Transcript 후천성 심장질환

Tricuspid Valve Disease
Endocarditis
Department of Thoracic & Cardiovascular Surgery
Seoul National University Hospital
&
Tricuspid Valve
Anatomy
• Normal tricuspid valve area ; 10.5 cm2
• Normal valve diameter ; 40 - 45 mm
• No actual tricuspid annulus ; attached to
AV junction
• Tricuspid valve ring is related to the base
of AV, membranous septum, CFB, RCA,
CS, bundle of His
Tricuspid Valve
Anatomy
• View of tricuspid valve and surgical importance
Tricuspid Regurgitation
Pathophysiology
• The most common presentation of tricuspid regurgitation
is secondary, functional rather than organic from mostly
MS, MR or in isolated aortic valve disease
• As pulmonary hypertension develops leading to right
ventricular dilation, tricuspid annulus will dilate
• The circumference of annulus lengthens primarily along
the attachments of the anterior and posterior leaflets .
• The septal leaflets is fixed between the fibrous trigones,
preventing lengthening.
• As the annular & ventricular dilation progresses, chordal
papillary muscle complex becomes functionally shortened
• This combination prevents leaflet apposition, resulting in
valvular incompetence
Tricuspid Valve Disease
Etiology
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Mostly secondary (functional) to valve pathology
Eisenmenger’s syndrome
Primary pulmonary hypertension
Marfan syndrome and other myxomatous disease
Blunt or penetrating chest trauma
Dilated cardiomyopathy in the late stages
Infectious endocarditis
Carcinoid syndrome
Rheumatic disease of the tricuspid valve is always
associated with mitral valve
Functional Tricuspid Regurgitation
Process of annular dilatation
• Pathological process of tricuspid annular dilatation. Arrows designate
the intercommissural distance that increases with dilatation and that
is measured intraoperatively.
Functional Tricuspid Regurgitation
Prerequisite
• For the tricuspid valve to leak, the tricuspid annulus
and hence the right ventricle has to be dilated
• In addition to tricuspid dilatation, three important
factors determine whether TR occurs: the preload,
afterload, and right ventricular function.
• This may explain why TR is difficult to accurately
assess because these factors can interfere with regard
to the severity of TR under different conditions.
Functional Tricuspid Regurgitation
Controversies
• Early investigators advocated a conservative approach,
arguing that functional TR, often secondary to
pulmonary hypertension and concomitant mitral valve
disease, should spontaneously improve after mitral
valve repair
• Subsequent studies, however, have demonstrated that
TR does not necessarily regress after repair of left-sided
valve lesions
• Uncorrected TR increases both postoperative morbidity
and mortality and is associated with poor long-term
results with medical management alone
Tricuspid Regurgitation
Clinical presentation
• Fatigue & weakness related to reduction
of cardiac output
• Right heart failure lead to ascites, venous
engorgement, hepatospenomegaly,
pulsatile liver, pleural effusions &
peripheral edema
• In late stage, cachexia, cyanosis, jaundice
& AF is common
Tricuspid Regurgitation
Signs
Tricuspid Stenosis
Clinical presentation
• Most commonly rheumatic, rare isolated stenosis
• Fatigue & malaise related to reduction of CO
• As the right atrial pressure increases, venous
congestion leads to distention of jugular veins,
hepatomegaly, ascites, pleural effusion, & peripheral
edema
• Anatomic features are similar to mitral stenosis with
fusion and shortening of chordae & leaflet thickening
• The right atrial wall thickens and chamber dilates
Tricuspid Valve Disease
Indications for surgery
• Repair of tricuspid stenosis is indicated for
class III-IV symptoms, including hepatic
congestion, ascites, and peripheral edema that
are refractory to medical treatment
• Repair of tricuspid regurgitation is indicated
for severe symptoms or when moderate-tosevere functional TR is present at left-sided
valve surgery.
Repair is especially important if PVR is
elevated.
Tricuspid Valve Repair
Bicuspidalization
Plicating the annulus along the posterior leaflet
Flexible ring placed, ring can be above coronary sinus
Tricuspid Regurgitation
Tricuspid valve annuloplasty
Tricuspid Regurgitation
Tricuspid valve annuloplasty
• Modified DeVega annuloplasty
Tricuspid Regurgitation
Tricuspid valve annuloplasty
• Suture bicuspidization is performed by placement of a 2-0 pledgetsupported Ethibond mattress suture from the anteroposterior to the
posteroseptal commissures along the posterior annulus.
Tricuspid Regurgitation
Tricuspid valve annuloplasty
• Carpentier-Edwards ring annuloplasty
Tricuspid Valve Annuloplasty
Cosgrove-Edwards System
Annular sutures extend from the posteroseptal to the anteroseptal
commissure and are placed through the polyester velour band of the
annuloplasty system
Tricuspid Valve Annuloplasty
Cosgrove-Edwards System
A measured plication of the annulus adjacent to the anterior & posterior
leaflets is achieved and the conduction system is not jeopardized.
Traumatic Tricuspid Regurgitation
Clover technique
Surgical steps of the clover technique
Tricuspid Regurgitation
Tricuspid valvuloplasty
• Partial Commissure Closure & Leaflet Cleft Repair
Tricuspid Regurgitation
Partial annuloplasty
Tricuspid Valvuloplasty
Edge-to-edge valve plasty
A U-shaped 5-0 polypropylene stitch reinforced with small pericardial pledgets passes
through the middle point of the free edges of the tricuspid leaflets. The anterior leaflet is
anchored to the facing edges of posterior and septal leaflets to create a triple orifice
tricuspid valve.
Tricuspid Valve Disease
Operative management
• Results be interpreted with early & late
results of mitral & double valve procedures
• Indications ; NHYA functional class III & IV
• TV repair is preferable to valve replacement
- Due to unfavorable complications of TVR
(TE, thrombosis, anticoagulation problems)
Tricuspid Valve Annuloplasty
Risk factors for late failure
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Greater preoperative TR grade
Preoperative TR without concomitant MR
Higher postoperative PASP
NYHA, preoperative PASP, preoperative RV
dysfunction, recurrent MR were not significant
risk factors.
Tricuspid Regurgitation
Results of operative treatment
• Clinical and surgical management of tricuspid valve
disease have evolved from conservative approaches,
that is, spontaneous regression after correction of leftsided lesions, to a more interventionist care.
• At present, it is well known that tricuspid regurgitation
grades 3+ and 4+ that are not surgically corrected or
that reappear after operation are prognostic factors of
poor long-term outcome.
• Dysfunction after tricuspid valve repair requiring
reoperation was associated with a high hospital
mortality
Tricuspid Valve Replacement
Prosthetic valve choice
• The choice of prosthesis follows the algorithm similar
to that used for valve replacement in other cardiac
valve positions ( demonstrating equality )
• The patient’s age, anticoagulation considerations in
women and social issues must be considered
• Degenerative changes were less for bioprosthesis in
the tricuspid position than in the mitral, however ,
thrombus and pannus formation were more frequent
in the tricuspid position
• Prostheses with more than 27mm internal diameter
do not have clinically significant gradient
• Recommend a mechanical valve to young patients
who do not have a contraindication to anticoagulation
Tricuspid Valve Replacement
Mitral homograft
Prosthetic Valve Endocarditis
Infective Endocarditis
Introduction
• Rates of infective endocarditis in the general
population have remained relatively constant and are
estimated to be 5.0 to 7.0 cases per 100,000 personyears in the United States
• Contemporary causes of infective endocarditis include
intravenous drug use (IVDU), use of prosthetic valves,
sclerotic disease in the elderly, and nosocomial infection
• Although high mortality remains associated with
infective endocarditis, surgical treatment has greatly
increased survival versus antibiotic treatment alone
Early aggressive surgical intervention is often indicated
to optimize surgical results
Infective Endocarditis
Development
• Endocarditis usually develops in individauls with
underlying structural cardiac defects who develop
bacteremia with organisms likely to cause endocarditis
• Surgical and dental procedures and instrumentations
involving mucosal surfaces or contaminated tissue cause
transient bacteremia that rarely persists for more than
15 minutes
• Bacteremia may lodge on damaged or abnormal heart
valves or on the endocardium or the endothelium near
anatomic defects, resulting in bacterial endocarditis or
endarteritis.
• Although bacteremia is common following many invasive
procedures, only certain bacteria commonly cause
endocarditis
Active Infective Endocarditis
Introduction
• Depending on how promptly the disease is diagnosed
and appropriate antibiotics are started, on the virulence
of the microorganism, and on whether the infected
valve is native or prosthetic, surgery may become
indispensable to save the patient’s life and eradicate the
infection
• Staphylococcus aureus was the most common
microorganism, & less virulent streptococcus viridans,
always respond to antibiotics alone is erroneous,
because these bacteria can cause extensive damage to a
heart valve and surrounding tissues if inadequately
treated
Infective Endocarditis
Modified Duke Criteria
[Major criteria]
Blood culture positive for IE
(A) Typical microorganisms consistent with IE from 2 separate blood cultures:
(1) Viridans streptococci, Streptococcus bovis, HACEK group, staphtlococcu aureus; or
(2) Community-acquired enterococci, in the absence of a primary focus
(B) Microorganisms consistent with IE from persistently positive blood cultures, defined as follows;
(1) At least 2 positive cultures of blood samples drawn 12h apart; or
(2) All of 3 or a majority of ＞ 4 separate cultures of blood (with first and last sample drawn at least 1h apart)
(C) Single positive blood culture for Coxiella burnetii or antiphase I IgG antibody titer e ＞ 1:800
Evidence of endocardial involvement
(A) Echocaridiogram positive for IE (TEE recommended in patients with prosthetic valves, rated at least “possible
IE” by clinical criteria, or complicated IE [paravalvular abscess]; TEE as first test in other patients), defined as follows;
(1) Oscillating intracardiac mass on valve of an alternative anatomic explanation; or
(2) Abscess; or
(3) New vavular regurgitation (worsening or changing of pre-existing murmur not sufficient)
[Minor criteria]
(A) Predisposition: predisposing heart condition or injection drug use
(B) Fever: temperature ＞ 38℃
(C) Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial
hemorrhage, conjunctival hemorrhages, and Janeway’s lesions
(D) Immunologic phenomena: glomerulonephritis, Osle’s nodes, Roth’s spot, and rheumatoid factor
(E) Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological
evdence of active infection with organism consistent with IE
Infective Endocarditis
Modified Duke Criteria (Diagnosis)
Definite infective endocarditis
Pathologic criteria
(1) Microorganisms demonstrated by culture or histologic examination of a vegetation, a
vegetation that has embolized, or an intracardiac abscess specimen; or
(2) Pathologic lesions; begetation or intracardiac abscess confirmed by histologic
examination showing active endocarditis
Clincal criteria
(1) 2 major criteria; or
(2) 1 major criterion and 3 minor criteria; or
(3) 5 minor criteria
Possible infective endocarditis
(1) 1 major criterion and 1 minor criterion; or
(2) 3 minor criteria
Rejected
(1) Firm alternate diagnosis explaning evidence of infective endocarditis; or
(2) Resolution of infective endocarditis syndrome with antibiotic therapy for ＜ 4 days; or
(3) No pathologic evidence of infective endocarditis at surgery or autopsy, with antibiotic
therapy for ＜ 4 days; or
(4) Dose not meet criteria for possible infective endocarditis, as above
Infective Endocarditis
Situations of high complication
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Prosthetic cardiac valves
Left-sided infective endocarditis
Fungal infective endocarditis
Previous infective endocarditis
Prolonged clinical symptoms(>3 months)
Cyanotic congenital heart disease
Patients with systemic to pulmonary shunt
Poor clinical response to antimicrobial therapy
Infective Endocarditis
Need for surgical intervention
 Vegetation
• Persistent vegetation after systemic embolization
• Increase in vegetation size after 4 weeks of antimicrobial therapy
 Valvar dysfunction
• Acute aortic or mitral regurgitation with ventricular dilatation
• Heart failure unresponsive to medical therapy
• Valve perforation or rupture
 Perivalvar extension
• Valvar dehiscence, rupture, or fistula
• New heart block
• Large abscess or extension of abscess despite appropriate
antibiotic therapy
Prosthetic Valve Endocarditis
Early
Onset
< 60 days
Organism Staphylococci;
Late
> 60 days
Streptococci;
S.epidermidis,aureus. S.viridans, Gr D.
Gr(-) organisms.
Staphylococci.
Fungi, Diphteroids.
Fungi, Diphteroids
Streptococci.
* Risk of PVE: greatest at 5wks following valve implantation
Prosthetic Valve Endocarditis
Pathology
• Mechanical valve;
Sewing ring, valve ring abscess,
valve dehiscence, paravalvular leak
• Tissue valve;
Valve leaflets
– greater success of antibiotic therapy
Infective Endocarditis
Paraannular ring abscess
Infective Endocarditis
Causes of negative blood cultures
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Rt-sided endocarditis
Bacteria free-stage: very “chronic” SBE
Uremia
Poor bacteriologic sampling techniques
Fastidious organisms needing special
growth requirements
• Prior administration of antibiotics
• Nonbacterial causes of endocarditis
Native Valve Endocarditis
Surgical indications
• Presence of moderate-to-severe CHF
• Persistent sepsis
• Evidence of local extension producing annular or
myocardial abscesses, conduction disturbance, or
intracardiac fistula
• Systemic embolization
• Enlarging vegetations, threatened embolization
Infective Endocarditis
Surgical indications
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Progressive heart failure
Significant heart failure: fails to improve
Major embolism, large vegetation ( >1cm )
Persistent bacteremia despite antibiotics
Fungal endocarditis
Patients with intravascular devices
Heart block
PV dehiscence or obstruction
Relapse
Infective Endocarditis
Tricuspid valve lesion
• Increasing due to rising incidence of IV drug
abuse
• Surgical treatment is necessary when continued
sepsis, moderate to severe HF, multiple
pulmonary emboli(+)
• Intensive medical Tx, valvectomy, valve
replacement; aggressive counseling should be
offered due to high incidence of recidivism
Endocarditis Prophylaxis
Cardiac conditions
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High-risk category
• Prosthetic cardiac valves, including bioprosthetic and
homograft valves
• Previous bacterial endocarditis
• Complex cyanotic congenital heart disease
• Surgical systemic pulmonary shunt or conduits
Moderate-risk category
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Most other congenital cardiac malformations
Acquired valvar dysfunction
Hypertrophic cardiomyopathy
Mitral valve prolapse with valve regurgitation and/or
thickened leaflets
Endocarditis Prophylaxis
Cardiac conditions
Negative-risk category (not greater than general)
• Isolated secundum ASD
• Surgical repair of ASD, VSD, or PDA ( without residua
beyond 6 months )
• Previous coronary artery bypass graft surgery
• Mitral valve prolapse without regurgitation
• Physiologic, functional, or innocent heart murmur
• Previous Kawasaki disease without valve dysfunction
• Previous rheumatic fever without valvar dysfunction
• Cardiac pacemakers( intravenous and epicardial ) and
implanted defibrillators
Infective Endocarditis
Prophylactic regimens for procedures
Situation
Agent
Srandard general
Amoxicillin
Regimen
Adult; 2.0g orally 1 hour before procedure
Child; 50mg/kg orally
Unable to oral intake
Ampicillin
Adult; 2.0g IM or IV, 30 m before procedures
Child; 50mg/kg 30 min. before
Allergic to penicillin
Clindamycin Adult; 600mg, Child; 20mg/kg 1 h before
Cephalexin
Adult; 2g,
Child; 50mg/kg 1 h before
Azithromycin Adult; 500mg, Child; 15mg/kg 1 h before
or Clarithromycin
Allergic & unable to
Clindamycin or
Oral intake
Cefazolin
Adult; 1g,
Child; 25mg/kg 30 min. before procedure
Prosthetic Heart Valve
Bioprosthetic
Durability
less
Bleeding Cx.
less
Thromboemboism less
Rheology

Indication
pregnant woman
, old age
Focus(BE)
leaflet
Mechanical
more
more
more
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most pts
sewing ring
Prosthetic Valve Endocarditis
Gross findings
Tissue Valve
Mechanical Valve
Redo Cardiac Valve Operation
Considerations
• Careful preoperative study
Chest lateral, Chest CT, Cardiac catheterization &
angiography
• Femoral dissection
• Blood-saving procedure
Autotransfusion, cell saver, aprotinin
• Automatic implantable cardioverter defibrillator
• Tissue valve(cusp tear) > mechanical valve(TE,
SBE)
Infective Endocarditis
Management in septic shock
• Nitric oxide has been implicated in these derangements.
Exposure to endotoxin and cytokines can trigger a de
novo synthesis of the inducible, calcium-dependent
isoform of nitric oxide synthase.
• Methylene blue inhibits this process by decreasing
intracellular cyclic guanosine monophosphate
concentrations through guanylate cyclase inhibition,
thus blocking its vasodilator properties.
• Methylene blue increases arterial pressure, systemic
vascular resistance, and left ventricular stroke work
but does not increase cardiac output, oxygen delivery,
or oxygen consumption. 4
Infective Endocarditis
Indications for surgery
• Infective endocarditis have continued to evolve,
but frequently include new severe valvular
regurgitation, intractable heart failure, abscess
formation, conduction abnormalities, recurrent
embolic events, organism involved(fungal
endocarditis), and presence of prosthetic
material
• While mortality has improved from 30% to 15%
over the past two decades, it remains substantial
Infective Endocarditis
Echocardiographic diagnosis
• Three echocardiographic findings are
considered to be major criteria for the
diagnosis of endocarditis: (1) presence of
vegetations defined as mobile echodense masses
implanted in a valve or mural endocardium; (2)
presence of abscess; or (3) presence of a new
dehiscence of a valvular prosthesis
• With the development of TEE imaging, the
noninvasive detection of vegetations has
substantially improved
Infective Endocarditis
Causes of operative deaths
• Often multifactorial, but the main reasons were
multiorgan failure, low cardiac output syndrome,
intractable sepsis, coagulopathy , technical errors,
stroke, pulmonary embolism, acute myocardial
infarction, ruptured aortic root, valve dehiscence,
retroperitoneal bleeding, and right ventricular failure
• The predictors of operative mortality includes
preoperative shock, prosthetic valve endocarditis, S
aureus, and paravalvular abscess.
Infective Endocarditis
Results of operative treatment
• Surgery for endocarditis continues to be challenging &
associated with high operative mortality & morbidity
• Age, shock, prosthetic valve endocarditis, impaired
ventricular function, and recurrent infections adversely
affect long-term survival
• Long-term survival is satisfactory, particularly for
patients with native valve endocarditis & differences
between native and prosthetic valve endocarditis are
likely multifactorial and include higher operative
mortality, more complex operations, and such patient
variables as older age and worse ventricular function
Anticoagulation
Anticoagulation
Policy for prostheisis
1. Mechanical valves:
All patients should be anticoagulated with coumadin.
In addition, all patients would receive aspirin and persantine.
Persantine is discontinued after 3 months.
2. Porcine or bovine valves:
a) Aortic valve replacement:
Aspirin and persantine starting on the 5th postoperative day for 3 months.
No anticoagulants per se need be given.
b) Mitral and tricuspid valve replacement:
ⅰ) Children with chronic atrial fibrillation or proven intra-atrial clot should
be anticoagulated with coumadin, sapirin and persantine permanently.
ⅱ) Patients in sinus rhythm should be anticoagulated with coumadin,
aspirin, and persantine for a period of 3 months.
All drugs to be discontinued at 3 months.
c) Pulmonary valve replacement:
No anticoagulants are required. ASA is recommended indefinitely.
3. Homograft pulmonary or aortic valve:
No anticoagulants are required. ASA is recommended indefinitely.
Anticoagulation
 Protocol for children
British Columbia children’s Hospital Policy
1. Mechanical valve:
All patients with mechanical valve on the left side of the circulation should be
anticoagulated with coumadin for three months. Coumadin is discontinued after
three months and replaced by ASA(10 ㎎/㎏ per day) plus persantine (3 ㎎/㎏/day)
indefinitely. Patients in atrial fibrillation or with a history of thromboembolism
require life time anticoagulation (coumadin). Patient is then fully anticoagulated
with coumadin when 18 years of age.
2. Porcine or bovine valves:
All patients require coumadin for three months. Coumadin is discontinued after
3 months and replaced by ASA(10 ㎎/㎏ per day) and persantine (3 ㎎/㎏/day).
3. Homograft valve replacement:
all patients require ASA(10 ㎎/㎏ per day).
N.B. no heparin is given postoperatively as coumadin is started after 48 hours (per mouth or
Nasogastric tube). Prothrombin time is to be kept between 1-¹/₂to 2 times normal (15-20second)
Anticoagulation
Prothrombin time & INR
• Determine by %
• INR(international normalized ratio)
• Mechanical vs. bioprostheis
• Cardiac rhythm ; atrial fibrillation
• Location of valve; aortic, mitral, tricuspid
• Age ; old or young
Anticoagulation
Prothrombin time & INR
Anticoagulation
Drug interaction with warfarin
Potentiation
Acetaminophen
Alcohol(if liver D.)
Amiodarone
Chloral hydrate
Cefazolin
Cimetidine
Clofibrate
Erythromycin
Floxin antibiotics
Fluconazole
Isoniazid
Lovastatin
Metronidazole
Omeprazole
Phenylbutazone
Phenytoin
Propranolol
Quinidine
Tamoxifen
Inhibition
Azathioprine
Barbiturates
Carbamazepine
Chlordiazepoxide
Cholestyramine
Cyclosporine
Narcillin
Sucralfate
No Effect
Alcohol (if no liver D.)
Antacids
Atenolol
Bumetanide
Diltiazem
Famotidine
Ibuprofen
Ketorolac
Ketoconazole
Metoprolol
Nizatidine
Ranitidine
Vancomycin
Mechanical Valve Implantation
Pathogenesis of thromboembolism
• The pathogenesis is a complex phenomenon, occurring through an
interaction of a of prosthesis-related and patient-related factors
• Damaged perivalvular tissue and deposition of fibrinogen on the
valve surface activate platelets as soon as blood starts flowing
across the valve and this leads to immediate platelet adhesion and
aggregation, and within 24 hours after surgery, platelet deposition
on the Dacron sewing ring can be imaged radiographically
• Coagulation factors are also directly activated after valve
implantation, leading to further clot formation as a result of the
inherent thrombogenicity of the prosthetic material and sites of
denuded tissue (valve excision site)
• Transprosthetic turbulent flow leads to regional increases in shear
stress, structurally damaging the endocardium, causing a loss of
local resistance to thrombosis.
Mechanical Valve Implantation
Thromboembolic mechanism
• Strong risk factor for thromboembolic complications, especially in
the first three to six months after surgery
• First, the pathologic sequelae of the patients' inherent valvular
disease (atrial fibrillation, dilated left atrium, and dilated left
ventricle) may predispose to areas of stasis and thrombus
formation
• Second, the increased thromboembolic risk early reflect
incomplete endothelial proliferation on the raw intracardiac
surfaces, sewing ring, and suture knots in the initial postoperative
period
• Early thromboembolic risk can also be attributed to
inconsistencies of oral anticoagulation management.
• During the first six months, the thromboembolic risk is up to seven
times greater than in the after months and years.
Mechanical Valve Implantation
Early thromboembolic risk
• The early thromboembolic risk associated with the
placement of a mechanical prosthesis depends on the
complex interactions between the recipient and valve,
the intrinsic thrombogenic properties of the mechanical
valve components, and the diligent management of
postoperative anticoagulation.
• Variable or inadequate anticoagulation, defined as an
INR 25% or more below the therapeutic range, has
been demonstrated to increase the incidence of
thromboembolism 2 to 6 times, especially in the
postoperative period
Mechanical Valve Implantation
Anticoagulation therapy
• In patients not receiving anticoagulation therapy, the
average rate of major thromboembolism is estimated to
be 4 to 8 per 100 patient-years and this risk is reduced
to 2.2 per 100 patient-years with antiplatelet therapy,
and further reduced to 1 per 100 patient-years with
oral warfarin
• Recommended, in their most recent guidelines, that
contemporary mechanical valves in the aortic position
be anticoagulated with a target INR of 2.0 to 3.0, and
mechanical valves in the mitral position be
anticoagulated with a target INR of 2.5 to 3.5 [.
Mechanical Valve Implantation
Antiplatelet therapy
• In the absence of anticoagulation, antiplatelet therapy
seems to be insufficient to prevent thrombi.
• Because platelet aggregation occurs despite
anticoagulation, the co-administration of antiplatelet
agents with anticoagulation has been advocated to
reduce the frequency of thromboembolic complications
• Recommended that the addition of aspirin (80 to 100
mg/day) to warfarin be strongly considered for all
patients with mechanical valves, for patients who have
had an embolus while on warfarin therapy, those with
vascular disease, or those with hypercoagulability
Mechanical Valve Implantation
Early anticoagulation strategies
• The three common early postoperative anticoagulation
strategies (1) oral warfarin starting on postoperative
day one, without the use of therapeutic heparin
anticoagulation; (2) intravenous unfractionated heparin
beginning in the early hours after surgery, oral
warfarin starting on postoperative day one, and the
continuation of heparin until a therapeutic INR has
been achieved; (3) low molecular weight heparin
(LMWH) beginning in the early hours after surgery,
oral warfarin starting on postoperative day one, and
the continuation of LMWH until a therapeutic INR has
been
Mechanical Valve Implantation
Strategies
• Oral warfarin alone
Aanticoagulation with oral warfarin alone has been
advocated as the safest regimen
• Intravenous unfractionated heparin and oral warfarin
Because the risk of thromboembolism is greatest in the
early postoperative period (within 24 hours), with oral
anticoagulation starting on the first postoperative day
• 3. Low molecular weight heparin and oral warfarin
Better safety profile with less thrombocytopenias, less
bleeding, a more predictable and rapidly reached
anticoagulant effect, the possibility of self-administration
without laboratory monitoring, and shorter hospital stays
Anticoagulation
Thromboembolic level (TEL)
• TEL 1; Presence of nonobstructive thrombus in the
vicinity of the prosthetic valve as identified by
clinical imaging (echocardiography);
• TEL 2; Documented evidence of peripheral limb
and visceral embolization (solid organs, coronary
thrombus);
• TEL 3; Documented evidence of central nervous
system embolization (transient ischemic attack or
cerebrovascular accident);
• TEL 4; Prosthesis thrombosis requiring
thrombolysis or emergency surgery;
• TEL 5; A fatal thromboembolism.
Anticoagulation
Bleeding level (BL)
• BL 1; Mild bleeding such as recurrent epistaxis or
periodontal bleeding (more than two events) and
gastrointestinal bleeds not requiring hospitalization
or transfusions;
• BL 2; Documented large pericardial effusion (>1 cm
thickness on echocardiography);
• BL 3; G-I bleeding requiring hospitalization,
transfusion, endoscopic intervention or surgery;
• BL 4; Documented cardiac tamponade requiring
intervention;
• BL 5; Documented CNS hemorrhage
• BL 6; Fatal bleeding.
Anticoagulation
Tissue valved conduit replacement
• Small patients with a greater mismatch between
conduit size and normal valve size, prophylactic
anticoagulation is recommended.
• Due to the initially good overall performance, the
Contegra bovine jugular vein conduit has become our
preferred device for RVOT reconstruction.
• Anticoagulated with heparin during their hospital stay
followed by aspirin (10 mg/d) after discharge until they
gain a weight of 5 to 6 kg. Since the introduction of this
regimen we have not observed any other case of conduit
valve thrombosis
Anticoagulation
Systemic-pulmonary shunt
• PTFE conduit in Fontan patient received warfarin for
6-12 months for anticoagulation to maintain an INR
between 2.5 and 3.0. In addition, they were
administered aspirin (5 mg/kg per day), which was
continued indefinitely.
• Trend in recent years toward using smaller shunts has
contributed to a decrease in perioperative mortality due
to excessive pulmonary blood flow but perhaps also to
an increase in the incidence of shunt thrombosis
• Shunt size is made more difficult by variations in
technique such as the location of the proximal end of
the shunt and its length
Anticoagulation
Tissue valve implantation
• Warfarin was given to patients in sinus rhythm for the
first 3 months postoperatively, then aspirin at a dose of
150 mg.
• Keep on warfarin in patients in chronic atrial
fibrillation and maintain the INR between 2.5 and 3.5.
• Aanticoagulate our patients with tissue valves for the
first 3 months postoperatively because the
thromboembolic risk outweighs the risk of bleeding in
this group of patients
• Thromboembolic rates in patients with aortic
pericardial valves parallel those observed in patients
with aortic porcine valves
Ideal Anticoagulation
Factors of clinical situations
• Valve replacement
MVR, AVR, DVR, TVR
Mechanical vs. tissue
• Bentall operation
• Mitral ring annuloplasty
• Graft replacement of large vein
• Pulmonary embolism, deep vein thrombosis
• Atrial fibrillation, LA thrombi
Ideal Anticoagulation
Ideal levels of INR
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•
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•
•
Mitral valve replacement( 2.5 to 3.5 INR )
Aortic valve replacement(2.0 to 3.0 INR)
Tricuspid valve replacement
Pulmonary valve replacement
Annuloplasty rings
Extracardiac conduit Fontan operation
Prosthetic angioplasties
Anticoagulation
Choice of prosthesis
• The incidence of anticoagulation-related
complications such as bleeding and
thromboembolic events increase sharply with
advanced age
• Oral anticoagulation is required lifelong, some
may argue that implantation of bioprostheses
should be preferred instead of mechanical
prostheses in order to reduce the risk of
anticoagulation-related complications with
advanced age
Postoperative Blood Loss
Factors
•
•
•
•
•
•
•
•
Prior intake of antiplatelet drugs
Endothelial response to cardiopulmonary bypass
Systemic inflammatory response
Systemic hypothermia
Heparin excess and heparin rebound
Platelet dysfunction and fibrinolysis
Type of operation, reoperation, duration of CPB
Presurgical anticoagulation status
Hemostasis
Physiology
• Vascular function, which consists of three discrete
layers; intima, media, and adventitia.
The intima comsists of a monolayer of
nonthrombogenic endothelial cells and an internal
elastic membrane.
The media consists of smooth muscle cells and the
adventitia, external elastic lamina and membrane and
supportive connective tissues.
• The platelets, which must be normal in both number
and function
• The plasma protein, which include procoagulants,
anticoagulants, and fibrinolytic proteins
Anticoagulants
Warfarin
• Interfere with vitamin K –mediated formation of
clotting factors, including prothrombin as well as factor
II, VII, IX and X, ; warfarin may also block the release
of prothrombin from the liver
• The absorption of vitamin K , as well as warfarin, is
influenced by bile salts , dietary fat and in addition,
affected by gastrointestinal tract transit time and
intrinsic hepatic function and oral antibiotics that alter
the gut flora
• The maximam teratogenic action occurs between 6 and
9 weeks of pregnancy(oral anticoagulants cross the
placenta and produces fetal abnormality)
Anticoagulants
Warfarin
• Action; interfere with hepatic synthesis of vitamin K –
dependent coagulation factors(II, VII, IX,X)
• Stability; protect from light in IV form(inject over 1-2
minutes)
• Dose adjustment in hepatic disease
• Dietary consideration; foods in high vitamin K inhibit
anticoagulant effect
• Contraindications; hypersensitivity to warfarin or any
components of formulation of bleeding tendency
• Adverse reaction; bleeding is major and others
nonspecific & some allergic
Warfarin
Pharmacokinetics
• Onset of action; anticoagulation effect from oral 36-72
hours, peak therapeutic effect 5-7 days, INR increase
in 36-72 hours, IV administer as a slow bolus injection
2-5mg/day
• Absorption; rapid , oral
• Stability; protect from light in IV form(inject over 1-2
minutes)
• Duration; 2-5 days
• Metabolism; hepatic
• Half life elimination; 20-60 hours
Aspirin
Pharmacokinetics
• Mechanism of action;Inhibits prostaglandin synthesis,
acts on the hypothalamus heat-regulating center to
reduce fever, blocks prostaglandin synthetase action
which prevents formation of the platelet-aggregating
substance thromboxane A2
• Duration; 4-6 hours, rapid absorption, & rapid
dstribution and cross the the placenta and enter fetal
circulation and also enters breast milk
• Metabolism; hydrolyzed to salycylate(active) by
esterase in GI mucosa, RBC, blood; primarily by
hepartic conjugation; metabolic pathways are
saturable
Aspirin
Actions
Mechanism
• Aspirin inhibits platelet aggregation by irreversible
inhibition of platelet cyclooxygenase and thus inhibits the
generation of thromboxane A2
 Child dose
• Antiinflammatory, 60-80mg/day/Kg in every 4-6 hours
• Antiplatelet effects; 3-5mg/Kg– 5-10mg/Kg in single dose
• Mechanical prosthetic valve 6-20mg/Kg in single dose
 Adult dose
• 75-325mg/day in CABG, 80-325mg/day in PTCA, 160325mg in stent, 30-325mg/day to prevent stroke(upto
1300mg)