indications for surgery. Reversal of flow seen in the descending aorta is a sign of severe

aortic valve insufficiency. More sophisticated techniques can quantify the regurgitant volume, such

as evaluating the regurgitant jet velocity/time integral.

Treatment

For asymptomatic patients with moderate aortic insufficiency and normal ventricular dimensions, no

treatment is necessary. Patients with severe aortic valve insufficiency and normal ventricular size should be

followed every 6 months with assessment of symptoms and echocardiography. Some advocate the use of

afterload reduction agents to reduce the volume of regurgitant blood, but no evidence demonstrates

reduced need for surgery. Symptomatic patients who are not candidates for surgery should be treated with

afterload reduction agents, such as calcium channel blockers or inhibitors of angiotensin-converting enzyme.

Diuretics and salt restrictions may help in alleviating heart failure symptoms.

For operative candidates, development of heart failure symptoms is an indication for surgery. Asymptomatic

patients with decreased left ventricular systolic function or elevated left ventricular end systolic volumes

should also undergo operative treatment. Because ventricular dilation is associated with irreversible changes

at the cellular level, intervention is best performed before these permanent changes occur.


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Management strategy for patients with chronic severe aortic regurgitation. Preoperative coronary angiography

should be performed routinely, as determined by age, symptoms, and coronary risk factors. Cardiaccatheterization and angiography may also be helpful when there is discordance between clinical findings and

echocardiography. "Stable" refers to stable echocardiographic measurements. In some centers, serial follow-up

may be performed with radionuclide ventriculography (RVG) or magnetic resonance imaging (MRI) rather than

echocardiography (echo) to assess left ventricular (LV) volume and systolic function. AVR, aortic valve

replacement; DD, end-diastolic dimension; EF, ejection fraction; eval, evaluation; SD, end-systolic dimension.

Surgical Techniques

As with most other cardiac surgical procedures, median sternotomy is the standard incision utilized for access


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to the aortic valve. The pericardium is opened longitudinally, and the reflection is mobilized off of the great

vessels. The pulmonary artery and aorta are separated as they emanate from the heart, taking care to avoid

injury to the takeoff of the right pulmonary artery or the left main coronary artery. The patient is

anticoagulated with 300 IU heparin, and an activated clotting time of at least 400 seconds is confirmed.

Cannulation for CPB is performed, using the distal ascending aorta or the transverse aortic arch to maximize

the distance between the aortic cross-clamp and the aortotomy. Venous return is via the right atrial

appendage. CPB is initiated, and the left ventricle is vented via a catheter advanced from the right superiorpulmonary vein. The patient is cooled systemically to 32 C. An aortic cross-clamp is applied to the distal

ascending aorta just proximal to the CPB cannula. The heart is arrested with cold blood cardioplegia solution

with dextrose, phosphate, and potassium at 8 C. The cardioplegia is delivered antegrade down the coronary

arteries using a catheter in the aortic root. Cardioplegia is also delivered retrograde via a balloon-tipped

catheter in the coronary sinus. If severe aortic valve insufficiency is present, only retrograde cardioplegia can

be delivered. Once diastolic cardiac arrest is achieved, the ascending aorta is opened transversely

approximately 12 cm above the takeoff of the right coronary artery. The aortotomy is extended two thirds

of the circumference of the aorta, providing excellent visualization of the valve, the coronary ostia, and the

ventricular outflow tract.

Excision of the stenotic aortic valve can be time consuming and requires meticulous attention to detail. The

extensive calcifications can extend deep into the annulus and up the wall of the aortic root or down along the

anterior leaflet of the mitral valve. The calcium buildup must be debrided aggressively enough to allow

proper seating of the valve prosthesis without a paravalvular leak while avoiding residual outflow tract

obstruction. However, overaggressive debridement can result in perforations of the aortic wall, ventricular

septal defect, or unhinging of the mitral leaflet with resultant severe mitral regurgitation. In cases of

endocarditis, any granulation tissue or residual vegetations must be removed and debrided to avoid

recurrent infection of the implanted prosthetic. The outflow tract and aortic root is thoroughly irrigated to

ensure removal of loose deposits and debris.

Once the native valve has been removed and the annulus satisfactorily debrided, the outflow tract is sized

using tools provided by each manufacturer of valve prostheses. The appropriately sized valve is selected and

secured in place. Mechanical valve prosthetics are implanted using a pledgeted mattress technique, leaving

the pledgets on the aortic side. This eliminates the likelihood of the bulky pledgets interfering with the diskmechanisms on the ventricular surface. Alternatively, if a bioprosthetic valve is selected, the pledgets can be

oriented on the ventricular side of the annulus. This allows supra-annular seating of the bioprosthetic and

implantation of a slightly larger valve. The sutures are then placed through the sewing cuff of the prosthetic,

and the valve is lowered into the surgical field. The sutures are tied, ensuring that the valve has seated

properly to the annulus. The ostia of the coronary arteries should be inspected and clearly free of

impingement by the prosthetic valve. The aortotomy is then closed with running polypropylene suture,

occasionally reinforced with Teflon felt in the older patient with a thin aortic wall.

The patient is then gradually weaned from CPB, thoroughly deairing with gentle suction applied using the left

ventricular vent and the aortic root catheter. The valve is carefully inspected using the transesophageal

echocardiogram for competency and adequacy of the size. There should be no paravalvular leak, and the

gradients across the valve should be low. Elevated pulmonary artery pressures or reduced cardiac outputshould alert the surgeon of the possibility of an unrecognized paravalvular leak.

Occasionally, the aortic annulus and aortic root are small, allowing implantation of an undersized valve,

creating postoperative pressure gradients and leaving the patient with residual left ventricular outflow tract

obstruction. A variety of maneuvers can be performed to enlarge the aortic root. A Nicks procedure involves

extending the aortotomy obliquely down the noncoronary sinus and across the aortic annulus into the

anterior leaflet of the mitral valve. The defect is closed with a small diamond-shaped patch of Dacron or

pericardium. The reconstructed annulus is now increased in size approximately 24 mm, allowing upsizing of


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the chosen prosthetic. A Konno procedure involves creating an anterior longitudinal aortotomy, extending

into the right coronary sinus and across the right ventricular outflow tract. The muscular interventricular

septum is opened below the annulus, allowing expansion of the annulus beyond 4 mm. This procedure is

typically performed in children to allow insertion of a prosthetic for congenital stenosis, which will allow for

increased flow with the child's growth.

Aortic valve endocarditis also poses unique surgical challenges. The infective process often results in abscess

formation and occasionally intracardiac fistulas. The most important first step in addressing these problems is

aggressive debridement of infected and devitalized tissue. Not only will residual infection colonize the

implanted prosthetic but inadequate debridement with securing of the prosthetic to infected and devitalized

tissue will lead to dehiscence with need for early reoperation. Abscesses are common within the intervalvular

fibrous body. The annular defect should be covered with a pericardial patch. Often, the entire root requires

excision, requiring replacement with a valved conduit and reimplantation of the coronary ostia. Results for

endocarditis are dependent on the clinical status of the patient at the time of surgery as well as the etiology

of the infection. Intravenous drug users carry the worst prognosis, in large part related to recurrence of their

addiction with subsequent reinfection.

Heart Failure

Heart failure is a progressive disorder in which damage to the heart causes weakening of the cardiovascular

system. It manifests by fluid congestion or inadequate blood f low to tissues. Heart failure progresses by underlying

heart injury or inappropriate responses of the body to heart impairment.

Heart failure may result from one or the sum of many causes. It is a progressive disorder that must be managed in

regard to not only the state of the heart, but the condition of the circulation, lungs, neuroendocrine system and

other organs as well. Furthermore, when other conditions are present (e.g. kidney impairment, hypertension,

vascular disease, or diabetes) it can be more of a problem. Finally, the impact it can have on a patient

psychologically and socially are important as well.

Heart failure is a cumulative consequence of all insults to the heart over someone's life. It is estimated that nearly

5 million Americans have heart failure. The prevalence of heart failure approximately DOUBLES with each decadeof life. As people live longer, the occurrence of heart failure rises, as well as other conditions that complicate its

treatment. Even when symptoms are absent or controlled, impaired heart function implies a reduced duration of

survival. Fortunately, many factors that can prevent heart failure and improve outcome are known and can be

applied at any stage.

SmptomsFluid Congestion

If the heart becomes less efficient as a pump, the body will try to compensate for it. One way it attempts to do this

is by using hormones and nerve signals to increase blood volume (by water retention in the kidneys). A drop in

blood flow to the kidneys will also lead to fluid retention. Blood and fluid pressure backed up behind the heart

result in excess salt water entering the lungs and other body tissues. However, it is important to note that not all

swelling due to fluid retention is a reflection of heart failure.

Clinical symptoms due to fluid congestion:

shortness of breath edema (pooling of fluid in lungs and body)


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Reduced Blood Flow to the Body

The heart's inability to pump blood to the muscles and organs isn't always apparent in early stages of heart failure.

Often times, it is unmasked only during increases in physical activity. In advanced heart failure, many tissues and

organs may not even receive the oxygen they require for functioning at rest.

Clinical symptoms due to poor blood flow to the body:

difficulty exercising fatigue dizziness (due to low blood pressure)

The symptoms and physical changes of heart failure have several different classifications based on their location

and mechanism.

Right vs. Left Sided Heart Failure

1. Right Heart Failure - The inability of the right side of the heart to adequately pump venous blood into thepulmonary circulation. This causes a back-up of fluid in the body, resulting in swelling and edema.

2. Left Heart Failure - The inability of the left side of the heart to pump into the systemic circulation. Back-upbehind the left ventricle causes accumulation of fluid in the lungs.

As a result of those failures, symptoms can be due to:

1. Forward Heart Failure - The inability of the heart to pump blood at a sufficient rate to meet the oxygendemands of the body at rest or at exercise.

2. Backward Heart Failure - The ability of the heart to pump blood at a sufficient rate ONLY when heartfilling pressures are abnormally high.

3. Congestive Heart Failure - Fluid in the lungs or body, resulting from inadequate pumping from the heartand high heart filling and venous pressures.

Symptoms and SignsSwollen Ankles or Legs

Swollen ankles or legs, known as peripheral

edema, may be a result ofright-sided heart

failuresince fluid cannot be pumped to the

lungs at an efficient rate. In right-sided heart

failure, fluid backs up in the veins, leaks out

of capillaries and accumulates in tissues. Also,

a decrease in blood flow to the kidneys can

lead to an increase in fluid retention.

Diuretics are often prescribed to get rid of

this excess fluid and reduce the strain on theheart.

In the absence of heart failure, peripheral

edema may commonly be due to obesity or

venous insufficiency with stretched venous

valves.

Shortness of Breath

Shortness of breath can be caused by

congestion in the lungs. This congestion is

known as pulmonary edema. One sign to

watch out for is whether your shortness of

breath is worse when you lay f lat. Orthopnea

is the shortness of breath which occurs when

blood kept in the legs by gravity returns to

the chest when you lay down.

Shortness of breath can also occur at night.Shortness of breath that comes on suddenly

at night is known as paroxysmal (par-ox-iz-

mal) nocturnal dyspnea.
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Angina

Angina is chest or arm discomfort due to a

blockage of the coronary arteries. Heart cells

typically do not get enough oxygen when

blood flow to the heart muscle is reduced.

Often, angina comes on with exertion and isrelieved by rest. This is because your heart

may have an adequate blood supply when it

is not working very hard but not when under

stress. Other common causes of chest pain

unrelated to the heart are chest muscle, bone

or joint disease, and acid in the esophagus.

Fatigue

Fatigue is often attributed to getting old or

being out of shape. However, if this condition

persists for long periods of time, it may be

the result of heart failure. Sluggishness may

be the result of your organs not gettingenough oxygen. You may feel as tired after

getting up in the morning as you did when

you went to bed. Let your doctor know if this

happens on a regular basis.

Weight Gain or Loss

Excess fluid in the body may cause an

increase in weight. Similarly, when excess

fluid is excreted, your weight may fall. Weightincreases by about two pounds for each extra

quart of fluid. You may notice that your

weight has risen before you notice swelling of

the ankles or extremities. Inform your doctor

of changes of more than five pounds.

Loss of Appetite

Fluid accumulation in the digestive organs

can cause you to feel full. You may also feel

bloated. You may want to try eating smallermore frequent meals instead of the

traditional three large meals a day.

Causes

For heart failure to occur, there must be an unresolved impairment of the heart that

compromises its ability to work as a pump. The source of this can be a cutoff of blood supply, an

increase in workload due to high blood pressure caused by non-functioning valves or a geneticpredisposition. Heart failure can be worsened by a poor diet and lifestyle. Its development

follows the scheme below:


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Coronary Artery Disease (CAD)

This is the most common cause of heart failure in the U.S. today. CAD causing obstruction to the

coronary arteries prevents blood flow and, therefore, oxygen delivery to the heart. CAD is a

manifestation of atherosclerosis, which can affect any artery of the body. Risk factors for CAD

also include smoking, high cholesterol, hypertension, and diabetes.

Hypertension

This is more commonly known as high blood pressure. It is a condition that is treatable and

simple to diagnose with a blood pressure cuff. Although most individuals will not have symptoms,hypertension is detected by a simple measurement with a blood pressure cuff and stethoscope. It

is also a risk factor for CAD, stroke, peripheral vascular disease, or kidney impairment.

Valvular Heart Disease

A condition that occurs when the valves between the chambers of the heart are faulty, either due

to birth defect or injury.

Cardiomyopathy

A disease of the heart muscle. This can be one of many varieties. It can arise because of genetic

causes, a viral infection, or consumption of toxins (lead, alcohol, etc.). In peripartum

cardiomyopathy, women who have recently given birth can develop heart muscle impairment. In

many cases, the condition is called "idiopathic", which means it has occurred of uncertain origin

or cause.

In addition to those causes above, the following factors also can play a role in determining if heart

ailure will affect you:

1. family history of heart failure2. diabetes3. marked obesity


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4. heavy consumption of alcohol, or drug abuse5. failure to take medications6. large salt intake in diet7. sustained rapid heart rhythms

Many other conditions can actually simulate heart failure symptoms - it is important to seek

evaluation from a medical professional for a definitive diagnosis. Some of these are:

1. lung impairment2. anemia3. kidney impairment4. pericardial disease(rare)

Diagnosis

Chest X-ray

Your doctor can use an x-ray to look at your heart, lungs, and blood vessels. He or she can see if

your heart is enlarged or if there is fluid around your lungs. Pulmonary congestion shows up as

cloudy areas on the x-ray. A chest x-ray requires only a brief exposure to x-rays and is generally

considered safe.

Echocardiogram

Theechocardiogramis a procedure used to visualize the pumping action of the heart. It is an

ultrasound examination of the heart that can also measure blood flow into and out of the heart.

Electrocardiogram

This test also known as an "ECG" or "EKG", measures the electrical activity of the heart. An

electrocardiogram can check the heart's rhythm, evidence of enlargement, and the presence of aprior or recent heart attack. Electrical wires with adhesive ends are attached to the skin on your

chest, arms, and legs. The electrical activity of the heart is then recorded on a piece of paper.

Tracer Studies

Radioactive tracers given through a hand or arm IV are another tool used in the diagnosis of heart

failure. Radioactivity is detected as the blood moves through the heart. In this way, doctors can

outline the chambers of the heart, measure the ejection fraction, and assess blood flow to regions
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of the heart

Acquired Heart Dx

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