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Cardiac Surgery: Answers
179
murmur of MR. There may be left atrial dilatation and LV enlargement,
depending on the
presence and severity of MR. Involvement of
other valves may occur. Tricuspid valve
prolapse may occur in
40% of patients with MVP. Pulmonic and aortic valve prolapses
occur
in 2% to 10% of patients with MVP. There is an increased
incidence of associated secundum
atrial septal defect and/or
left-sided atrioventricular bypass tracts and supraventricular
arrhythmias.
The natural history of asymptomatic MVP is heterogeneous and
can vary from benign
and normal life expectancy to adverse with
significant morbidity or mortality. The spectrum
of MR ranges
from absent to severe. The most frequent predictor of cardiovascular
mortality
is moderate to severe MR and, less frequently, an
LV ejection fraction less than 0.50.
Echocardiographic evidence
of thickened MV leaflets (5 mm or greater) is also a predictor
of
complications related to MVP. In
most patients, the MVP syndrome is associated with a
benign
prognosis. The age-adjusted survival rate for both men
and women with MVP is
similar to that of individuals without
this entity.
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.
Nesta F, Leyne M, Yosefy C, et al. New locus for autosomal dominant mitral valve prolapse
on chromosome 13: clinical insights from genetic studies. Circulation. 2005;112:2022-
30.
Freed LA, Acierno JS Jr, Dai D, et al. A locus for autosomal dominant mitral valve prolapse
on chromosome 11p15.4. Am J Hum Genet. 2003;72:1551-9.
2.35 Answer: A
A diagnosis of infective endocarditis (IE) is based on the presence of either major or
minor clinical criteria. Major criteria in the Duke strategy
included IE documented by data
obtained at the time of open
heart surgery or autopsy (pathologically definite) or by well-
defined
microbiological criteria (high-grade bacteremia or fungemia)
plus echocardiographic
data (clinically definite). To maintain
the high specificity of blood culture results for IE, the
Duke
criteria required that some patients with high-grade bacteremia
with common IE
pathogens also fulfill secondary criteria. For
example, bacteremia resulting from viridans
streptococci and
members of the HACEK group of fastidious Gram-negative rods,
which are
classic IE pathogens but uncommonly seen in patients
without IE, are given primary
diagnostic weight. In contrast,
S aureus and Enterococcus faecalis commonly cause both IE
and
non-IE bacteremias. The Duke criteria therefore gave diagnostic
weight to bacteremia
with staphylococci or enterococci only
when they were community acquired and without an
apparent primary
focus; these latter types of bacteremia have the highest risk
of being
associated with IE.
The Duke criteria incorporated echocardiographic findings in
the diagnostic strategy.
Major diagnostic weight was given to
only 3 typical echocardiographic findings: mobile,
Shahzad G. Raja
180
echodense
masses attached to valvular leaflets or mural endocardium; periannular
abscesses;
or new dehiscence of a valvular prosthesis.
Six common but less specific findings of IE also were included
as minor criteria in the
original Duke schema: intermittent
bacteremia or fungemia, fever, major embolic events,
nonembolic
vascular phenomena, underlying valvular disease or injection
drug use, and
echocardiographic abnormalities that fell short
of typical valvular vegetations, abscesses, or
dehiscence. Clinically
definite IE by the Duke criteria required the presence of 2
major
criteria, 1 major criterion and 3 minor criteria, or 5
minor criteria. In the mid- to late 1990s,
direct analyses of
the Duke criteria were made in 11 major studies, including nearly 1700
patients composed of geographically and
clinically diverse groups (adult, pediatric, older
adult [>60
years old], patients from the community, patients with and without
injection drug
use, and patients with both native and prosthetic
valves). These studies confirmed the high
sensitivity
and specificity of the Duke criteria and the diagnostic utility
of echocardiography
in identifying clinically definite cases.
Moreover, a retrospective study of 410 patients showed
good
agreement (72% to 90%) between the Duke criteria and clinical
assessment by infectious
disease experts blinded to underlying
IE risk factors.
Table. Definition of Terms Used in the Modified Duke Criteria for the Diagnosis of
Infective Endocarditis
Major criteria
Blood culture positive for IE
Typical microorganisms consistent with IE from 2 separate blood cultures: Viridans streptococci,
Streptococcus bovis, HACEK group, Staphylococcus aureus; or community-acquired enterococci
in the absence of a primary focus; or
Microorganisms consistent with IE from persistently positive blood cultures defined as follows: At
least 2 positive cultures of blood samples drawn >12 h apart; or all of 3 or a majority of ≥ 4
separate cultures of blood (with first and last sample drawn at least 1 h apart)
Single positive blood culture for Coxiella burnetii or anti–phase 1 IgG antibody titer >1:800
Evidence of endocardial involvement
Echocardiogram positive for IE (TEE recommended for patients with prosthetic valves, rated
at least "possible IE" by clinical criteria, or complicated IE [paravalvular abscess]; TTE as
first test in other patients) defined as follows: oscillating intracardiac mass on valve or supporting
structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative
anatomic explanation; or abscess; or new partial dehiscence of prosthetic valve; new valvular
regurgitation (worsening or changing or preexisting murmur not sufficient)
Minor criteria
Predisposition, predisposing heart condition, or IDU
Fever, temperature >38°C
Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, and Janeway‘s lesions
Immunologic phenomena: glomerulonephritis, Osler‘s nodes, Roth‘s spots, and rheumatoid factor
Microbiological evidence: positive blood culture but does not meet a major criterion as noted above
*
or serological evidence of active infection with organism consistent with IE
Echocardiographic minor criteria eliminated
Modifications shown in boldface.
*Excludes single positive cultures for coagulase-negative staphylococci and organisms that do not cause
endocarditis.
IE, infective endocarditis; IDU, intravenous drug user; TEE, transesophageal echocardiography; TTE,
transthoracic echocardiography.
Cardiac Surgery: Answers
181
Several refinements have been made recently to both the major
and minor Duke criteria.
As noted above, in the original Duke
criteria, bacteremia resulting from S aureus was
considered
to fulfill a major criterion only if it was community acquired
because ample
literature has suggested that this parameter is
an important surrogate marker for underlying
IE. An increasing
number of contemporary studies, however, have documented IE
in patients
experiencing nosocomial staphylococcal bacteremia.
For example, of 59 consecutive patients
with S aureus IE, 45.8%
had nosocomially acquired infections and 50.8% had a removable
focus of infection. In a more recent analysis of 262 patients
at Duke University Medical
Center who had hospital-acquired
S aureus bacteremia, 34 (13%) were subsequently
diagnosed with
definite IE. Therefore, the modified Duke criteria (Table)
recommend the
inclusion of S aureus bacteremia as a major criterion,
regardless of whether the infection is
nosocomially acquired
(with or without a removable source of infection) or community
acquired.
References
Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: diagnosis, antimicrobial
therapy, and management of complications: A Statement for Healthcare Professionals
From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council
on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology,
Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association:
endorsed by the Infectious Diseases Society of America. Circulation. 2005;111:e394-
434.
Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criteria for the diagnosis
of infective endocarditis. Clin Infect Dis. 2000;30:633-638.
Fowler VG Jr, Sanders LL, Kong LK,et al. Infective endocarditis due to Staphylococcus
aureus: 59 prospectively identified cases with follow-up. Clin Infect Dis. 1999;28:106-
114.
Stockheim JA, Chadwick EG, Kessler S, et al. Are the Duke criteria superior to Beth Israel
criteria for the diagnosis of infective endocarditis in children? Clin Infect Dis.
1998;27:1451-1456.
Heiro M, Nikoskelainen J, Hartiala JJ, et al. Diagnosis of infective endocarditis: sensitivity of
the Duke vs von Reyn criteria. Arch Intern Med. 1998;158:18-24.
2.36 Answer: B
The AHA Prevention of Infective Endocarditis Committee recommended
that prophylaxis
be given only to a high-risk group of patients
before dental procedures that involve
manipulation of either
gingival tissue or the periapical region of the teeth or perforation
of
oral mucosa (Table). High-risk patients were defined
as those patients with underlying cardiac
conditions associated
with the highest risk of adverse outcome from infective endocarditis,
not
necessarily those with an increased lifetime risk of acquisition
of infective endocarditis.
Prophylaxis is no longer recommended
for prevention of endocarditis for procedures that
involve the
respiratory tract unless the procedure is performed in a high-risk
patient and
involves incision of the respiratory tract mucosa,
such as tonsillectomy and adenoidectomy.
Prophylaxis is no longer
recommended for prevention of infective endocarditis for GI
or GU
procedures, including diagnostic esophagogastroduodenoscopy
or colonoscopy. However, in
high-risk patients with
infections of the GI or GU tract, it is reasonable to administer
antibiotic
Shahzad G. Raja
182
therapy to prevent wound infection or sepsis. For
high-risk patients undergoing elective
cystoscopy or other urinary
tract manipulation who have enterococcal urinary tract infection
or colonization, antibiotic therapy to eradicate enterococci
from the urine before the procedure
is reasonable.
Table. Endocarditis prophylaxis
Prophylaxis against infective endocarditis is recommended for the following patients:
• Patients with prosthetic heart valves and patients with a history of infective
endocarditis. (Level of Evidence: C)
• Patients who have complex cyanotic congenital heart disease (e.g., single-ventricle
states, transposition of the great arteries, tetralogy of Fallot). (Level of Evidence: C)
• Patients with surgically constructed systemic pulmonary shunts or conduits. (Level of
Evidence: C)
• Patients who have undergone valve repair. (Level of Evidence: C)
• Patients who have hypertrophic cardiomyopathy when there is latent or resting
obstruction. (Level of Evidence: C)
• Patients with MVP and auscultatory evidence of valvular regurgitation and/or thickened
leaflets on echocardiography. (Level of Evidence: C)
Prophylaxis against infective endocarditis is not recommended for the following patients:
• Patients with isolated secundum atrial septal defect. (Level of Evidence: C)
• Patients 6 or more months after successful surgical or percutaneous repair of atrial
septal defect, ventricular septal defect, or patent ductus arteriosus. (Level of
Evidence: C)
• Patients with MVP without MR or thickened leaflets on echocardiography. (Level of
Evidence: C)
• Patients with physiological, functional, or innocent heart murmurs, including patients
with aortic valve sclerosis as defined by focal areas of increased echogenicity and
thickening of the leaflets without restriction of motion and a peak velocity less than
2.0 m per second. (Level of Evidence: C)
• Patients with echocardiographic evidence of physiologic MR in the absence of a
murmur and with structurally normal valves. (Level of Evidence: C)
• Patients with echocardiographic evidence of physiological TR and/or pulmonary
regurgitation in the absence of a murmur and with structurally normal valves. (Level
of Evidence: C)
References
Nishimura RA, Carabello BA, Faxon DP, et al; American College of Cardiology/American
Heart Association Task Force. ACC/AHA 2008 guideline update on valvular heart
disease: focused update on infective endocarditis: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines: endorsed by
the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography
and Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118:887-96.
Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: diagnosis, antimicrobial
Therapy, and Management of Complications: A Statement for Healthcare Professionals
From the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council
on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology,
Cardiac Surgery: Answers
183
Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association:
endorsed by the Infectious Diseases Society of America. Circulation. 2005;111:e394-
434.
2.37 Answer: C
The majority (80%) of cases of endocarditis
are due to streptococcal and staphylococcal
organisms. The latter
species is also the most frequent organism in endocarditis resulting
from
intravenous drug abuse. Eighty percent of tricuspid valve
infection is by Staphylococcus
aureus. This organism is also
a frequent cause of infective endocarditis in patients with
insulin-dependent diabetes mellitus. With prosthetic valve endocarditis,
a wide spectrum of
organisms can be responsible within the first
year of operation. However, in "early" prosthetic
valve endocarditis,
usually defined as endocarditis during the first 2 months after
surgery,
Staphylococcus epidermidis is the predominant offending
organism. Late-onset prosthetic
valve endocarditis follows the
profile of native valve endocarditis, that is, streptococci
(viridans) and staphylococci. Enterococcus faecalis and E. faecium
account for 90% of
enterococcal endocarditis, which is usually
associated with malignancy or manipulation of the
genitourinary
or gastrointestinal tract. Gram-positive and Gram-negative bacilli
are relatively
uncommon causes of endocarditis. In recent years,
the HACEK group of organisms
(Haemophilus, Actinobacillus, Cardiobacterium,
Eikenella, and Kingella species) has become
an important cause
of endocarditis. These organisms cause large vegetations (greater
than 1
cm), large-vessel embolism, and congestive heart failure.
They should be considered along
with fungal endocarditis when
large vegetations are noted. Fungi, especially Candida, are
important causes of endocarditis in patients with prosthetic
valves, compromised immune
systems, and intravenous drug abuse.
References
Bonow RO, Carabello BA, Chatterjee K, et al. 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) developed in collaboration with the Society of Cardiovascular
Anesthesiologists endorsed by the Society for Cardiovascular Angiography and
Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2006;48:e1-148.
Baddour LM, et al. Infective endocarditis: diagnosis, antimicrobial Therapy, and Management
of Complications: A Statement for Healthcare Professionals From the Committee on
Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular
Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and
Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the
Infectious Diseases Society of America. Circulation. 2005;111:e394-434.
2.38 Answer: B
Predisposing factors for infective endocarditis are cardiac
abnormalities that disrupt the
endocardium by means of a jet
injury, as well as the presence of blood-borne microorganisms
that colonize these abnormal surfaces. Congenitally bicuspid
aortic valve is the most common
predisposing lesion for endocarditis
of the aortic valve. Other congenital abnormalities of the
aortic valve, degenerative calcific aortic stenosis, aortic insufficiency
secondary to connective
Shahzad G. Raja
184
tissue disorders, and rheumatic aortic
valve disease, are also predisposing lesions for
infection. Depending
on the virulence of the offending microorganism, normal aortic
valves
can also be affected. Patients with prosthetic heart valves
have a constant risk of developing
infective endocarditis.
It is difficult to determine the incidence and prevalence of
native aortic valve
endocarditis in the general population because
this disease is continuously changing. The
annual incidence
of infective endocarditis is estimated to range from 1.7 to
7.0 episodes per
100,000 person-years in North America.
Patients with prosthetic aortic valves are reported to have
an incidence of infective
endocarditis of 0.2 to 1.4 episodes
per 100 patient-years, which varies with the type of aortic
valves. Approximately 1.4% of patients undergoing
aortic valve replacement develop
prosthetic valve endocarditis
during the first postoperative year.
References
Lamas CC, Eykyn SJ. Bicuspid aortic valve—a silent danger: analysis of 50 cases of infective
endocarditis. Clin Infect Dis. 2000; 30:336-41.
Dyson C, Barnes RA, Harrison GA. Infective endocarditis: an epidemiological review of 128
episodes. J Infect. 2000; 40:87-93.
Tleyjeh IM, Steckelberg JM, Murad HS, et al. Temporal trends in infective endocarditis: a
population-based study in Olmsted County, Minnesota. JAMA. 2005; 293:3022-8.
2.39 Answer: D
The microbiology of infective endocarditis of the aortic valve is affected by whether the
infection is hospital- or community-acquired. Furthermore, the microbiology also depends on
whether the valve is native or prosthetic. Native aortic valve endocarditis is most commonly
caused by Staphylococcus aureus
and Streptococcus viridans. S. aureus is extremely virulent
and able to cause endocarditis of normal aortic valves. S. viridans is not as
virulent and causes
infection that often follows a lengthy and chronic course. Staphylococcus epidermidis and
various other streptococci
can also cause endocarditis.
Endocarditis due to gram-negative bacteria is uncommon. However, it is associated with
serious
complications and is often resistant to antibiotic therapy. Haemophilus,
Actinobacillus, Cardiobacterium,
Eikenella, and Kingella (the HACEK group) are gram-
negative
bacilli grouped together due to their typical fastidiousness
requiring a prolonged
incubation period before growth. Endocarditis
due to the HACEK group is also uncommon.
Fungal endocarditis
is rare but extremely serious. Usual causative agents for fungal
endocarditis are Candida albicans and Aspergillus
fumigatus.
The microbiology of prosthetic aortic valve endocarditis is
dissimilar to that of the native
valve. Prosthetic valve
endocarditis has been arbitrarily classified as early and late. Early
endocarditis
occurs within the first 2 months after surgery. Late endocarditis occurs after 2
months. However, it is possible that many cases
of prosthetic valve endocarditis that occur
during the first
year after surgery are the result of infection at the time of implantation
of the
artificial heart valve. This may be especially applicable
when the infection is caused by the
HACEK group of bacteria. Early
prosthetic valve endocarditis is the result of contamination
of the
valve at the time of implantation by perioperative bacteraemia.
Staphylococcus
epidermidis, S. aureus, and Enterococcus faecalis
are among the more common bacteria
responsible for early
prosthetic valve endocarditis. The sources of
late prosthetic valve
Cardiac Surgery: Answers
185
endocarditis are more difficult to determine.
Bacteraemia is presumably the major cause of
late endocarditis. Although
streptococci and staphylococci are common causative agents in
these
patients, multiple microorganisms can cause late prosthetic valve
endocarditis.
Hospital-acquired infections are often caused by S. aureus or other
staphylococci.
In a small number of cases of aortic valve endocarditis,
no microorganism can be cultured
from either the blood or surgical
specimens. This is called "culture-negative endocarditis,"
but
it is important to exclude fastidious microorganisms and
every effort should be made to
establish their identity.
References
Alexiou C, Langley SM, Stafford H, et al. Surgery for active culture-positive endocarditis:
determinants of early and late outcome. Ann Thorac Surg. 2000; 69:1448-54.
Moon MR, Miller DC, Moore KA, et al. Treatment of endocarditis with valve replacement:
the question of tissue versus mechanical prosthesis. Ann Thorac Surg. 2001; 71:1164-71.
Kang N, Wan S, Ng CS, Underwood MJ. Periannular extension of infective endocarditis. Ann
Thorac Cardiovasc Surg. 2009;15:74-81.
2.40 Answer: B
The most common presentation of tricuspid regurgitation (TR) is secondary to cardiac
valvular
pathology (mostly mitral valve disease) on the left side of
the heart. As pulmonary
hypertension develops, leading to right
ventricular dilatation, the tricuspid valve annulus will
dilate.
The circumference of the annulus lengthens primarily along the
attachments of the
anterior and posterior leaflets. The septal
leaflet is fixed between the fibrous trigones,
preventing lengthening. As the annular and ventricular dilatation progresses,
the chordal
papillary muscle complex becomes functionally shortened.
This combination prevents leaflet
apposition, resulting in valvular
incompetence commonly referred to as functional tricuspid
regurgitation.
Eisenmenger syndrome and primary pulmonary hypertension lead
to the same
pathophysiology of progressive right ventricular
dilatation, tricuspid annular enlargement, and
valvular incompetence.
A right ventricular infarction produces either disruption of
the
papillary muscle or a severe regional wall motion abnormality
that prevents normal leaflet
apposition by a tethering effect
on the leaflets, leading to regurgitation. Marfan syndrome and
other variations of myxomatous disease affecting the mitral
and tricuspid valves can lead to
prolapsing leaflets, elongation
of chordae, or chordal rupture, producing valvular
incompetence.
Blunt or penetrating chest trauma may disrupt the structural
components of the
tricuspid valve. Dilated cardiomyopathy in
the late stages of biventricular failure and
pulmonary hypertension
produces TR. Infectious endocarditis can destroy
leaflet tissue,
mostly in drug addicts with staphylococcal infection.
The carcinoid syndrome leads to either focal or diffuse deposits
of fibrous tissue on the
endocardium of valve cusps, cardiac
chambers, intima of the great vessels, and coronary
sinus. The
white fibrous carcinoid plaques, if present on the ventricular
side of the tricuspid
valve cusps, adhere the leaflet tissue
to the right ventricular wall, preventing leaflet
coaptation.
Rheumatic disease of the tricuspid valve is always associated
with mitral valve
involvement, and the deformity of the tricuspid
tissue results in a tricuspid valve stenosis as
well as regurgitation.
Shahzad G. Raja
186
References
Morrison DA, Ovitt T, Hammermeister KE. Functional tricuspid regurgitation and right
ventricular dysfunction in pulmonary hypertension. Am J Cardiol. 1988; 62:108-12.
Raja SG, Dreyfus GD. Surgery for functional tricuspid regurgitation: current techniques,
outcomes and emerging concepts. Expert Rev Cardiovasc Ther. 2009;7:73-84.
2.41 Answer: C
The bioprostheses, either porcine or pericardial
valves, have excellent freedom from
degeneration and re-replacement
for structural valve degeneration. In 1984, Cohen and
colleagues
reported on six simultaneously implanted and then explanted
valves from the
mitral and tricuspid positions. Degenerative
changes were less extensive for the bioprosthetic
valves in
the tricuspid position than in the mitral position. However,
thrombus formation and
pannus formation (interpreted as organized
thrombotic material) were observed more
frequently in the tricuspid
position.
Nakano‘s review of the Carpentier-Edwards pericardial
xenograft reported a freedom
from structural degeneration of
100% at 9 years, but nonstructural dysfunction was 72.8%.
The
cause of nonstructural dysfunction was pannus formation on the
ventricular side of the
cusps. This finding is often subclinical.
Echocardiographic follow-up revealed a 35%
incidence of this
anatomic finding in patients with at least 5 years of follow-up.
Guerra
reported similar changes in simultaneously explanted
porcine valves. The tricuspid position
had less structural tissue
degeneration and calcification than the mitral position. The
report
described the presence of pannus formation on the ventricular
side of the cusps in tricuspid
porcine valves. The pannus interfered
with cuspal pliability and function.
Nakano‘s 2001 report of bioprosthetic tricuspid valves
reported an 18-year freedom from
reoperation of 63%. The
freedom from structural deterioration was 96%, and nonstructural
dysfunction was 77%. Reoperation replacing previously placed
bioprosthetic valves occurred
in 12 of 58 survivors. In 6 of
the 12 patients, the primary indication for reoperation was
tricuspid dysfunction, and 7 of the 12 had pannus formation
on the ventricular side of the
cusps. This rate
of degeneration and the subclinically high incidence of pannus
formation,
often eventually leading to reoperation, are major
concerns. Tricuspid bioprosthetic valves
require echocardiographic
follow-up. Possible anticoagulation of bioprosthetic valves
in the
tricuspid position can reduce the incidence of pannus
formation. The reported data in the
literature categorize this
pannus formation as nonstructural degeneration.
In the tricuspid position it is always possible to place large
bioprosthetic or mechanical
valves. Prostheses with more than
a 27 mm internal diameter do not have clinically significant
gradients. Therefore, hemodynamic performance is rarely an issue
for tricuspid valve
replacement. The data demonstrate excellent
results with modern bileaflet mechanical valves.
Series comparing
bioprosthetic and mechanical valves have been consistent in
demonstrating
equality during the period of follow-up. The development
of thrombus on a bileaflet valve can
be treated successfully
with thrombolysis.
A recent review by Filsoufi and a meta-analysis of biologic
or mechanical prostheses in
the tricuspid position both conclude
that there is no survival benefit of a bioprothesis over a
mechanical
valve.
Cardiac Surgery: Answers
187
References
Cohen SR, Silver MA, McIntosh CL, Roberts WC. Comparison of late (62 to 104 months)
degenerative changes in simultaneously implanted and explanted porcine (Hancock)
bioprosthesis in the tricuspid and mitral positions in six patients. Am J Cardiol.
1984;53:1599-1602.
Nakano K, Eishi K, Kosakai Y, et al. Ten-year experience with the Carpentier-Edwards
pericardial xenograft in the tricuspid position. J Thorac Cardiovasc Surg. 1996;111:605-
12.
Nakano K, Ishibashi-Ueda H, Kobayashi J, et al. Tricuspid valve replacement with
bioprostheses: long-term results and causes of valve dysfunction. Ann Thorac Surg.
2001;71:105-9.
Guerra F, Bortolotti U, Thiene G, et al. Long-term performance of the Hancock porcine
bioprosthesis in the tricuspid position. A review of forty-five patients with fourteen-year
follow-up. J Thorac Cardiovasc Surg. 1990;99:838-45.
Filsoufi F, Anyanwu AC, Salzberg SP, et al. Long-term outcomes of tricuspid valve
replacement in the current era. Ann Thorac Surg. 2005; 80:845.
Rizzoli G, Vendramin I, Nesseris G, et al. Biological or mechanical prostheses in tricuspid
position? A meta-analysis of intrainstitutional results. Ann Thorac Surg. 2004; 77:1607-
14.
2.42 Answer: A
Coronary artery bypass grafting (CABG) has been considered the
gold standard for
treating multivessel coronary artery disease,
mainly because of its higher rate of complete
revascularization,
reflected by a lower need for repeat revascularizations compared
with
percutaneous coronary intervention (PCI).
Whereas the risk difference of CABG versus balloon angioplasty
for repeat
revascularization in a large-scale meta-analysis
proved to be 34% at 3 years, this difference
decreased to 15%
when coronary stents were used. In terms of clinical safety
end points, the
recently reported 5-year follow-up of the Arterial
Revascularization Therapies Study (ARTS),
Argentine Randomized
Trial of Coronary Angioplasty With Stenting Versus Coronary
Bypass
Surgery in Patients With Multiple Vessel Disease (ERACI-II),
and the Medicine, Angioplasty
or Surgery Study for Multi-Vessel
Coronary Artery Disease (MASS-II) reported no difference
in
death rates between the 2 revascularization strategies. Conversely,
the Stent or Surgery
(SoS) trial recently demonstrated a significantly
lower survival in patients treated with PCI
compared with CABG
at 6 years.
In a recently published meta-analysis, patient-level data of the above-mentioned
randomized trials were pooled to make a more precise estimate
of the relative long-term
safety and efficacy of PCI with stenting
and CABG for multivessel coronary artery disease, to
assess
the relative treatment effect in several high-risk subgroups,
and to assess the
heterogeneity of the treatment effect.
A total of 3051 patients were included in this analysis between
June 1995 and June 2000
(1205 in ARTS, 450 in ERACI-II, 408
in MASS-II, and 988 in SoS). In total, 1533 were
randomized
to CABG, and 1518 were randomized to PCI. Eighty-nine percent
of patients
allocated to PCI underwent the assigned treatment
compared with 96% of those assigned to
CABG.
Shahzad G. Raja
188
Although 3-vessel disease was more frequent in the CABG group
compared with the PCI
group (40.0% versus 36.1%, respectively;
P=0.017), complete revascularization was
performed in 89.4%
of the CABG patients compared with 62.0% of the PCI patients
(P<0.001). The hospital stay was significantly longer in
the CABG group (median, 8 days;
interquartile range, 1 to 4
days) compared with the PCI group (median, 3 days; interquartile
range, 6 to 11) (P<0.001).
Five-year follow-up was complete for 97% of all patients (100%
in ARTS and ERACI-II,
97.5% in MASS-II, and 91.6% in SoS). At
5 years, the cumulative incidence of death, MI,
and stroke was
similar in patients randomized to PCI with stenting versus CABG
(16.7%
versus 16.9%, respectively; Hazard Ratio [HR], 1.04; 95% CI, 0.86 to
1.27; P=0.69). Repeat
revascularization, however, occurred significantly
more frequently after PCI compared with
CABG (29.0% versus 7.9%,
respectively; HR, 0.23; 95% CI, 0.18 to 0.29; P<0.001). Because
of the substantial difference in the repeat revascularization
rates between both treatment
modalities, major adverse cardiac
and cerebrovascular event rates were significantly higher in
the PCI group than in the CABG group (39.2% versus 23.0%, respectively;
HR, 0.53; 95%
CI, 0.45 to 0.61; P<0.001).
For the composite end point of death, stroke, and MI, no heterogeneity
in treatment was
found between patients with diabetes and those
without diabetes. In patients with diabetes, the
cumulative incidence of death was 12.4% in the PCI group compared
with 7.9% in the CABG
group (P=0.09). In patients without diabetes,
the cumulative incidence of death was 7.7% in
the PCI group
compared with 8.3% in the CABG group (P=0.55). The cumulative
incidence
of death, stroke, or MI in diabetics was similar after
PCI with stenting and CABG (21.4%
versus 20.9%, respectively;
P=0.9). However, the HR for repeat revascularization in the
diabetic subgroup was 0.18 (95% CI, 0.11 to 0.29) as a result
of a 3-fold-higher cumulative
incidence of repeat revascularization
in the PCI group (29.7% versus 9.2%; P<0.001).
The cumulative 5-year incidence of death was similar between
PCI and CABG in both
the 2-vessel disease (7.6% versus 7.3%,
respectively; P=0.87) and the 3-vessel disease
(10.2% versus
9.5%, respectively; P=0.71) subgroups. The cumulative incidence
of death,
stroke, and MI was similar between PCI and CABG in
both the 2- and 3-vessel subgroups.
However, repeat revascularization
rates were significantly higher in the PCI group in patients
with 2-vessel and in those with 3-vessel disease (29.0% versus
7.2%, P<0.001; and 28.9%
versus 7.8%, P<0.001, respectively),
resulting in a significantly lower incidence of the
combined
major adverse cardiac and cerebrovascular events in the CABG
cohort for both 2-
and 3-vessel disease.
References
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