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Cardiac Surgery: Answers

169

Current recommendations for patients with bicuspid aortic valve and dilated

ascending aorta are as follows:

Class I

1. Patients with known bicuspid aortic valves should undergo an

initial transthoracic

echocardiogram to assess the diameters

of the aortic root and ascending aorta. (Level of

Evidence:

2. Cardiac magnetic resonance imaging or cardiac computed

tomography

is indicated in

patients with bicuspid aortic valves

when morphology

of the aortic root or ascending aorta

cannot

be assessed accurately

by echocardiography. (Level of Evidence:

3. Patients with bicuspid aortic valves and dilatation of

the aortic

root or ascending aorta

(diameter greater than 4.0

cm) should

undergo serial evaluation of aortic root/ascending

aorta

size

and morphology by echocardiography, cardiac magnetic

resonance,

or computed

tomography on a yearly basis. (Level

of Evidence:

4. Surgery to repair the aortic root or replace

the ascending aorta

is indicated in patients

with bicuspid aortic

valves if the

diameter of the aortic root or ascending aorta

is greater than

5.0 cm or if the rate of increase in diameter

is 0.5 cm per

year or more. (Level of Evidence: C)

5. In patients

with bicuspid valves undergoing AVR because of severe

AS or

AR, repair

of the aortic

root

or replacement of the ascending aorta is indicated if the

diameter

of the aortic

root or ascending aorta is greater than

4.5 cm.

(Level of Evidence: C)

Class IIa

1. It is reasonable to give beta-adrenergic blocking agents to

patients with bicuspid valves

and dilated aortic roots (diameter

greater than 4.0 cm) who are not candidates for surgical

correction

and who do not have moderate to severe AR. (Level of Evidence:

2. Cardiac magnetic resonance imaging or cardiac computed

tomography

is reasonable in

patients with bicuspid aortic valves

when aortic

root dilatation is detected by

echocardiography

to further quantify

severity of dilatation and involvement of

the ascending

aorta.

(Level of Evidence: B)

References

Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focused update incorporated into the

ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a

report of the American College of Cardiology/American Heart Association Task Force on

Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the

Management of Patients With Valvular Heart Disease): endorsed by the Society of

Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and

Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118:e523-661.

Braverman AC, Güven H, Beardslee MA, et al. The bicuspid aortic valve. Curr Probl

Cardiol. 2005;30:470-522.

Ferencik M, Pape LA. Changes in size of ascending aorta and aortic valve function with time

in patients with congenitally bicuspid aortic valves. Am J Cardiol. 2003; 92: 43-6.

Fedak PW, Verma S, David TE, et al. Clinical and pathophysiological implications of a

bicuspid aortic valve. Circulation. 2002;106:900-4.

Nistri S, Sorbo MD, Marin M, et al. Aortic root dilatation in young men with normally

functioning bicuspid aortic valves. Heart. 1999;82:19-22.

Shahzad G. Raja

170

2.27 Answer: D

Aortic valve replacement (AVR) in asymptomatic patients remains a controversial topic,

but it is generally agreed that AVR is indicated

in patients with left ventricular (LV) systolic

dysfunction. LV systolic dysfunction

is defined as an ejection fraction below normal at rest.

The

lower limit of normal is assumed to be 0.50 in the current AHA guidelines.

AVR is also recommended in patients with severe LV dilatation

(end-diastolic dimension

greater than 75 mm or end-systolic

dimension greater than 55 mm), even if ejection fraction is

normal. The majority of patients with this degree of dilatation

will have already developed

systolic dysfunction because of

afterload mismatch and will thus be candidates for valve

replacement

on the basis of the depressed ejection fraction. The elevated

end-systolic

dimension in this regard is often a surrogate for

systolic dysfunction. The relatively small

number of asymptomatic

patients with preserved ejection fraction despite severe increases

end-systolic and end-diastolic chamber size should be considered

for surgery, because they

appear to represent a high-risk group

with an increased incidence of sudden death, and the

results of valve replacement in such patients have thus far

been excellent. In contrast,

postoperative mortality is considerable

once patients with severe LV dilatation develop

symptoms or

LV systolic dysfunction.

Patients with severe AR in whom the degree of LV dilatation

has not reached but is

approaching these threshold values (e.g.,

LV end-diastolic dimension of 70 to 75 mm or end-

systolic dimension

of 50 to 55 mm) should be followed with frequent echocardiograms

every

4 to 6 months, as noted previously. In addition,

AVR may be considered in such patients if

there is evidence

of declining exercise tolerance or abnormal hemodynamic responses

exercise, for example, an increase in pulmonary artery wedge

pressure greater than 25 mm Hg

with exercise.

Several patient subgroups develop LV systolic dysfunction with

less marked LV

dilatation than observed in the majority of patients

with uncomplicated AR. These include

patients with long-standing

hypertension in whom the pressure-overloaded ventricle has

reduced

compliance and a limited potential to increase its chamber size;

patients with

concomitant CAD, in whom myocardial ischemia may

develop with increasing myocardial

wall stress, resulting in

LV dysfunction; and patients with concomitant MS, in whom the

left

ventricle will not dilate to the same extent as in patients

with pure AR. In such patients, it is

particularly important

that LV ejection fraction and not merely systolic dimension

monitored. Women also tend to develop symptoms and LV dysfunction

with less LV

dilatation than men; this appears to be related

to body size, because these differences are not

apparent when

LV dimensions are corrected for body surface area. Hence, LV

dimensions

alone may be misleading in small patients of either

gender, and the threshold values of end-

diastolic and end-systolic

dimension recommended above for AVR in asymptomatic patients

(75 and 55 mm, respectively) may need to be reduced in such

patients. There are no data with

which to derive guidelines

for LV dimensions corrected for body size, and clinical judgment

is required.

A decrease in ejection fraction during exercise should not be

used as the only indication

for AVR in asymptomatic patients

with normal LV systolic function at rest, because the

exercise

ejection fraction response is multifactorial, and the strength

of evidence is limited.

The ejection fraction response to exercise

has not proved to have independent prognostic

value in patients

undergoing surgery. The change in ejection fraction with

exercise is a

relatively nonspecific response related to both

severity of volume load and exercise-induced

Cardiac Surgery: Answers

171

changes in preload and peripheral resistance that develop

early in the natural history of AR.

AVR should also not be recommended

in asymptomatic patients with normal systolic function

merely

because of evidence of LV dilatation as long as the dilatation

is not severe (end-

diastolic dimension less than 75 mm or end-systolic

dimension less than 55 mm).

Patients who demonstrate progression of LV dilatation or progressive

decline in ejection

fraction on serial studies represent a higher-risk

group who require careful monitoring, but

such patients often

reach a new steady state and may do well for extended periods

of time.

Hence, AVR is not recommended until the threshold values

noted above are reached or

symptoms or LV systolic dysfunction

develop. However, prompt referral to AVR once

patients develop

symptoms, subnormal ejection fraction, or progressive LV dilatation

results

in significantly better postoperative survival than

if AVR is delayed until symptoms or LV

systolic function becomes

more severe.

It is recommended that patients with bicuspid valves should

undergo elective repair of the

aortic root or replacement of

the ascending aorta if the diameter of these structures exceeds

5.0 cm. Such surgery should be performed by a surgical team

with established expertise in

these procedures. Others have

recommended a value of 2.5 cm per m

or greater as the

indication

for surgery. If patients with bicuspid valves and associated

aortic root enlargement

undergo AVR because of severe AS or

AR, it is recommended that repair

of the aortic root or

replacement of the ascending aorta be

performed if the diameter of these structures is greater

than

4.5 cm.

References

Bonow RO, Carabello BA, Chatterjee K, et al: 2006 Writing Committee Members; American

College of Cardiology/American Heart Association Task Force. 2008 Focused update

incorporated into the ACC/AHA 2006 guidelines for the management of patients with

valvular heart disease: a report of the American College of Cardiology/American Heart

Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998

Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by

the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography

and Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118:e523-661.

Klodas E, Enriquez-Sarano M, Tajik AJ, et al. Aortic regurgitation complicated by extreme

left ventricular dilation: long-term outcome after surgical correction. J Am Coll Cardiol.

1996;27:670-7.

Borger MA, Preston M, Ivanov J, et al. Should the ascending aorta be replaced more

frequently in patients with bicuspid aortic valve disease? J Thorac Cardiovasc Surg.

2004;128:677-83.

2.28 Answer: E

Homografts for AVR have a similar rate of structural valve degeneration (SVD) as

bioprosthesis. O‘Brien et al. reported: 1) in 1987, a 0% incidence of SVD at 10 and 15 years

in 192 viable cryopreserved valves; 2) in 1991, the ―assumed‖ SVD of 410 cryopreserved

valves at 15 years was 15%; 3) in 2001, at 15 years, the reoperation rate for SVD off

cryopreserved valves in those age 0 to 20 years at time of prosthetic heart valve (PHV)

implantation was 53%, in those age 21 to 40 was 15%, in those age 41 to 60 years was 19%,

and in those age >60 years was 16%.

Shahzad G. Raja

172

A review of mechanical valves comprising 95 published series, 37,253 valves, and

187,220 valve-years of follow-up and of biological valves (porcine, pericardial, and

homograft) comprising 70 published series, 24,202 valves, and 132,519 valve years of

follow-up showed: 1) there is no significant difference among the various mechanical valves

for thromboembolism, and also among the various bioprosthesis; this is also true for rates of

thrombosis, bleeding, endocarditis, and leak; 2) the incidence of thromboembolism is higher

in patients with mitral PHV than in those with aortic PHV; 3) bioprosthesis are not free of

thromboembolic risk, but the risk is lower than with use of a mechanical valve; 4)

complication rates with use of the same brand of PHV varies widely; and 5) the risk of SVD

with all currently used mechanical valves is ―negligible‖.

Despite nearly four decades of experience, the role of pulmonary valve

autotransplantation (Ross procedure) in the treatment of aortic valve disease in adults and

children continues to evolve and remains controversial. As the picture of late results has

unfolded, alternating waves of enthusiasm and caution have characterized its use and have led

to ongoing refinements in indications and operative technique. At present, it is seen as

indispensable in the treatment of aortic valve disease in infants and small children (for whom

no satisfactory replacement alternative exists and for whom growth is essential), attractive for

adolescents and young adults who wish to avoid anticoagulants because of childbirth and

lifestyle considerations, a reasonable option for selected adults who desire biologic solutions

with potentially better durability than conventional bioprostheses, and contraindicated for the

elderly and those with connective tissue disorders. Young patients with bicuspid aortic valve

are the most common potential recipients, but also the most controversial, because of the risk

of autograft dilatation.

References

O‘Brien MF, Stafford E.G., Gardner MA, et al. A comparison of aortic valve replacement

with viable cryopreserved and fresh allograft valves, with a note on chromosomal studies.

J Thorac Cardiovasc Surg. 1987;94:812-23.

O‘Brien MF, McGiffin DC, Stafford EG., et al. Allograft aortic valve replacement: long-term

comparative clinical analysis of the viable cryopreserved and antibiotic 4 degrees C

stored valves. J Card Surg. 1991;6(4 Suppl):534-43.

O‘Brien MF, Harrocks S, Stafford EG, et al. The homograft aortic valve: a 29-year, 99.3%

follow up of 1,022 valve replacements. J Heart Valve Dis. 2001;10:334-44.

Grunkemeier GL, Li HH, Naftel DC, et al. Long-term performance of heart valve prostheses.

Curr Probl Cardiol. 2000 ;25:73-154.

Cameron DE, Vricella LA. What is the proper place of the Ross procedure in our modern

armamentarium? Curr Cardiol Rep. 2007;9:93-8.

2.29 Answer: A

Prosthetic valve endocarditis (PVE) is a catastrophic complication of valve replacement.

Prosthetic valve endocarditis is defined as infection occurring in a prosthetic heart valve with

overall incidence of 0.32 to 1.2% per patient year and cumulative risk of 5% at 10 years. In

the past, surgery for PVE was associated with a mortality of 25%–60%. Earlier diagnosis,

better myocardial protection, and improved surgical approaches have led to better survival

results in PVE.

Cardiac Surgery: Answers

173

Aortic homograft has been the conduit of choice for aortic root and left ventricular

outflow tract (LVOT) reconstruction after extensive debridement and removal of the infected

prosthesis. Homografts mold well to the debrided aortic annulus, have excellent

hemodynamic performance even in small sizes, and do not need anticoagulation. Even if

concomitant mitral repair/replacement is required, the presence of homograft would not

interfere with this, and the anterior mitral leaflet attached to the homograft may be useful as a

patch. Technique of homograft insertion depends on extent of debridement performed. Most

procedures for aortic PVE require homograft insertion by the full-root technique; presence of

subannular abscesses require the homograft to be anchored to the LVOT at the

interventricular septum and anterior mitral leaflet to exclude these abscesses, avoiding the

atrioventricular bundle if possible.

References

Mihaljevic T. Invited commentary. It would not be wise to completely abandon the use of

homograft root replacement in particular in patients with prosthetic valve endocarditis

and aortic root abscess. Ann Thorac Surg. 2007;84:1942.

Lopes S, Calvinho P, de Oliveira F, Antunes M. Allograft aortic root replacement in complex

prosthetic endocarditis. Eur J Cardiothorac Surg. 2007;32:126-30

Sabik JF, Lytle BW, Blackstone EH, et al. Aortic root replacement with cryopreserved

allograft for prosthetic valve endocarditis. Ann Thorac Surg. 2002;74:650-9.

Lytle BW. Surgical treatment of prosthetic valve endocarditis. Semin Thorac Cardiovasc

Surg. 1995;7:13-9.

2.30 Answer: A

Mitral stenosis (MS) is an obstruction to left ventricular (LV) inflow at the level of the

mitral valve (MV) as

a result of a structural abnormality of the MV apparatus, which

prevents

proper opening during diastolic filling of the left

ventricle. The predominant cause of MS is

rheumatic carditis.

Isolated MS occurs in 40% of all patients presenting with rheumatic

heart

disease, and a history of rheumatic fever can be elicited

from approximately 60% of patients

presenting with pure MS. The ratio of women to men presenting with isolated MS is 2:1.

Congenital malformation of the MV occurs rarely and is observed

mainly in infants and

children. Acquired causes of MV obstruction,

other than rheumatic heart disease, are rare.

These include

left atrial myxoma, ball valve thrombus, mucopolysaccharidosis,

and severe

annular calcification.

In patients with MS due to rheumatic fever, the pathological

process causes leaflet

thickening and calcification, commissural

fusion, chordal fusion, or a combination of these

processes. The result is a funnel-shaped mitral apparatus in which the

orifice of the mitral

opening is decreased in size. Interchordal

fusion obliterates the secondary orifices, and

commissural fusion

narrows the principal orifice.

The normal MV area is 4.0 to 5.0 cm

. Narrowing of the valve

area to less than 2.5 cm

typically occurs before the development

of symptoms. With a reduction in valve area by the

rheumatic

process, blood can flow from the left atrium to the left ventricle

only if propelled by

a pressure gradient. This diastolic transmitral

gradient is the fundamental expression of MS

and results

in elevation of left atrial pressure, which is reflected back

into the pulmonary

venous circulation. Decreased pulmonary venous

compliance that results in part from an

increased pulmonary

endothelin-1 spillover rate may also contribute to increased

pulmonary

Shahzad G. Raja

174

venous pressure. Increased pressure and distension

of the pulmonary veins and capillaries can

lead to pulmonary

edema as pulmonary venous pressure exceeds that of plasma oncotic

pressure. In patients with chronic MV obstruction, however,

even when it is severe and

pulmonary venous pressure is very

high, pulmonary edema may not occur owing to a marked

decrease

in pulmonary microvascular permeability. The pulmonary arterioles

may react with

vasoconstriction, intimal hyperplasia, and medial

hypertrophy, which lead to pulmonary

arterial hypertension.

An MV area greater than 1.5 cm

usually does not produce symptoms

at rest. However, if

there is an increase in transmitral

flow or a decrease in the diastolic filling period, there will

be a rise in left atrial pressure and development of symptoms.

From hydraulic considerations,

at any given orifice size, the

transmitral gradient is a function of the square of the

transvalvular

flow rate and is dependent on the diastolic filling period.

Thus, the first

symptoms of dyspnea in patients with mild MS

are usually precipitated by exercise, emotional

stress, infection,

pregnancy, or atrial fibrillation with a rapid ventricular response.

As the

obstruction across the MV increases, decreasing effort

tolerance occurs.

As the severity of stenosis increases, cardiac output becomes

subnormal at rest and fails

to increase during exercise.

The degree of pulmonary vascular disease is also an important

determinant of symptoms in patients with MS. A second

obstruction to flow develops from

increased pulmonary arteriolar

resistance, which may protect the lungs from pulmonary

edema. In some patients, an additional reversible obstruction

develops at the level of the

pulmonary veins. The low

cardiac output and increased pulmonary arteriolar resistance,

which

results from functional and structural changes (alveolar

basement membrane thickening,

adaptation of neuroreceptors,

increased lymphatic drainage, and increased transpulmonary

endothelin

spillover rate), contribute to the ability of a patient with

severe MS to remain

minimally symptomatic for prolonged periods

of time.

Although MS is best described as a disease continuum, and there

is no single value that

defines severity, for the AHA/ACC guidelines,

MS severity is based on a variety of

hemodynamic and natural

history data using mean gradient, pulmonary artery

systolic

pressure, and valve area as follows: mild (area greater

than 1.5 cm

, mean gradient less than 5

mm Hg, or pulmonary

artery systolic pressure less than 30 mm Hg), moderate (area

1.0 to 1.5

, mean gradient 5 to 10 mm Hg, or pulmonary artery

systolic pressure 30 to 50 mm Hg),

and severe (area less than

1.0 cm

, mean gradient greater than 10 mm Hg, or pulmonary artery

systolic pressure greater than 50 mm Hg).

References

Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focused update incorporated into the

ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a

report of the American College of Cardiology/American Heart Association Task Force on

Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the

Management of Patients With Valvular Heart Disease): endorsed by the Society of

Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and

Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118:e523-661.

Wood P. An appreciation of mitral stenosis, I: clinical features. Br Med J. 1954;4870:1051-

63.

Rowe JC, Bland EF, Sprague HB, et al. The course of mitral stenosis without surgery: ten-

and twenty-year perspectives. Ann Intern Med. 1960;52:741-9.

Cardiac Surgery: Answers

175

Olesen KH. The natural history of 271 patients with mitral stenosis under medical treatment.

Br Heart J. 1962;24:349-57.

Roberts WC, Perloff JK. Mitral valvular disease: a clinicopathologic survey of the conditions

causing the mitral valve to function abnormally. Ann Intern Med. 1972;77:939-75.

Edwards JE, Rusted IE, Scheifley CH. Studies of the mitral valve, II: certain anatomic

features of the mitral valve and associated structures in mitral stenosis. Circulation.

1956;14:398-406.

2.31 Answer: C

The natural history of patients with untreated MS has been defined

from studies in the

1950s and 1960s. Mitral stenosis

is a continuous, progressive, lifelong disease, usually

consisting

of a slow, stable course in the early years followed by a progressive

acceleration

later in life. In developed countries,

there is a long latent period of 20 to 40 years from the

occurrence

of rheumatic fever to the onset of symptoms. Once symptoms develop,

there is

another period of almost a decade before symptoms become

disabling. Overall, the 10-year

survival of untreated patients

presenting with MS is 50% to 60%, depending on symptoms at

presentation. In the asymptomatic or minimally symptomatic patient, survival

is greater than

80% at 10 years, with 60% of patients having

no progression of symptoms. However, once

significant

limiting symptoms occur, there is a dismal 0% to 15% 10-year

survival rate. Once

there is severe pulmonary

hypertension, mean survival drops to less than 3 years. The

mortality of untreated patients with MS is due to progressive

pulmonary and systemic

congestion in 60% to 70%, systemic embolism

in 20% to 30%, pulmonary embolism in 10%,

and infection in 1%

to 5%. In North America and Europe, this classic history

of MS has been

replaced by an even milder delayed course with

the decline in incidence of rheumatic fever.

The mean

age of presentation is now in the fifth to sixth decade;

more than one third of

patients undergoing valvotomy are older

than 65 years. In some geographic areas, MS

progresses more

rapidly, presumably due to either a more severe rheumatic insult

or repeated

episodes of rheumatic carditis due to new streptococcal

infections, resulting in severe

symptomatic MS in the late teens

and early 20s. Serial hemodynamic and Doppler-

echocardiographic

studies have reported annual loss of MV area ranging from 0.09

to 0.32