Transcript Fate of Fresh Autologous Pericardium as Cardiovascular implant

Diseases of Pericardium
Seoul National University Hospital
Department of Thoracic & Cardiovascular Surgery
Pericardium
Anatomy
• The pericardial sac is composed of the fibrous and the
serous pericardium
• Fibrous pericardium is the tough external fibroelastic
outermost layer of the pericardium & the inner layer,
serous pericardium, is the smooth mesothelial layer
• The inner layer pericardium consists of outer parietal
and inner visceral layer
• Outer parietal layer sits on the inner aspects of fibrous
pericardium and the inner visceral layer of serous
pericardium is the mesothelial component of epicardium
• Epicardium consists of an inner fibroelastic connective
tissue layer & outer superficial mesothelial membrane
Pericardium
Developmental anatomy
• During embryologic development, heart invaginates
into the serous pericardium and is coated by the inner
visceral layer of serous pericardium
• At the roots of great vessels, the investing inner visceral
layer of serous pericardium is continuous with the
outer parietal layer of serous pericardium
• The potential space between the outer parietal layer of
serous pericardium and the inner visceral layer of
serous pericardium is pericardial space and normally
contains only a small amount of serous fluid and the
pressure is subatmospheric under normal condition
Pericardium
Anatomy
Pericardium
Physical protection of adhesion
1. Loss of mesothelial integrity
1) Mechanical damage
surgical swabs, instruments desiccation, cold stretching,
blood spilling
2) CPB
2. Pathogenesis of adhesion
1) Deposition of fibrin in damaged area
2) Loss of fibrinolytic activity
3. Methods of preventing adhesion
1) pericardial meshing, padding
2) Dextran pericardial washing
3) pericardial substitute
4) Pharmacologic agents (methyl PD)
5) primary closure
Diseases of Pericardium
Classification
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Effusive pericarditis
Constrictive pericarditis
Cardiac tamponade
Postoperative pericardial effusion
Postoperative cardiac tamponade
Postpericardiotomy syndrome
Congenital defect
Neoplastic process
Benign mass
Pericardial cyst
Pneumopericardium
Chylopericardium
Effusive Pericarditis
 Definition
Inflammatory stimulation of the pericardium which results
in the accumulation of appreciable amounts of pericardial fluid
 Etiology
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Idiopathic ; common
Viral
; often
Uremic
Tuberculosis
Purulent
Neoplastic
Traumatic
Traumatic with hemopericardium
Drug-induced
Effusive Pericarditis
 Symptoms and signs
• Vary depending on the etiology and the speed with
which the pericardial fluid has accumulated
• The quality of pericardial fluid also play a role in
symptomatology
 Diagnosis
• History, physical examination, chest radiography,
echocardiography
 Theray
• Medical and surgical management
Pericardium
• Computed tomography scan of chest – pericardial fluid is seen
around the heart
Constrictive Pericarditis
 Definition
Chronic inflammatory process of fibrous and serous
layers of the pericardium that leads to pericardial
thickening and compression of the cardiac chambers,
ultimately with an associated significant reduction in
cardiac function
 Etiology
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Idiopathic
Viral
Tuberculosis
Effusive
Postcardiotomy
Radiation induced
Constrictive Pericarditis
History
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Galen ; Cicatrical thickening in animal in A.D 160
Lower ; Acute & chronic pericarditis in 1669
Lancisi ;Autopsy description in 1728
Pick ; A clinical report in 1896
Rehn & Sauerbruck ; Successful partial
pericardiectomy in 1913 in German
• Church, Beck ; Successful series in 1929, 1931 in States
Constrictive Pericarditis
Pathophysiology
• Clinical features derives from basic abnormalities of
diastolic function
• Ventricular filling is impaired and ventricular stroke
volume reduced as a result of reduced compliance of
fused cardiac and pericardial mass.
• For a brief period in early diastole, ventricular filling is
rapid. However, the limit of ventricular distensibility
is reached rapidly, and right ventricular pressure pulse
displays an early diastolic dip and then a high diastolic
plateau ( square root sign )
Constrictive Pericarditis
 Symptoms and signs
• Rare in childhood
• Easy fatigability, DOE and even syncope on exertion
• Jugular venous distention, distant heart sound,
hepatomegaly, ascites in advanced cases
 Diagnosis
• Lack of cardiac enlargement and calcification on chest
radiography , pericardial thickening but not always on
echocardiography and CT
• Equalization of mean RA, PA wedge, RVED and LVED
pressure help differentiate constrictive pericarditis to
LV failure on cardiac catheterization
 Therapy
• Medical and surgical early pericardiectomy
Constrictive Pericarditis
Natural history
• Knowledge of surgically untreated patients is incomplete
• The interval between the etiologic event and onset of
clinical evidence of constriction varies between the few
months and many years, and the factors that determine
rate of progression are unknown
• Atrial fibrillation commonly occurs at some stage and
results in sudden deterioration in circulatory status
• Once signs and symptoms develop, only a semi-invalid
life can be led over an interval of 5 to 15 more years
• When the clinical syndrome includes ascites, progression
is more rapid, particularly in children
Constrictive Pericarditis
 Pressure tracing
• The plateaued end-diastolic pressure of the right ventricle
& equalization of diastolic pressures in all cardiac chamber
Constrictive Pericarditis
Clinical spectrum
• The advent of antitubercular chemotherapy brought
down the mortality for tuberculous pericarditis from
90% to about 40%
• In tuberculous pericarditis, institute the antitubercular
therapy for a minimum period of 12 months
• The role of corticosteroids in the management of
tuberculous pericarditis is controversial
• The diagnosis of constrictive pericarditis remains a
challenge and is achieved by echocardiography,
computed tomography, magnetic resonance imaging,
and cardiac catheterization
Constrictive Pericarditis
Distinction to restrictive cardiomyopathy
• Differentiation of constrictive pericarditis to from
restrictive cardiomyopathy with diastolic ventricular
dysfunction can be quite challenging
• Clinical assessment, MRI, cardiac catheterization,
echocardiography, radionuclide ventriculography &
endomyocardial biopsy neeeded
• For patients with constrictive pericarditis, early
complete surgical pericardiectomy remains the only
definitive treatment
Pericardiectomy
Definitions
• Total pericardiectomy was defined as wide excision of the
pericardium with the phrenic nerves defining the posterior
extent, the great vessels including the intrapericardial
portion of and superior vena cava–right atrium junction
defining the superior extent, and the diaphragmatic surface,
including the inferior vena cava–right atrium junction
defining the inferior extent of the pericardial resection.
• Constricting layers of the epicardium were removed
whenever possible
• Any excision less than total was considered partial.
Pericardiectomy
Surgical techniques
• The objective is to remove all pericardium from the
cardiac structures including the right & left ventricle,
right & left atrium, aorta, pulmonary artery, SVC, IVC,
pulmonary veins
• In epicardial peel is adherent, a cross-hatching waffle
procedure, or multiple incision of peel ( turtle cage
operation ) allow myocardial expansion.
• On the ventricular surface, dissection may proceed
outside the epicardium in the area of coronary arteries,
but the dissection over the great arteries and atria
should remove the overlying epicardium
• Management is curative surgical pericardiectomy and
should be instituted rapidly once diagnosis is made
Pericardiectomy
Surgical approach
• Left anterolateral thoracotomy was the preferred
option in the setting of purulent pericarditis to avoid
sternal infection
• Median sternotomy approach was preferred in the
following cases: (1) annular constrictive pericarditis,
(2) calcific pericardial patch compressing the right
atrium & right ventricular outflow tract, (3)
extracardiac intrapericardial mass, (4) presence of a
gradient between the superior & inferior venae cavae
& right atrium 2 mm Hg or greater, (5) constriction
after previous open heart surgery, and (6) recurrent
constrictive pericarditis after partial pericardiectomy
Pericardiectomy
Surgical results
• Regardless of the operative approach or the extent of
pericardial resection, a subset of patients with
constrictive pericarditis will develop low-output
syndrome after pericardiectomy
• Poor results, with persistent elevation of ventricular
filling pressures, have been variously attributed to
inadequate decortication, fibrous invasion of the
myocardium, atrophy of myocardial fibers,
"remodeling" of the ventricles, worsening tricuspid
regurgitation, and postoperative mitral regurgitation
secondary to papillary muscle elongation
Constrictive Pericarditis
Results of surgical treatment
• Survival
Early death
Time-related survival
• Modes of death
• Incremental risk factors
Preoperative functional class
High RV end-diastolic pressure
Previous radiation therapy over chest
• Hemodynamic results
• Functional status
• Reoperation
Cardiac Tamponade
Characteristics
• Accumulation of fluid within the pericardial space can
cause a rise in pericardial pressure that leads to
impairment of ventricular diastolic filling as defined
cardiac compression
• All intracardiac pressures will equalize during diastole
• The end result of this physiologic state is a lack of left
heart filling, leading to a lack of cardiac output and
shock
• Initial compensatory mechanisms such as tachycardia
will precede & herald the eventual state of circulatory
collapse
Cardiac Tamponade
Diagnosis
• Beck’s triad
Elevated CVP
Decreased arterial pressure
Muffled heart tones
• Pulsus paradoxicus
• Kussmaul’s sign
Postpericardiotomy Syndrome
Definition
• Pericardial inflammation secondary to either cardiac
muscle damage or surgical cardiotomy associated with
pain, friction rub, and occasionally ECG changes
suggestive of ischemia.
• Unclear etiology & thought to be an autoimmune
disorder
• Symptoms typically appear 3 – 6 weeks after
pericardiotomy including fever, arthralgia, progressive
pericardial effusion, and sometimes pleural effusion
• Usually lymphocytosis, elevated ESR; eosinophilia and
elevated C reactive protein may be present
Postpericardiotomy Syndrome
 Etiology
• Unclear and is thought to be an autoimmune disorder;
concurrent fresh or reactivated viral illness is also felt
to play a role in triggering the immunologic response
& seasonal variation with a higher incidence in winter
 Therapy
• Initial bed rest & nonsteroidal antiinflammatory agents
Indomethacin or salicylates ( 60-80mmg/Kg/day )
• Prednisolone for refractory cases or recurred case
• Surgical intervention for difficult case
Pericardial Defect
Congenital defects
• A rare group of lesions which range from isolated
defects to complete absence of pericardium
• Three types are complete absence, left-sided defect
(most common), and right-sided defect.
• Patients may be completely asymptomatic or have
exertional or nonexertional chest pain, cardiac
arrhythmias, syncope, sudden death, or incarceration
of myocardium
• Surgery is indicated for arrhythmia, cardiac torsion,
cardiac herniation, or debilitating chest pain
• Surgical repair involves pericardial reconstruction
( pericardioplasty) using xenograft or Gore-tex
Chylopericardium
Definition
• A chylous effusive process of the pericardium
and cause either acute or chronic cardiac
tamponade
Etiology
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Idiopathic
Posttraumatic
After thoracic surgery
Postpericardiotomy
Neoplastic in origin
Chylopericardium
After cardiac surgery
• Incidence
0.2%, frequent after Fontan operation
• Etiology
Thoracic duct injury ; most common
Damage of lymphatics of pericardium
Elevation of systemic venous pressure
Congenital lymphatic dysplasia (Down syndrome)
• Treatment
Diuresis & dietary modification ( low-fat mediumchain trigliceride ), parenteral nutrition, repeated
centesis.
Exploration to ligate after 2 weeks medical failure
with pleuropericardial window or pericardiostomy
Pericardial Reentry
Surgical adhesion
• Lead to more difficult sternal reentry and cardiac
dissection, to blunted visibility of distinct cardiac
structures, to potential injury of cardiac structures
(including the atria, ventricles, and coronary arteries),
as well as to an increased risk of surgical bleeding, all
associated with an increase in morbidity and mortality.
• Reoperations due to adhesions are more timeconsuming, and because of the increased difficulty they
are associated with a greater level of stress for the
individual surgeon.