13 - Cardiovascular Sciences Forum

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CARDIOVASC SCI FORUM - Jan/Mar - 2010; 5 (1): 1 - 49
CONTENTS
EDITORIAL
Rheumatic Fever – Facing this challenge in Brazil and worldwide (English)
Moisés Ezequiel Chissonde
08
ORIGINAL ARTICLE / ARTIGO ORIGINAL
Is there a histological difference between decellularized aortic tissue and pulmonic
trunk tissue? (English)
Torsten Christ, Pascal Maria Dohmen, Sebastian Holinski, Melanie Schönau, Wolfgang Konertz
13
Vídeo-assisted “No touch” Saphenous Vein Harvesting (English)
Otoni M. Gomes, Melchior Luiz Lima, Elton Francisco Nunes Batista, Michael R. Dashwood (By invitation),
Domingos S. Souza (By invitation)
19
Rabbit and Human Compared Mesenteric Arterial Anatomy (English)
Pedro Henrique Lima Prata, Walter Ferraz Flávio Júnior, Lucas Ferreira Santana , André Santiago da Silva, Luiz
Alberto B. Porto, Luciano Dantes de Paula, Otoni M.Gomes
23
Effect o Exercise o Entricular Remodeling After Experimental Myocardial
Infarction in Rabbits (English)
29
Manuel Rodríguez, Germán E. González, Celina Morales, Carlos Bertolasi, Ricardo Jorge Gelpi
HOW TO DO / COMO FAZER
Economic Roller Ventilador for Small Animals (Português)
Otoni Moreira Gomes
34
UPDATING ARTICLE /ARTIGO DE ATUALIZAÇÃO
Esophageal Protection During Atrial Fibrillation Ablation. (English)
Protección Esofágica Durante Ablación de Fibrilación del Atrio. (Spañol)
Proteção Esofágica Durante Ablação de Fibrilação Atrial. (Português)
Henrique César de Almeida Maia, Simone Nascimento dos Santos, Benhur Davi Henz, Luiz Roberto Leite da Silva
37 / 41 / 44
UPCOMING EVENTS
47
Cardiovasc Sci Forum 2010; 5(1): 8-12
EDITORIAL
Rheumatic fever, facing this challenge
in Brazil and worldwide
Febre Reumática; enfrentando este
desafio no Brasil e no mundo
Moisés Ezequiel Chissonde
Rheumatic Fever is a bacterial,
inflammatory, non-suppurative and autoimmune disease of the connective tissue. It
results from delayed complications of of the
streptococcal pharyngotonsillitis. The causal
agent is Lancefield’s Beta-Hemolitic Group A
Streptococcus, or streptococcus pyogenes.
Between 1 and 4 weeks after
infection the patient presents inflammation
and pain on joins (poliarthritis), carditis,
neurological manifestations (chorea) and
dermatological lesions (Erythema marginatum
and subcutaneous nodules). In absence
of treatment patients with carditis develop
permanent injury of valves, heart failure due
to stroke and atrial fibrilation1.
Rheumatic affects mainly children and
adolescents between 5 and 15 years old (peak
of incidence at 12 years old), with genetic
predisposition in and under socioeconomic
and sanitary difficult conditions. The results of
some studies suggest that the girls are more
affected than boys, the reason is unknown.
It is the main cause of acquired cardiac
disease among children and young adults. The
incidence is 10/100.000 children/year. The
prevalence of the rheumatic carditis among
scholar children in developed countries, is
0,6/1000. In developing countries is above
7/1000. In Brazil, the prevalence is 35/1.0002.
Its estimated that 2.5% to 4% of
children with pharyngitis , develop rheumatic
fever. According to IBGE (Brazilian Institute
of Geo-statistics), in Brazil are registered 10
million cases of bacterial tonsillitis per year.
30 thousand of them develop rheumatic
Fever and half of them (15 thousand) may
have heart lesions1.
Transmission and clinic signals occur
as result of genetic factors (susceptibility
of the patient) and immunologic factors.
There are 3 immunologic phenomena: Direct
action of the bacteria in the tissues; action
of the bacterium toxins in affected tissues
(mainly streptolysin); and autoimmune/
hipersensibility reactions.
Due to molecular mimicry (antigenic
similarity) of streptococcal proteins with some
human tissues, the antibodies produced
against bacterium have crossed reaction
against structures/of the patient (sinovia,
joints cartilage, myocardium, cardiac valves,
neurons of the caudate and subtalamic
nucleus). Once affected these structures,
appears the clinical manifestations of the
rheumatic fever. The most common are
arthritis, the carditis, the valve disease and
chorea. Its common also to find residual
injuries in heart as calcification ans fibrosis3.
There is a particularity in Australian
aboriginal people. Among them, the causal
agent of rheumatic fever is a pyodermic
streptococci strain which causes skin infection.
In children of this ethnic group, Rheumatic
Fever is not preceded by pharyngitis, but by
pyoderma. Infections from Coxsackie virus B
is also able to provoke valve injuries3,4.
Arthritis. Occurs in 75% of patients
and it is characterized by mono-arthritis of
Correspondence:
Moisés Ezequiel Chissonde, MD
Rua Pedro Domingos Vitali,160, Pq. Itália
Campinas – SP, Brasil - CEP: 13036-180
E-mail: echissonde@ yahoo.com.br
great joints (knees, ankles, fists and elbows),
painful (it can generate pseudo-paralysis).
The arthritis is migratory, non-symmetric and
persists for 1 or 2 days in each joint.
Rheumatic Carditis. Uses to be a
pancarditis (endocarditis, myocarditis and
pericarditis). It occurs in 40 to 70% of the
patients. It can have mild presentation or involve
definitive cardiac sequelae. It is the main factor
of burden and mortality. Endocarditis uses to
affect the valvular tissue, mainly, mitral valve,
followed by aortic valve and rarely pulmonary
and tricuspid. Miocarditis culminates with
the rupture of chordae tendinae, resulting in
cardiomegaly, heart failure and pulmonary
congestion. Occasionally it is possible to find
pericarditis and pericardium stroke.
Sydenham Chorea. Occurs between 1
and 12 months after the streptococcal infection
and affects 5%-36% of patients. It consists on
generalized, uncoordinated, involuntary and
abrupt movements, which affects face, lips,
eyelids and tongue. Usually the mother or the
patient relates slips when walking, dysarthria,
easy falls, drop of objects (plates, cups, books),
has difficulties of writing and has emotional
lability. Symptoms are precipitated by stress
situations and reduced by rest or sleep.
Erythema Marginatum and subcutaneous
nodules. This symptoms are rare, but very
specific to rheumatic fever. Erythema is an
evanescent, macular, nonpruritic rash with pale
centers and rounded or serpiginous margins.
Lesions vary greatly in size and occur mainly
on the trunk and proximal extremities, not on
the face. It is more common in patients with
chronic carditis.
Subcutaneous nodules are firm, painless,
freely movable nodules, usually located over
extensor surfaces of the joints and tendons.
The diagnosis of rheumatic fever is
clinical and is based on modified Jones’ criteria
(American Heart Association)5. Diagnosis is
made by evidence of previous infection by
group A streptococcus (Elevation ASL or rapid
test BHGAS) + 2 major criteria or 1 major criteria
+ 2 minor.
Laboratory tests. They confirm the
diagnosis of inflammation and streptococcal
infection and allow control of the evolution
and assessment of therapeutic response. ASLO
dosage, Erythrocyte sedimentation rate (ESR)
and C-reactive protein (CRP) are the most
commonly used.
According to the Brazilian Guidelines,
treatment should involve 3 phases: General
Measures (hospitalization, rest and control of
fever), Eradication of streptococci (Eradication
of streptococci and prevention recurrence
and sequelae), Treatment of symptoms.
The approach is summarized in Table 1.
The approach of cardiac sequelae toward
preservation of patient life is made by surgical
or per-cutaneous intervention6.
The third world countries has 79% of
all rheumatic fever world patients. Asia, Africa,
Latin America and Mediterranean are the most
affected regions, with up to 1% of school-age
children affected.
Table 1: Primary and secondary prophylaxis of rheumatic fever
Rheumatic Fever affects 18 million
people. Only the Rheumatic Carditis is present in
15 million people. There are 470.000 new cases
of rheumatic fever every Year2. Approximately 3
million develops valve lesions and congestive
heart failure. These, require repeated hospital
admissions and long medical treatment with
drugs that are difficult to manage (anticoagulants,
for example). Many cases, require cardiac
surgery or interventionist procedure within next
5 -10 years. About 30% die within 12 -20 years.
Rheumatic disease leads to premature death. A
study in India found that age of death is around
24,4 years old7.
Rheumatic
heart
disease
causes
functional and psychosocial limitations, resulting
in decline of productivity, reduction on life
quality and temporary or permanent absence in
school or professional activities8.
All these factors involve high costs for
health programs and have a significant economic
impact on the lives of patients and their families.
A Brazilian study showed that 22% of patients
with rheumatic fever had high rate of repetition
in school, and 5% of patients parents lost their
jobs as result of their absences9.
After introduction of penicillin on the
approach of infections, the incidence became
reduced. From 77/100.00 in the 1930s declined
to 30/100.00 in the 1970s and 10/100.000
in the 1980s. In United States the incidence
today is less than 1 case/100.000 inhabitant10.
In developing countries the rate of incidence
is 20.3/100.000. The highest rates are among
Pacific indigenous peoples of Australia and New
Zealand, with 374 new cases/100.000 inhab,
followed by Asia with 37.6 new cases/100.000
inha2.
Prevalence of rheumatic heart disease in
the world today is 1.3/1.000. In the developed
countries this rate is 0.3 / 1000. In developing
countries still remains above 2/10003 and in
these countries, rheumatic disease is responsible
for 12% to 65% of hospital admissions related
to cardiovascular diseases. The overview of
prevalence in the world is illustrated (Figure 1) . In
the 90s the U.S. had a prevalence of 0.6/1.000,
Japan 0.7/1.000, Asia 0,4-21/1.000, Africa 0,315/1.000 and South America 1-17/100.000.
Currently U.S. and developed countries
have a prevalence of 0.3/1.000, Asia 0,221/1.000, Africa 1,8-5,7/1.000 and South
10
Figure 1: Worldwide prevalence of Rheumatic cardiac disease
Source: Lancet Infectious diseases 2005.
America 2 - 4.1/100.000. The highest rates are
registered in sub-Saharan Africa (5.7/1.000),
among Indigenous people in Pacific, Australia
and New Zealand (3.5/1.000) and Central Asia
and Caucasus (2.2/1.000)2.
Actually there are 349.000 deaths/
year2. During 2002, China, India, Pakistan,
Indonesia and Bangladesh had highest rates,
with over 10.000 deaths each one11. In the lack
of antibiotic prophylaxis 1- 2% of patients die
per year. When prophylaxis is used the rate is 0
- 0.6%/deaths/year.
The prevalence of rheumatic fever in
Latin America is 2.8/1.000. Bolivia and Brazil
have the highest rates with 5.7 and 3.6/1.000
respectively2. In the region, is responsible for
7% of hospitalizations among children and
3% among all ages. In Chile and Venezuela
the disease is notifiable and in Brazil is part of
the health primary care program12. Due to the
scarcity of statistic data, this editorial focuses
on Brazilian reality.
The prevalence of rheumatic heart
disease in Brazil is 1-7/1.000. In all the
regions of the country the incidence is falling1.
According to the Government Health System
(SUS) data, the mortality rate among patients in
public hospitals was 6.8% in 2005 and 7.5% in
200413. The management of rheumatic fever
and its complications has an annual social cost
over 51 million dollars. This was a conclusion
of a research9 which observed 100 patients
under 18 years old during 12 months. In this
this period, the total cost was U$319/patient/
year in the SUS and U$ 684,351/patient/year in
the private hospitals system. Direct and indirect
expenses consumed 1.3% of annual family
incomes. The loss of working days by parents
of patients was 22.9% (901 days/year), due to
repeated visits, hospitalizations and surgeries.
About 5% of parents lost their jobs. Sick
children showed poor academic performance
(repetition rate of 22%).
Surgeries and Interventionist procedures
had expended of 94 million of Brazilian Reals
in 2005 and 100 million in 20071. In 2004
30% of cardiac surgeries performed were due
to rheumatic heart disease.
Brazilian government pays about U$D
4.000,00/surgery. In the other side, the cost
of primary prophylaxis is less than U$D 1,00
for a single dose of Benzathine penicillin and
secondary prophylaxis costs less than U$D
16,00/year/patient. According to a recent
study that involved 6 Brazilian states, the
rate of recurrence of rheumatic fever after
treatment is 21.5%14. The great achievement
on this matter in Brazil, was the creation of
the Brazilian Program for Rheumatic Fever
Prevention (PREFERE) in 2003, by government.
It aims to reach school community (students,
teachers, parents and workers) with information
about the disease. Encourages early diagnosis
among children and referral of suspected
cases to health professionals for appropriate
treatment13.
In 1954 World Health Organization
(WHO) held the first meeting about rheumatic
fever burden and mortality. In 1972 created
prevention programs in 7 countries of Africa,
Asia and America. In 1999 defined the
prevention of rheumatic fever as priority15 and
in 1966 began to establish research centers for
diagnosis of streptococcal infections in China,
Philippines and Vietnam. These centers support
control programs14. These programs have been
adopted in several countries, resulting in the
decline of the incidence, prevalence and costs
with the disease and its complications.
Currently there are 3 programs sponsored
by the World Health Organization. Two of
them cover 22 countries in collaboration with
local governments. In countries contemplated
as Cuba, Martinique, Pakistan, Zambia and
Philippines, incidence and prevalence have
fallen significantly. A 3rd program in partnership
with WHO and UNESCO (United Nations
Fund for Education and Culture) provides
literature in different languages, to support
several control programs across the world.
The World Heart Federation (WHF) works on
international partnerships to provide resources
to control programs in developing countries
and advocates creation of statistical databases
in several countries, to register rheumatic heart
disease data (diagnosis, classification, severity,
secondary prophylaxis, cardiac surgery and
deaths)16.
Production of vaccines against group A
streptococci is the great challenge for the future.
Researches for that are been running for more
than 18 years. There are over 200 serotypes
and streptococcal immunity must be available
for each one of them. This is the major difficult.
Some researches suggest that a twelvevalency
vaccine (with fragments from 12 serotypes) may
bring protection with 85% of effectiveness13.
In Brazil there is a research project,
held by InCor Immunology Laboratory, at
Hospital das Clínicas, University of São Paulo,
involving more than 12 reserchers17 which uses
fragments of M1 serotype (the most common).
Initial tests reveals that the vaccine achieved
50% protection in mice. Results are expected
In human. Another study is held at Rockefeller
University in USA. The researchers aim to
produce a multivalent vaccine resulting from the
combination of fragments from M-serotype and
Escherichia Coli18. Pharmaceutical companies
are also investing in researches for this
purpose. Rheumatic fever and rheumatic heart
disease are public health challenges especially
in developing countries. Among aboriginal , as
part of etiopathogenic approach, it is essential
to consider pyoderma.
Diagnose and treatment of of rheumatic
fever sequelae carries high economic costs to
patients, their families and society. It is very
important that governments promote control
programs, which may include training and
clinical screening of symptomatic children. The
use of echo cardiogram increases greatly the
diagnostic accuracy and the detection of mild
cases, with chances to develop sequelae. It is
important to ensure access to this diagnosis
method to people, especially in countries with
low-income populations.
The great hope for prevention and
eradication of disease is the production of a
vaccine against streptococcus. Researches are
going on toward this goal.
11
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2. Carapetis, Jonathan R, The Current Evidence
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2009]
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7. Kumar R, Raizada A, Aggarwal AK, Ganguly
NK. A community-based rheumatic fever/
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12
CHRIST, T et al - Tissue engineering of heart valves
ORIGINAL ARTICLE
ARTIGO ORIGINAL
Is there a histological difference between decellularized
aortic tissue and pulmonic trunk tissue?
Existe diferença histológica entre os tecidos
descelularizados da aorta e do tronco pulmonar?
Torsten Christ, Pascal Maria Dohmen, Sebastian Holinski, Melanie Schönau, Wolfgang Konertz
Abstract
Background: Tissue engineering is a
promising approach to overcome problems
associated with biological heart valve prosthesis.
Key for creating tissue engineered heart valves
is the optimal scaffold, showing good biocompatibility and allowing in vivo assembling of
heart valves, which have regenerative potential.
This study investigated differences between
porcine aortic and pulmonic scaffolds.
Results: Evaluation in Haematoxylin/
eosin staining showed significant higher
(p<0.001) inflammatory reaction in scaffolds
than in aortic scaffolds after decellularization.
This was confirmed by staining for monocytes,
which could be seen significantly more
(p<0.001) in pulmonic tissue. Fibroblasts could
also be detected significantly more (p=0.001)
in pulmonic tissue.
Methods: Thirty Lewis rats were
investigated using the subdermal rat model.
We implanted respectively decellularized
aortic and decellularized pulmonic wall-tissue
specimens. Explantation was performed 2,
4 and 6 weeks after implantation. Afterwards
gross examination, histological evaluation
(Haematoxylin/eosin-staining,
Von-Kossastaining) and immunohistochemical evaluation
(Monocyte-staining, Fibroblast-staining) was
performed and semi-quantitative analysis
conducted.
Conclusion: Results indicate that
decellularization of pulmonic and aortic
tissue leads to different host reactions. In this
study-setup pulmonic tissue showed stronger
cellular infiltration especially with leucocytes.
Therefore we can assume higher inflammatory
potential of decellularized pulmonic tissue than
decellularized aortic tissue.
Keywords:
Tissue
engineering,
Decellularization, Recellularization, Inflammation, Rat subdermal model
Institution:Department of Cardiovascular Surgery,
Medical University Berlin, Charité Hospital, Berlin, Germany
Correspondence: Torsten Christ - Medical University Berlin, Charité Hospital Department of Cardiovascular Surgery / Charitéplatz 1
10117 Berlin-Germany
Phone: +4930450522092 / Fax: +4930450522921 /E-mail: [email protected]
13
INTRODUCTION
Tissue engineering is a promising
approach to overcome problems associated
with glutaraldehyd-fixed biological heart valve
prosthesis, such as calcification and degeneration,
which prospectively results in re-operations.1
Many studies occupy this matter evaluating
specific issues within tissue engineering. One
major topic is creating an optimal scaffold,
which shows no antigenic potential, allows
emigration of host cells and consequently the
in vivo assembling of heart valves, which are
able to remodel, regenerate and have growth
potential.2,3 Various approaches have been
presented. Mayer et al for example tried to work
with biodegradable polymer scaffolds.4 Others,
including our group, preferred biological
scaffolds to benefit from the given anatomy,
structure of the extracellular matrix5 and better
attachment of cells.5,6 A decellularized heart
valve was developed, which revealed in animal
experiments excellent hemodynamic properties
and repopulation by host cells without any signs
of calcification.7 This study was performed to
evaluate the histological difference between
decellularized porcine wall tissue from the aorta
and the pulmonic.
METHODS
All experiments were performed in
accordance with the Principles of Laboratory
Animal Care prepared by the National society
of Medical Research and the Guide for the Care
and Use of Laboratory Animals prepared by the
Institute of Laboratory Animal Resource and
published by the National Institute of Health
(NIH Publ. 85-23, Rev 1996). The study was
approved by the Ethical Committee of Charité
Hospital, Medical University Berlin. In thirty
Lewis rats decellularized tissue from porcine
pulmonic and aortic origin was implanted
in the subdermal model. Tissue specimens
sizing 1cm² were cut from porcine aortic walls
and pulmonics, which were purchased from a
local slaughterhouse. Tissue specimens have,
caused by the process of fabrication, an intimal
side, an adventitial side and four cutting edges.
Decellularization was performed as previously
described.7 In summary, after preparation
the tissue was stored in antibiotics (Penicillin,
14
Cardiovasc Sci Forum 2010; 5(1):13-18
Streptomycin and Amphotericin B (Gruenenthal,
Aachen, Germany) until decellularization was
performed. Decellularization was performed
with deoxycholic acid (Sigma Chemical Co., St.
Louis, Mo., USA) followed by ethanol treatment.
After decellularization, the tissue was again
stored in antibiotic solution as described above
till implantation. From 10 rats specimens were
explanted after 2 weeks, from another 10 rats
after 4 weeks and from the last 10 rats after 6
weeks. In the end 60 tissue specimens could
be analyzed.
Operation technique
Anesthesia of Lewis rats was induced
with
intra-peritoneal
injected
Trapanal
(Nycomed, Konstanz, Germany). After shaving
the rats back and its disinfection, 1 cm wide
cuts with a gap of 5 mm were set by scalpel.
Afterwards sufficiently sized subdermal pockets
for the tissue specimens were prepared as
previously published by Mako.8 In these pockets
we implanted respectively one decellularized
aortic and one decellularized pulmonic scaffold
in each of the thirty rats. After implantation
of tissue specimens the skin was closed with
intracutaneous sutures and the rats were
monitored till the end of narcosis.
Explantation
Anesthesia was performed as described
above. Subdermal pockets at the back of the
rats were re-opened. Tissue specimens were
removed along with surrounding tissue to rule
out harming the scaffolds. Afterwards gross
examination of scaffolds was performed and
rats were sacrificed in a CO2-chamber.
Histology
Tissue specimens were preserved as
usual. Histological examination was performed
to observe the cellular repopulation of the
tissue. Longitudinal sections were made from
the middle of the specimens.
Light Microscopy: Haematoxylin-eosin
staining was performed on all specimens to
allow general evaluation. For determination
of depth of infiltration the middle of the
longitudinal sections was analyzed with a scale
described in Figure 1. Von-Kossa staining was
used to identify present areas of calcification.
Immunohistochemistry: Staining for
host-fibroblasts (anti rat prolyl-4-hydroxylase,
clone 6-9H6; Acris, Herford, Germany) and
monocytes (CD 68, clone KP1; Acris, Herford,
Germany) was performed to evaluate depth of
respective infiltration with scales described in
figures 3 and 6. For determination of depth
of infiltration the middle of the longitudinal
sections was analyzed.
Statistics: For statistical analysis we
compared decellularized aortic scaffolds
with
decellularized
pulmonic
scaffolds,
independently from the implantation interval.
Group sizes for statistical analysis were therefore
respectively n=30. Semi-quantitative data was
expressed as mean and standard deviation.
Groups were compared with paired Wilcoxontests. Level for statistical significance was set at
p value <0.05. Data management and statistical
analysis were done with SPSS 16.0 (SPSS Inc.,
Chicago, Ill., USA).
RESULTS
Gross examination: All animals survived
without complications during follow-up till
explantation of specimens. While explanting
specimens we looked for signs of inflammation
especially blood vessel ingrowth, encapsulation
and accumulation of ichor. Strongest
inflammatory reaction could be seen after two
weeks, declining after four and six weeks. No
difference between pulmonic and aortic tissue
could be seen.
Von Kossa staining: Von Kossa staining
was performed in all specimens to show
calcification and none of the decellularized
scaffolds showed signs of calcification.
Haematoxylin/eosin
staining:
Haematoxylin/eosin staining revealed significant higher (p<0.001) depth of cellular
infiltration in 30 pulmonic scaffolds than in 30
aortic scaffolds (Figure 1). Between the different
implantation times regression of cellular
infiltration from two to six weeks could be seen.
Cellular infiltration was in all specimens higher
at the cutting edge than at the former intimal
side of the vessel (Figure 2).
Monocyte
staining:Staining
for
monocytes (CD 68 positive cells) revealed
significant higher depth of infiltration
(p<0.001) in 30 pulmonic scaffolds than in 30
aortic scaffolds (Figure 3). Between different
implantation times regression of monocytic
Cardiovasc Sci Forum 2010; 5(1):13-18
infiltration from two to six weeks could be seen.
Furthermore we saw in all specimens a higher
infiltration of monocytes at the cutting edge than
at the former intimal side of the vessel (Figure
4).
Fig.1- Cellular infiltration in Haematoxylin-Eosin staining.
(Legend: 0 =<10% beneath Intima, 1 = >10% beneath Intima,
2 =>20% beneath Intima, 3 =>30% beneath Intima,
4 =>40% beneath Intima, 5 =>50% beneath Intima)
Fig. 2- Hematoxylin-eosin staining of decellularized aortic
specimen (right: former Intima, left: former Adventitia, bottom:
cutting Edge).
Fig. 3- CD-68 positive cell infiltration (Legend: Meaning per 1:400
lens coverage:0 = under 1/3 of lens coverage, 1 = 1/3 till 2/3 of
lens coverage, 2 = 2/3 till 1 of lens coverage, 3 0 = above one lens
coverage).
15
Fig. 4- CD-68 staining of decellularized pulmonic specimen with
higher infiltration at the cutting edge (right) than at the former
intimal side of the vessel (top).
Figure 6. Fibroblast infiltration (Legend: Meaning per 1:400 lens
coverage: 0 = under 1/3 of lens coverage, 1 = 1/3 till 2/3 of lens
coverage, 2 = 2/3 till whole lens coverage, 3 = above one lens
coverage).
Fibroblast
staining:
Staining
for
fibroblasts (Figure 5) revealed infiltration in all
scaffolds. Significantly higher depth of infiltration
was observed in 30 pulmonic compared with
30 aortic scaffolds (p=0.001) olds (Figure 6).
Between different implantation times regression
of fibroblastic infiltration from two to six weeks
could be seen. Fibroblast infiltration was in all
specimens higher at the cutting edge than at the
former intimal side of the vessel.
Fig. 5. Fibroblasts in aortic decellularized scaffold at the former
intimal side of the vessel.
16
DISCUSSION
The host’s reaction to implanted heart
valve prothesis is essential in understanding
causes and mechanisms that lead to its
destruction or limitation of functionality.
Decellularization alters the host’s response
to the implanted tissue. But decellularized
tissue still leads to various reactions when
implanted. So, using tissue of different origin
for decellularization could optimize heart valve
prosthesis. Differences between decellularized
aortic and pulmonic tissue are therefore needed
to be investigated.
Beginning with haematoxylin/eosin
staining there was higher cellular infiltration
to be seen. Morphologically the main part of
cellular infiltration consisted of different types
of leukocytes. To confirm this, we furthermore
performed staining for CD 68 positive cells
(macrophages and monocytes), which are
among the first cells involved in inflammatory
responses or healing processes. It is to
consider that several types of macrophages are
also important in constructive or regenerative
processes.9 However, they are mainly involved
in destructive processes and so infiltration with
these cells indicates inflammatory response.
Meyer et al showed also in a rat allograft model
that decellularization (using protease inhibitors
and Triton X-100 as detergent) significantly
reduces cellular and humoral immune
response to allograft tissue.10 Our group could
show a reduction of human immunogenic
response to decellularized xenogenic heart
valves (using deoxycholic acid) compared to
cryopreserved valves.11 We could also show a
lack of calcification6 after using deoxycholic
acid based decellularization process like we
did in this study-setup. Results of Erdbruegger7
indicate that reduction of antigenic structures
comes along with better structural integrity and
with it functionality. Rieder et al found in an
in vitro study decellularized (detergent-based
decellularization with Triton X-100, sodiumdeoxycholate, octylphenyl-polyethyleneglycol)
xenogenic pulmonary valve tissue with different
proteins than in human pulmonary valve
tissue.12
They revealed that remaining potential of
decellularized pulmonary heart valves to attract
monocytic cells depends strongly on whether
porcine or human scaffolds were used. Naso et
al also showed that after decellularization (by a
detergent-based procedure (Tri-Col)) pulmonic
artery leaflets contained a significant unstable
collagen fraction and quantitatively different
fractions of collagen, lipids and elastin than
aortic leaflets.13 Of course other detergents for
decellularization were used and influence the
results. However in our in vivo study we also
showed significantly higher cellular infiltration
and inflammatory reaction in pulmonic
specimens compared to aortic specimens and
therewith confirmed the findings of Rieder and
Naso in this in vivo study.
Furthermore there was higher infiltration
at the cutting edge of the scaffolds. Various
publications report about antigenic potential
of fragmented or damaged collagen14, which
could along with the disintegration of the ECM
cause the deeper infiltration with inflammatory
cells. The data points out that reduction of the
antigenic structures due to decellularisation only
works by the extraction of cellular components.
ECM does not get altered with this process of
decellularization nor does the collagen get
cross linked.7 So damaged collagen persists
as antigenic structure. Therefore Courtman
suggested that cross-linking procedures could
be useful after decellularization.15
Immigration of fibroblasts can be
induced by several factors. In tissue engineered
heart valves the preferred way for them would
be to migrate to the place where the donor’s
fibroblasts before decellularization have been
and adopt their work of regenerating and
remodeling tissue. Fibroblasts also migrate
during inflammatory reactions after cellular
debris is phagocytized. In our experiment we
cannot clarify the cause of migration, but in
relation to the results of monocyte-staining
some conclusions can be drawn. Data displays
that decellularized pulmonic specimens show at
the same time higher infiltration with fibroblasts
and monocytes. So one could conclude that
fibroblast-infiltration in pulmonic tissue is
mainly part of an inflammatory process.
Limitations
Of course remodeling of decellularized
tissue was evaluated in a subdermal location,
which is markedly different from a blood contact
surface as would be the case in the in vivo use
of a decellularized heart valve. Nonetheless
cellular infiltration shows remarkable differences
between pulmonic and aortic tissue. Further
studies, which involve direct blood contact
and mechanical stress, have to confirm these
results.
CONCLUSION
Results of this study indicate that there is
a significant difference between the response to
decellularized porcine aortic and pulmonic wall
tissue in the rat subdermal model. Decellularized
pulmonic tissue shows higher inflammatory
potential than aortic tissue. Besides this,
destroyed collagen or a disintegration of extracellular matrix seems to increase inflammatory
reactions.
Acknowledgement:
We would like to thank Mrs. Krueger for
assistance in operating the animals and preparing
and staining the histological sections.
17
REFERENCES
1. Schoen FJ, Levy RJ. Founder’s Award, 25th
Annual Meeting of the Society for Biomaterials,
perspectives. Providence, RI, April 28-May 2,
1999. Tissue heart valves: current challenges
and future research perspectives. J Biomed
Mater Res 1999; 47:439-465.
2. Dohmen PM, Hauptmann S, Terytze A et
al. WF. In-vivo repopularization of a tissueengineered heart valve in a human subject. J
Heart Valve Dis 2007; 16:447-449.
3. Dohmen PM, da Costa F, Holinski S et al.
Is there a possibility for a glutaraldehyde-free
porcine heart valve to grow? Eur Surg Res
2006; 38:54-61.
4. Mayer JE, Jr., Shin’oka T, Shum-Tim D. Tissue
engineering of cardiovascular structures. Curr
Opin Cardiol 1997; 12:528-532.
5. Badylak SF. The extracellular matrix as a
scaffold for tissue reconstruction. Semin Cell
Dev Biol 2002; 13:377-383.
12. Rieder E, Seebacher G, Kasimir MT et al. Tissue
engineering of heart valves: decellularized porcine and
human valve scaffolds differ importantly in residual
potential to attract monocytic cells. Circulation 2005;
111:2792-2797.
13. Naso F, Gandaglia A, Spina M et al. Differential
quantitativ distribution of collagen, elastin, total lipid
and other components between leaflets and sectors of
aortic and pulmanary artery root before and after cell
removal. Presentation at the 3rd Biennial Heart Valve
Biology and Tissue Engineering Meeting of the Society
for Heart Valve Disease 2008.
14. Grabenwoger M, Grimm M, Eybl E et al. New
aspects of the degeneration of bioprosthetic heart valves
after long-term implantation. J Thorac Cardiovasc Surg
1992; 104:14-21.
15. Courtman DW, Errett BF, Wilson GJ et al. The role
of crosslinking in modification of the immune response
elicited against xenogenic vascular acellular matrices. J
Biomed Mater Res 2001; 55:576-586.
6. Dohmen PM, Ozaki S, Yperman J et al. Lack
of calcification of tissue engineered heart valves
in juvenile sheep. Semin Thorac Cardiovasc
Surg 2001; 13:93-98.
7. Erdbruegger W, Konertz W, Dohmen PM
et al. Decellularized Xenogenic Heart Valves
Reveal Remodeling and Growth Potential in
Vivo. Tissue Eng 2006; 12:2059-2068.
8. Mako WJ, Shah A, Vesely I et al.
Mineralization of glutaraldehyde-fixed porcine
aortic valve cusps in the subcutaneous rat
model: analysis of variations in implant site
and cuspal quadrants. J Biomed Mater Res
1999;45:209-213.
9. Asahara T, Murohara T, Sullivan A et al.
Isolation of putative progenitor endothelial cells
for angiogenesis. Science 1997; 275:964967.
10. Meyer SR, Nagendran J, Desai LS et al.
Decellularization reduces the immune response
to aortic valve allografts in the rat. J Thorac
Cardiovasc Surg 2005; 130:469-476.
11. da Costa FD, Dohmen PM, Duarte D et
al. Immunological and echocardiographic
evaluation
of
decellularized
versus
cryopreserved allografts during the Ross
operation. Eur J Cardiothorac Surg 2005;
27:572-578.
18
GOMES, Om et al - Vídeo-assisted “No touch” Saphenous Vein Harvesting
ORIGINAL ARTICLE
ARTIGO ORIGINAL
Vídeo-assisted “No touch” Saphenous Vein Harvesting
Dissecção Vídeo-assistida “No touch” da Veia Safena
Otoni Moreira Gomes1, Melchior Luiz Lima2, Elton Francisco Nunes Batista3,
Michael Richard Dashwood4 (By invitation), Domingos Sávio Ramos de Souza5 (By invitation)
Abstract
Backgrounds: The “No touch” Saphenous
vein harvesting is already confirmed as the
best venous graft protection procedure.
Objective: To report a successful case
of CABG with video-assisted saphenous vein
harvesting.
Conclusion: Video-assisted technique
improved the skin protection and the esthetic
result of the “No touch” saphenous vein
harvesting for coronary bypass graft.
Keywords: Coronary artery surgery, CABG,
Myocardium revascularization, Saphenous vein,
Lower legs vein disease, Video-assisted surgery
Method: In the right leg of a 74 years
old man, after general anesthesia and before
the thoracothomy, the “No touch” saphenous
vein harvesting was done by small separated
incisions with video-assisted technique.
Result: It was obtained satisfactory and
full protected vein harvesting with optimized
skin protection, and with best esthetic result
than observed with the reported routine full skin
open approach. The immediate and hospital
postoperative course were uneventful with
patient discharge in good clinical conditions.
1. Full Professor Cardiovascular Surgical Clinic Minas Gerais Federal University, Scientific Director São Francisco de
Assis Truth is Jesus Cardiovascular Foundation.Servcor.
2. Fellow MSc Postgraduation Cardiovascular Surgery São Francisco de Assis Truth is Jesus Cardiovascular Foundation,
Cardiovascular Surgeon CIAS Hospital Unimed-ES.
3. Associated Professor Surgical Clinic Dept. Espirito Santo Federal University, Specialist Video-Surgery Service CIAS
Hospital-UNIMED, Vitória-ES
4. Professor Departments of Clinical Biochemistry Royal Free and University College Medical School, London, UK
5. Professor Department of Thoracic and Cardiovascular Surgery, Örebro University Hospital, Örebro-Sweden
Correspondence:
Otoni Moreira Gomes
Rua José do Patrocínio, 522 - Santa Mônica
Belo Horizonte - MG, Brasil - CEP: 31525-160
E-mail: [email protected]
19
INTRODUCTION
The Sauvage et al.1 successful 1963
experimental demonstration in dogs
of the
saphenous vein grafts use for coronary artery
bypass was followed by Favaloro2, in 1968,
interposing short venous segments to replace
obstructed sections of coronary arteries or
by by-passing the diseased segment through a
bridge directly from the aorta (Favaloro, 19693;
Hahn et al., 19704.
Marty, Bouchardt and Cox5, em 1971,
pioneering first reported the degenerative
changes aspects of the saphenous vein used
in coronary by-pass graft, describing intimal
thickening and medial hypertrophy, particularly
affecting the middle circular layer in the first
observational stages. The intimal thickening
progressed, and the media later became largely
replaced by dense fibrous tissue;
No
aneurismal
dilatations
were
observed, but in 3 cases the grafts were
thrombosed. Almost 20 years later, in 1991,
Cox, Chiasson and Gotlieb6 confirmed the
importance of thrombosis, intimal thickening
and atherosclerosis in venous graft coronary
bypass failure.
Angelini et al. em 19877 and Soyombo et
al., in 19938 linked the saphenous graft lesions
occurring during its harvesting and preparation
with the degenerative histopathology alterations
responsible for the postoperative thrombosis,
wall thickening and obstruction leading the
graft failure and coronary ischemia.
The first successful solution for the
venous graft preservation was pioneering
proposed by Souza, in 19969 with the no-touch
preparation technique, best preserving the
venous wall normal structure and also its vasa
vasorum nourishing circulation.
Tsui et al. in 200110 and Dashwood et
al. in 200711 confirmed the efficacy of the no
touch technique in the histology and physiology
preservation of the venous graft. Confirming
the good results of one randomized clinical
trial12,13.
To optimize the legs skin cicatrisation
and the esthetic results of the “no touch “
saphenous vein harvesting it was employed with
success the video-assisted technology.
20
CASE REPORT
One male patient, 74 years old, entered
CIAS Hospital-Unimed - ES, March 13, 2010, with
a history of 4 months of chest and back pain.
He was admitted to the Emergency Unit due to
a complaint of typical high-intensity precordial
pain and diagnosed acute myocardial infarction.
Immediately he was taken to the hemodynamics
room. On coronary arteriography, right coronary
artery was shown to be obstructed in 80%
in its proximal and medial third with a distal
thrombus. The patient underwent mechanical
revascularization of the right coronary artery
by percutaneous transluminal angioplasty
followed by three stents grafting. Despite good
hemodynamic recovery the angina symptoms
persisted and a new coronary angiography
confirmed multi vessel lesions and good distal
bed post critical lesions in the circumflex,
diagonal and anterior descending coronary
arteries.
Direct myocardial revasculatization
with extracorporeal circulation was performed
on April 5, 2010, with triple bypass: 1) left
internal thoracic artery was grafted to the left
anterior descending artery; 2) great saphenous
vein was grafted to diagonal branch; and 3)
saphenous veingraft to the marginal branch.
For these grafts, the “no touch” saphenous vein
harvesting was done after general anesthesia
and before thoracotomy employing the StrykerR
with 21 monitor with 1188HD camera, XenonR
x 8000 light magnifier and HopkinsR II optic 30o
10mm. Figure 1A is presenting the used video
surgical approach facilities; Figure 1B, the
successful removal of a long segment of “no
touch” right leg saphenous vein; Figure 1C, the
proximal mouth of the circunflex CABG with the
normal vein structure exhibited before its aortic
anastomosis and, Figure 1D the satisfactory
optimized skin protection, by small separated
incisions.
The immediate and hospital postoperative course were uneventful with patient
discharge in good clinical conditions.
Fig. 1A - D: See text
COMMENTS
This first case of vídeo-assisted
saphenous vein harvesting confirmed the
method advantage, reducing the skin damage
and improving an optimized esthetic result.
Growing the surgical team experience
and adding some technology improvement in
the video-assisted instruments may confirm the
technique as the best routine surgical procedure
for the “No touch” harvesting.
REFERENCES
1. Sauvage LR., Wood St. J, Eyer KM, Bill
AH Jr. Experimental coronary artery surgery:
preliminary observations of bypass venous
grafts, longitudinal arteriotomies and end-toend anastomoses. J. thorac. cardiovasc. Surg
1963; 46:826-31.
2. Favaloro RG. Sapbenous vein autograft
replacement of severe segmental artery
coronary occlusion: operative technique.
Ann. thorac. Surg. 1968;5:334-40.
3. Favaloro RG. Saphenous vein graft in the
surgical treatment of coronary artery disease.
J. thorac. cardiovasc. Surg. 1969;58:17853.
4. Hahn C, Faidutti B, Pelogonisios P. Chirurgie directe
desobliterations coronaires. 51 observations. Ann. chir.
thorac, cardiovasc. 1970;9:163-70.
5. Marti MC, Bouchardy B, Cox JN. Aorto-Coronary
By-Pass with Autogenous Saphenous Vein Grafts:
Histopathological Aspects. Virehows Arch. Abt. A Path.
Anat. 1971; 352: 255-266.
6. Cox JL, Chiasson DA, Gotlieb AI. Stranger in a strange
land: the pathogenesis of saphenous vein graft stenosis
with emphasis on structural and functional differences
between veins and arteries. Prog Cardiovasc Dis.
1991;34(1):45-68.
7. Angelini GD, Passani SL, Breckenridge IM, Newby
AC. Nature and pressure dependence of damage
21
induced by distension of human saphenous
vein coronary artery bypass grafts. Cardiovasc
Res. 1987;21(12):902-7.
8. Soyombo AA, Angelini GD, Bryan AJ, Newby
AC. Surgical preparation induces injury and
promotes smooth muscle cell proliferation in a
culture of human saphenous vein. Cardiovasc
Res. 1993;27(11):1961-7
9. Souza D. A new no-touch preparation
technique. Technical notes. Scand J Thorac
Cardiovasc Sur. 1996;30(1):41-4
10. Tsui JC, Souza DS, Filbey D, Bomfim V,
Dashwood MR. Preserved endothelial integrity
and nitric oxide synthase in saphenous vein
graft harvested by a “no-touch” technique. Br
J Surg. 2001;88(9):1209-15.
11. Dashwood MR, Dooley A, Shi-Wen X,
Abraham DJ, Souza DS. Does periadventitial
fat- derived nitric oxide play a role in improved
saphenous vein graft patency in patients
undergoing coronary artery bypass surgery? J
Vasc Res. 2007;44(3):175-81
12. Souza DS, Johansson B, Bojö L, Karlsson
R, Geiger H, Filbey D, et al. Harvesting the
saphenous vein with surrounding tissue fo
CABG provides long-term graft patency
comparable to the left internal thoracic artery:
results of a randomized longitudinal trial. J
Thora Cardiovasc Surg. 2006;132(2):373-8
13. Souza DSR, Gomes WJ. O futuro da
veia safena como conduto na cirurgia de
revascularização miocárdica. Rev Bras. Cir
Cardiovasc. 2008, vol. 23, n.3
22
PRATA, PHl et al - Rabbit and Human Compared Mesenteric Arterial Anatomy
ORIGINAL ARTICLE
ARTIGO ORIGINAL
Rabbit and Human Compared
Mesenteric Arterial Anatomy
Anatomia Arterial Mesentérica Comparada
em Humanos e Coelhos
Pedro Henrique Lima Prata1, Walter Ferraz Flávio Júnior1, Lucas Ferreira Santana1, André Santiago da
Silva1, Luiz Alberto Bomjardim Porto1, Luciano Dantes de Paula2, Otoni Moreira Gomes3
Abstract
Backgrounds: The anatomy of the rabbit
mesenteric artery is not well known and there
is no consensus in the nomenclature.
predominates through cranial mesenteric artery,
with scanty presence of mesenteric caudal
artery.
Objective: To document the anatomy
of the mesenteric arterial circulation in rabbits,
allowing further experimental studies.
Conclusion: The mesenteric arterial
circulation in the studied rabbits showed a
marked predominance of the cranial mesenteric
artery with no specific presence of the caudal
mesenteric trunk.
Method: Dissection and isolation of
the mesenteric arteries was performed in six
anesthetized rabbits, to be used for mesenteric
ischemia-reperfusion
investigation.
After
anatomy standard registration, photographic
and contrast angiography were also documented
. The data obtained was described in comparison
with literature on the anatomy corresponding
to other animal species and humans.
Keywords: Rabbit Anatomy, Mesenteric
circulation, Compared Anatomy
Result: In contrast to human and other
animals anatomy, with well defined importance
for superior and caudal mesenteric arteries
enteric nutrition, in rabbits, the enteric nutrition
1. Students School of Medicine Federal University of Minas Gerais
2. Coordinator Surgical Technique Discipline FUMG School of Medicine
3. Full Professor Surgery Department FM.UFMG School of Medicine; Scientific Coordinator of the São Francisco de
Assis Truth is Jesus Cardiovascular Foundation
Correspondence:
Pedro Henrique Lima Prata
Rua Sergipe,15 / 1103 - funcionários
23
Literature Review
The mesenteric vessels are responsible
for blood supply of small and large intestine of
reptiles, birds and mammals1.
For the rat and mouse, the cranial
mesenteric artery arises from the abdominal
aorta, giving off branches to the pancreas,
duodenum, and to various parts of the small
and large intestine, and directed its branches to
the cecum and colon, as the caudal mesenteric
artery, it irrigates parts of the rectum, and one
of its branches anastomose with a branch of the
cranial mesenteric artery2.3.
In domestic animals, the cranial
mesenteric artery originates caudal to the celiac
artery, with which it forms in some cases a
trunk. The caudal mesenteric artery is a single
vessel that originates near the terminal division
of the aorta, dividing after a short trip4-7.
In golden hamsters (Mesocricetus
auratus), the arrangement of the visceral
branches of abdominal aorta, abdominal
segments for the digestive tract, is similar to
other mammals such as guinea pig, rabbit, rat
and man 8, 9.
The cranial mesenteric artery of
the agouti (Dasyprocta agouti) divided by
bifurcation, trifurcation or four divisions, giving
rise to branches to various parts of the intestine
and pancreas. The caudal mesenteric artery
bifurcates, vascularizing the final portions of
the large intestine and rectum. Anastomoses
between branches originating in the cranial
mesenteric artery and some of the mesenteric
caudal artery were also observed10.
In the paca, the cranial mesenteric artery
sends branches to the pancreas and the right
colic artery irrigates the characteristic “floating”
colon of these animals, yet from the cranial
mesenteric artery emerge: the middle colic
artery, ileocolic artery, a large branch that goes
to a part of the large colon ileocecocólic artery,
irrigates the ileum, the cecum and the beginning
of the large colon, and a series of branches
jejunum, ileum and cecum, in these animals,
the caudal mesenteric artery arises just before
the termination of the aorta and the issues left
colic artery, which anastomoses with the middle
colic artery, and branches to the rectum11.
In remarks by angiography, the anatomy
of the abdominal and lower back in goats, pigs
24
and rabbits, reported that the cranial mesenteric
artery in these species, originates the following
branches: middle colic, which is the most
developed branch and this anastomoses, in
some studies, with the left gastroepiploic artery;
ileocecocólica artery, which, in goats and rabbits
is the first branch given, pancreaticoduodenal
artery, cranial already been identified as the first
branch given, and numerous jejunal arteries
that anastomose with each other, forming
arches. The caudal mesenteric artery is a vessel
slightly thickened and divides into cranial and
caudal branches12,13.
In humans, the abdominal aorta begins
at the aortic hiatus in the diaphragm, up to
the level of the 12th thoracic vertebra. Its first
branches are the inferior phrenic arteries right
and left, which contribute to the irrigation of
the diaphragm and often emits the superior
adrenal glands arteries. Just below the aortic
hiatus of the diaphragm, between the pillars, is
the origin of the celiac trunk, a short and wide
vessel that after a course of 1 to 3 cm is divided
into the left gastric artery, splenic (or splenic)
and common hepatic. The celiac artery is the
caudal part of the anterior intestine.
Superior mesenteric artery is the artery
of the midgut. It arises from the anterior part of
the aorta below the origin of the celiac trunk.
Irrigates a part of the pancreas, the entire small
intestine (except a part of the duodenum), and
large intestine from the cecum to near the left
colic flexure. In its origin, it is located posterior
to the pancreas and splenic vein. From top to
bottom, from before the left renal vein, the
uncinate process of the pancreas and the third
part of duodenum (horizontal); then penetrates
the root of the mesentery and travels to the
right iliac fossa.
Its
first
branch,
the
inferior
pancreaticoduodenal artery, passes to the
right and is divided into anterior and posterior
branches and enters the arterial arches in the
anterior and posterior head of the pancreas, as
stated earlier. There are several branches that
originate from a variable way from the concavity
(right) of the superior mesenteric artery and
supplies blood to the large intestine. These
branches are the ileocolic artery, right colic
and middle colic arteries. The anastomoses
among them contribute to the formation of the
circumflex artery. The ileocolic artery has two or
more branches with a variety of anastomoses
communicating them. These branches irrigate
the terminal part of ileum, cecum and appendix.
Jejunal and ileal arteries, varying in number,
arise from the convexity (left) of the superior
mesenteric artery. The first jejunal branch may
lead to inferior pancreaticoduodenal artery. The
superior mesenteric artery and its branches are
accompanied by veins and a large number of
nerve fibers and lymphatic vessels. The superior
mesenteric vein is commonly on the right.
The inferior mesenteric artery is the
artery of the hindgut. It is originated from the
aorta several centimeters above its bifurcation;
irrigates the distal part of the colon, meaning,
from near the left colic flexure to the ampulla
of the rectum. From its origin, it runs toward
lower and left on the psoas major, crosses the
upper opening of the pelvis and becomes the
superior rectal artery. Then crosses the left
common iliac artery, where the urethra it is
lateral, in the apex of the sigmoid mesocolon to
the rectum, where it divides into two branches,
which continue toward the bottom wall of the
rectum. Before crossing the upper opening of
the pelvis, the inferior mesenteric artery gives
rise to the left colic and sigmoid arteries. These
form arches that contribute to the marginal artery
that gives origin to the straight arteries which
reach the intestine. The anastomosis between
the left colic artery and middle at the height of
the left colic flexure are optimum (through the
marginal artery). The inferior mesenteric artery
and its branches are accompanied by nerve
fibers (inferior mesenteric plexus) and veins
and lymphatics. The artery is accompanied by
the inferior mesenteric vein at the bottom of
its path. The sigmoid arteries originate from
the mesenteric arteries just before the upper
opening of the pelvis.
Human Superior Mesenteric Artery14
Its first branch, the inferior pancreaticoduodenal artery, passes to the right and is
divided into anterior and posterior branches
and enters the arterial arches in the anterior
and posterior head of the pancreas, as stated
earlier. There are several branches that
originate from a variable way from the concavity
(right) of the superior mesenteric artery and
supplies blood to the large intestine. These
branches are the ileocolic artery, right colic
and middle colic arteries. The anastomoses
among them contribute to the formation of the
circumflex artery. The ileocolic artery has two or
more branches with a variety of anastomoses
communicating them. These branches irrigate
the terminal part of ileum, cecum and appendix.
Jejunal and ileal arteries, varying in number,
arise from the convexity (left) of the superior
mesenteric artery. The first jejunal branch may
lead to inferior pancreaticoduodenal artery. The
superior mesenteric artery and its branches are
accompanied by veins and a large number of
nerve fibers and lymphatic vessels. The superior
mesenteric vein is commonly on the right (Fig.
1).
Fig. 1 - Anatomy of the human superior mesenteric artery
The inferior mesenteric artery is the
artery of the hindgut. It is originated from the
aorta several centimeters above its bifurcation;
irrigates the distal part of the colon, meaning,
from near the left colic flexure to the ampulla of
the rectum. From its origin, it runs toward lower
and left on the psoas major, crosses the upper
opening of the pelvis and becomes the superior
rectal artery. Then crosses the left common iliac
artery, where the urethra it is lateral, in the apex
of the sigmoid mesocolon to the rectum, where
it divides into two branches, which continue
toward the bottom wall of the rectum. Before
crossing the upper opening of the pelvis, the
inferior mesenteric artery gives rise to the left
colic and sigmoid arteries. These form arches
that contribute to the marginal artery that gives
25
origin to the straight arteries which reach the
intestine. The anastomosis between the left
colic artery and middle at the height of the
left colic flexure are optimum (through the
marginal artery). The inferior mesenteric artery
and its branches are accompanied by nerve
fibers (inferior mesenteric plexus) and veins
and lymphatics. The artery is accompanied by
the inferior mesenteric vein at the bottom of
its path. The sigmoid arteries originate from
the mesenteric arteries just before the upper
opening of the pelvis.
sends branches to the pancreas, duodenum,
small intestine, colon and cecum, noting the
presence from 12 to 22 jejunal arteries in
rabbits14 (Fig. 3).
Anatomy of the rabbit
Mesenteric arteries of the cranial and
caudal rabbits are homologous to superior
mesenteric and inferior arteries of human
beings. The change in nomenclature is due
to human bipedalism opposed to cuniculidae
quadripedalism.
The cranial mesenteric artery of the
rabbit sends the middle colic artery, the caudal
pancreatic-duodenal artery, the right colic artery,
a branch of ileocolic, and a common trunk, the
jejunal arteries. The caudal mesenteric artery,
some authors allude to the fact that this vessel
is divided into the left colic and cranial rectal
artery, which leave the sigmoid arteries8.
It was noted in all observed rabbits and
in the literature that the cranial mesenteric artery
is a large vessel that arises from the abdominal
aorta (Fig. 2), a fact that is also observed in
humans.
Fig. 3 - Cranial mesenteric artery of rabbit (Bt) resulting in the
ileocolic artery (Ic) and the jejunal arteries (Aj)13.
The caudal mesenteric artery of the rabbit
is a single vessel and very narrow, with source
near the end of the abdominal aorta, dividing
after a short path, at left colic and cranial rectal
artery, from which leave the sigmoid arteries13.
In the rabbits studied, the presence of
the caudal mesenteric artery cannot always be
evidenced by the macroscopic study neither
angiography (Fig. 4)
Fig. 4- Angiography demonstrating the dominance of a cranial
mesenteric (AT-Aorta, AC-celiac artery, mesenteric-MC)
Fig. 2- Cranial view of the abdominal cavity of an adult rabbit;
abdominal aorta (A) originating the celiac artery (Ac) and the
cranial mesenteric (Am)13.
In rabbits, as well as in humans, the
cranial mesenteric artery is a single vessel
whose origin is caudal to the celiac artery. It
26
Regarding the mesenteric venous
circulation, Heath and House reported that in
rabbit, portal vein is formed by the junction
of the gastrolienal that caudally, extends to
the right, with the mesenteric vein that is
directed cranially, is relatively larger, forming
the vein mesenteric artery and tributaries of the
pancreaticduodenal (15, 16). Barone et al. present
in the board, the hepatic portal vein originating
from three tributaries vein: a common ileocolic, a
jejunal vein and a common pancreaticduodenal
vein flow(17). In humans, these three vessels
drain into the superior mesenteric vein.
Brick et al.18 demonstrated that in
rabbit portal vein is formed after the joint
of the cranial mesenteric vein and caudal
mesenteric vein; also receiving tributaries from
the stomach, spleen and pancreas. Contribute
to the formation of the hepatic portal vein the
following venous components: gastrolienal
vein, the inferior pancreaticduodenal, jejunal
vein trunk, the cranial mesenteric vein, left
colic vein, right colic vein, middle colic vein
and mesenteric vein flow.
The cranial mesenteric vein formed by
a common jejunal trunk and an ileocolic trunk:
the common jejunal trunk is formed by the
union of eight to eighteen jejunal veins; the
ileocecocolic trunk is made after the meeting
of the colic veins, lymph nodes and ileal in
different arrangements and number (Figs. 5
and 6).
Fig. 6- Isolated cranial artery and vein of the rabbit.
The caudal mesenteric vein is formed by
the union of cranial rectal veins and left colic
vein, which establishes a common anastomotic
arc along the wall of the descending colon. As
tributaries of the hepatic portal vein, there is a
jejunal vein, a duodenojejunal vein, a right colic
vein, middle colic vein and a pancreaticduodenal
vein18.
REFERENCES
1. Morandini. C.. Zoologia. 2. ed., São Paulo,
Nobel, 1968 .
2. Greene, G. C.. Circulatory System. In:
Greene, G. C. (Ed.). Anatomy of mamimals.
Transactions of the American Philosophical,
New York, USA, 1955; p.177-235.
3. Habel R, StrombergMW. Anatomy and
embryology of the laboratory rat. Wörthsee,
Germany, Biomed Verlag. 1986.
4. Schwarze E, Schröder L. Compendio de
Anatomia Veterinaria: Aparato Circulatório y
Piel. Zaragoza, Acribia, 1972
5. Ghoshal N. G. Coração e artérias. In: Getty,
R (Ed.). Anatomia dos Animais Domésticos.
Rio de Janeiro, Interamericana. 1981, p.560562.
6. Nickel R, Schummer A, Seiferle E, Sack W
O. The circulatory system, the skin, and the
cutaneous organs of the domestic mammals.
Berlin, Verlag Paul Parey,1981.
Fig. 5- Schematic figure highlighting the veins that form
the hepatic portal system of the New Zealand rabbit
(Oryctolagus cuniculus Linnaeus,1758). (1) gastrospleic
vein, (2) pancreatoduodenal vein, (3) duodenal branch,
(4) duodenojejunal branch, (5) jejunal trunk, (6) cranial
mesenteric vein, (7) ileocecal trunk, (8) ileocecocolic trunk, (9)
right colic vein, (10) middle colic vein, (11) left colic vein, (12)
caudal mesenteric artery (17).
7. Gomes OM. Cirurgia Experimental. São
Paulo, Sarvier, 1978
8. Barone R. Artères. In: Barone R (Ed.).
Anatomie Comparée des Mammifères
domestiques Esplancnologie. Paris, Éditions
Vigot. 1996, p.327-347..
27
9. Orsi AM, Pinto e Silva P, Mello-Dias
S, Oliveira M. C. Considerações sobre a
remescência da aorta abdominal do hamster
dourado (Mesocricetus auratus). Revista
Brasileira de Pesquisas Médicas e Biológicas,
1975;8 (5- 6): 459-462.
10.Carvalho M.A.M.,Miglino M. A., Di Dio
L. J. A., Melo A. P. F. Artérias mesentéricas
cranial e caudal em cutias (Dasyprocta aguti).
Journal of Veterinary Science Federal University
of Uberlândia, 1999;5 (2): 17-24.
11. Machado M. R. F, Nogueira T. M. R,
Miglino, M. A., Artoni S. M. B, Araújo M.L,
Gianonni M.L.. Ramificação da artéria
mesentérica cranial e artéria mesentérica
caudal da Paca (Agouti paca, Linnaeus, 1766).
Anais do Congresso Brasileiro de Anatomia,
Ceará, Brasil, 1996, p.29.
12. Nayar K.N.M, Singh G, Singh Y, Singh
A. P, Singh G. R. Comparative arteriographic
anatomy of the abdominal viscera and lumbar
region in goats, dogs, pigs and rabbits. Indian
Journal of Animal Sciences, 1983;53 (12):
1310-1419.
13. Machado M.R.F,Souza S.V, Oliveira T.C,
Cortellini L.M.F, Barbosa R.R. Suprimento
arterial dos intestinos do coelho da raça Nova
Zelândia (Oryctolagus cuniculus).Biotemas
2007; 21(1):101-105.
14. Gray H. The superior mesenteric artery
and its branches. In: Gray H. Gray’s Anatomy
of the Human Body. 1918.
15. Heath T, House B.. Origin and distribution
of portal blood in the cat and rabbit. American
Journal of Anatomy 1970;127 (2):71-80.
16. Toens C, Krones C, Blum, U, Fernandez
V, Grommes J. F, Hoelzl F, Stumpf, M,
Klinge U, Shumpelick V. Int J Colorectal Dis.
2006;21:332-338.
17. Barone R. et al. Atlas d’anatomie du lapin.
Paris, Masson, 1973, p.138.
18. Brick A. J, Miglino M. A, Machado G. V,
Santos T. C.. Formação da veia porta-hepática
em coelhos da raça Nova Zelândia Branco
(Oryctolagus cuniculus Linnaeus, 1758). Braz. J.
vet. Res. anim. Sci. 2006;43 (1):87-94
28
rodríguez, m et al - Effect o Exercise o Entricular Remodeling After
Experimental Myocardial Infarction in Rabbits
ORIGINAL ARTICLE
ARTIGO ORIGINAL
Effect o Exercise on Ventricular Remodeling After
Efeito do Exercício no Remodelamento Ventricular
Após Infarto Miocárdico Experimental em Coelhos
Manuel Rodríguez, Germán E. González, Celina Morales, Carlos Bertolasi, Ricardo Jorge Gelpi*
Abstract
Backgrounds: The effect of exercise
on ventricular remodeling after myocardial
infarction (MI) is under discussion.
Objective: The aim was to evaluate
whether moderate exercise initiated at early
stages of MI modifies the degree of ventricular
dilation.
Method: New Zealand rabbits were used,
considering 3 groups: “sham group” (G1, n=7);
“MI sedentary group” (G2, n=4), rabbits were
subjected to the ligature of a prominent branch
of the left coronary artery, and, group with MI
and moderate exercise (G3, n=6) on motordriven treadmill, after 18 days of evolution.
Rabbits were sacrificed at day 56 post-surgery,
and hearts were perfused using Langendorff
techni¬que. Left ventricular end diastolic
pressure (LVEDP)-volume curves were recorded.
The size of MI was determined by morphometric
analysis. MI size was (8±SEM) G 1: 0±0.00, G 2:
20.55±0.94 and G 3: 19.15±1.47
Results: In this study, the changes
observed in the group with sedentary MI
coincide with previous studies: the installation
of a MI generates ventricular dilation when the
size of the infarcted area exceeds a certain
limit. Such dilation can be evidenced through
the shifting of the diastolic component of the
pressure-volume curves towards the right. In
this study, hearts of the group with sedentary
MI show a degree of dilation that coincides with
previous reports. Interestingly, the group of MI
with moderate exercise shows a trend towards
greater dilation than the group with sedentary
MI.
Conclusion: Moderate exercise initiated at early stages of MI evolution has an
unfavourable effect on ventricular remodeling.
*: P < 0.05
Keywords: Experimental myocardial
Infarction, ventricular remodeling.
* Member of the Scientific Career CONICET
Laboratory of Cardiovascular Physiopatology, Department of Pathology, Faculty of Medicine, U.BA., Argentine.
29
INTRODUCTION
Among ischemic cardiopathies, myocardial
infarct (MI) is the most important due to its high
morbidity and mortality rates both in its acute
phase and in the long term.
The appearance of a MI can provoke
structural changes in the ventricular walls and
cavity, thus causing modifications in the shape and
size of the ventricle and - therefore - in ventricular
geometry. Such changes are known as ventricular
remodeling1.
This process is initiated rapidly postinfarct,
allowing to compensate, sharply, for the abrupt
loss of myocytes suffered, and may continue
even after histopathologic healing is completed,
provoking ventricular dilation1-4. Thus, the
evolution of ventricular remodeling can cause left
ventricular dysfunctions which can lead to heart
failure1-11.
During recent years, comprehension of
the physiopathologic mechanisms involved in
post myocardial infarction ventricular remodeling
has become increasingly important. A key role
has been attributed to parietal stress, both in
early5 and late1 stages. Physical exercise could be
capable of modifying the remodeling process, as
it acts by altering the load conditions of the left
ventricle.
The aim of this study was to evaluate
ventricu¬lar remodeling after myocardial infarction
(MI), under resting conditions and in the presence
of moderate exercise initiated at the early stages
of evolution, considering infarct size and degree
of ventricular dilation.
MATERIAL AND METHODS
1-Experimental model:
Female New Zealand rabbits were
used. A left lateral thoracotomy was performed
under general anesthesia. After performing
pericardiectomy, a 6-0 type silk thread was
passed around a prominent bran¬ch of the left
coronary artery (LCA) (equivalent to the anterior
descending artery in human beings). In order to
induce MI the LCA was ligated. Throughout the
observation period, the animals were kept in a
quiet and acclimatized environment, and were fed
with standard rabbit chow and water ad libitum.
2-Experimental groups:
Sham group, n=7: surgery was performed
on this group as described above, but without
inducing MI. Rabbits were allowed to follow the
30
natural course of evolution during 56 days.
-MI sedentary group, n=4: MI was induced
as descri¬bed above. Rabbits were allowed to
follow the natural course of evolution during 56
days.
-MI with moderate exercise group, n=6: MI
was in¬duced as described above and rabbits were
allowed to follow the natural course of evolution
during 56 days. Moderate exercise on treadmill
was added as from day 18 of evolution after MI.
The moderate exercise protocol established 3
sessions per week of 2 minutes per session, at a
speed of 17 m/min, avoiding physical adaptation
(endurance training).
Upon completion of the evolution period
both ventricular functions and morphologic
characteristics were studied.
3- Ventricular function studies:
On comple-tion of the period assigned
to each protocol the animals were weighed and
sacrificed by means of an overdose of thiopental
sodium (35 mg/kg). Chests were quickly opened
and the aortas isolated and cannulated.
Hearts were immediately excised and
placed in a perfusion system by means of the
cannulae, and were perfused according to
Langendorff’s modified technique in Krebs –
Henseleit solution at a constant temperature of
37 º C and balanced with 95% O2 - 5% CO2 for
oxygenation and to keep pH close to 7.4.
A latex balloon tied to a rigid polyethylene
tube was placed in the left ventricle and was
connected to a Deltram II (Utah Medical System)
pressure transducer, thus allowing to record
inner pressure of the left ventricle. Also coronary
perfusion pressure (CPP) was recorded by means
of a pressure transducer connected to the
perfusion line at a point immediately anterior to
the aortic cannulae. Coronary flow was regulated
to obtain a constant CPP close to 80 mm/Hg. Heart
rate was kept constant at close to 180 beats per
minute by means of two electrodes (Figure 1).
Fig. 1 - Schematic design of the perfussion system (Langendorff
technique).
Ventricular functions were measured
in the preparation thus obtained by recording
pressure/volu¬me curves of the left ventricle.
Considering the diastolic component (left
ventricular end-diastolic pressure, LVEDP) of
these curves it was possible to evaluate the
degree of ventricular dilation.
4- Macroscopic and microscopic morphologic studies:
Once the data corresponding to
ventricular functions were obtained hearts were
fixed in forma¬lin 10% and subsequently cut
transversally in slices from apex to base, and
slices were placed in paraffin and stained with
hematoxylin-eosin and Masson’s trichrome.
All slices were then processed by means of a
digital image analyzer (Image Pro® Plus 3.0) to
calculate size of infarct area as a percentage of
the compromised myocardial mass.
Data were calculated as the mean ±
S.E.M., assessed by ANOVA and followed by a
post-hoc test.
Fig.2- Curves corresponding to LVEDP at different intraventricular volumes (diastolic component of the pressure/volume
curve of the left ventricle) of the three considered groups.
DISCUSSION
Until about three decades ago, the early
treatment of MI included a very prolonged rest
period: patients were instructed to sharply
reduce their physical activity, and rest in bed
during at least two or three months.
RESULTS
Among the rational motives for such
procedure was the objective of keeping
Table I - shows the values corresponding
myocardial oxygen consumption at a low level.
to general parameters: animal weight and
At present physical activity is initiated during the
percentage of infarct area. There were no
early stages of convalescence and many patients
significant differences among the considered
are encouraged to participate in supervised
groups, with the exception of the non-existence
programs of regular exercise; in certain cases,
of an infarct in the sham group.
physical training is indicated.
Figure 2 - shows results corresponding
Among its beneficial effects there is
to LVEDP at different intraventricular volumes
an incre¬ase of vagal tonicity, restoration of a
(diastolic component of the pressure/volume
higher degree of heart rate variability, a favorable
curve of the left ventricle) of the three
effect on peripheral resistance, a decrease of
considered groups. It can be observed that
thrombolic phenomena and a feeling of wellthe curves corresponding to the groups with
being. However, there is a possibility that,
MI are situated at the right of the sham group,
within the population with recent MI, there may
indicating LV dilation, as a larger volume is
be some specific sub-populations for which
required to reach the same pressure.
physical training could prove to be harmful12, 13.
We noticed that this rightwards
Accordingly, it is extremely important to
displacement was higher in the MI with moderate
know the impact of exercise on post-MI ventricular
exercise group (*: P<0.05).
remodeling. Notwithstanding, the available data
Table I: General data
“Sham” MI Sedentary
MI + Moderate Exercise Group
Group
Group Body weight (g) 2139±54
2270±60
1938±29
Infarct size (%) 0.0±0.0
20.55±0.94
19.15±1.47
31
are limited, and frequently contradictory. Studies
in patients present several obstacles: certain
variables are difficult to control, coexistence of
MI with other pathologies or with different risk
factors, the presence of concomitant treatments,
non-scheduled abandonment, necessity of
considering a large number of patients, etc.
Many of these drawbacks can be avoided
through the use of animal models. On the other
hand, although hearts of experimental animal
models are different to human hearts, they
allow a far more effective and strict control of
variables, thus opening new possibilities for the
better understanding of ventricular remodeling
in MI14-16.
In the last few years, rabbits have been
used as suitable experimental models for the
study of myocardial ischemia and for studies
of exercise physiology. It has been pointed
out17 that this species could mimic myocardial
ischemia of the human heart without previous
episodes of angina, being a highly suitable
experimental animal for the study of MI resulting
from an acute occlusion of an artery without
previous significant stenosis and with a viable
myocardium.
In our study we have resorted to an
experimental model of isolated rabbit heart
which, upon standardization of LV load
conditions, allows to perform a detailed analysis
of ventricular functions under the strict control
of certain variables. We have used a protocol of
moderate exercise (avoiding the generation of
physiologic hypertrophy or “endurance training”),
and such physical activity was incorpo¬rated
at the early stages of the MI histopathologic
evolution, when cicatrization of infarct was still
not consolidated.
In this study, the changes observed
in the group with sedentary MI coincide with
previous studies: the installation of a MI
generates ventricular dilation when the size of
the infarcted area exceeds a certain limit. Such
dilation can be evidenced through the shifting of
the diastolic component of the pressure-volume
curves9 towards the right. In this study, hearts
of the group with sedentary MI show a degree
of dilation that coincides with previous reports610
. Interestingly, the group of MI with moderate
exercise shows a trend towards greater dilation
than the group with sedentary MI.
In view of this trend towards greater
32
dilation, and therefore greater parietal stress,
such modifications in ventricular geometry
represent an unfavorable effect with important
functional and prognostic implications. Thus,
exercise initiated at the early stages of MI could
present some unfavorable aspects.
On one hand, exercise could aggravate
infarct expansion. On the other hand, ventricular
dilation can evolve slowly and progressively
during months and even years, provoking
hemodynamic impairment, and furthermore,
it is linked to a decrease in the life-span, in
both cases proportionately to infarct size1-11. In
another direction, the periodical increase in the
consumption of systemic oxygen can increase the
cardiac workload, thus favoring the appearance
of ischemia in areas with a decreased coronary
reserve, unleashing manifest episodes of heart
failure or serious arrhythmia.
We have studied the degree of ventricular
dilation reached as consequence of MI, under
resting conditions and also in the presence of
moderate exercise on treadmill initiated at the
early stages of evolution. The data obtained
indicate that ventricular dilation occurred in the
MI sedentary group, and that moderate exercise
initiated at the early stages of MI evolution has an
unfavorable effect on ventricular remodeling.
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remodeling after myocardial infarction.
Experimental observations and clinical
implications. Circulation. 1990; 81: 11611172.
2. Roberts C.S., Maclean D., Maroko P.,
Kloner R.A. Early and late remodeling of the
left ventricle aftermyocardial infarction. Am. J.
Cardiol. 1984; 54: 407-410.
3. Gaudron P., Eilles C., Ertl G., Kochsiek
K. Adaptation to cardiac dysfunction after
myocardial infarction. Circulation. 1993; 87
(Suppl. IV): IV-83 - IV-89.
4. Gaudron P., Eilles C., Ertl G., Kochsiek
K. Compensatory and noncompensatory
left ventricular dilatation after myocardial
infarction: Time course and hemodynamic
consequences at rest and during exercise.
Am. Heart J. 1992; 123: 377-385.
anterior myocardial infarction (EAMI) trial. J. Am. Coll.
Cardiol. 1993; 22: 1821-1829.
5. Weisman H., Bush D., Mannisi J., Healy
Bulkley B. Global cardiac remodeling after
acute myocardial infarction: A study in the rat
model. J. Am. Coll. Cardiol. 1985; 5: 13551362.
13. Giannuzzi P., Temporelli P. L., Corrá U., Gattone
M., Giordano A., Tavazzi L., for the ELVD Study Group.
Attenuation of unfavorable remodeling by exercise
training in postinfarction patients with left ventricular
dysfunction. Circulation. 1997; 96: 1790-1797.
6. Pfeffer J.M., Pfeffer M.A., Fletcher
P.J., Braunwald E. Progressive ventricular
remodeling in rat with myocardial infarction.
Am. J. Physiol. 1991; 260: H1406-H1414.
14. Musch T.I., Moore R. L., Leathers D., Bruno A., Zelis
R. Endurance training in rats with chronic heart failure
induced by myocardial infarction. Circulation. 1986; 74
(2): 431-441.
7. Lamas G.A., Pfeffer M.A. Increased left
ventricular vo¬lume following myocardial
infarction in man. Am. Heart J. 1986; 111:
30-35.
15. Gaudron P., Hu K., Schamberger R., Budin M.,
Walter B., Ertl G. Effect of endurance training early or
late after coronary artery occlusion on left ventricular
remodeling, hemodynamics, and survival in rats with
chronic trasnsmural myocardial infarction. Circulation.
89: 402-412, 1994.
8. White H.D., Norris R.M., Brown M.A.,
Brandt P.W.T., Whitlock R.M.L., Wild C.J.
Left ventricular end systolic volume as
the major determinant of sur¬vival after
recovery
from
myocardial
infarction.
Circulation, 1987; 76 (1): 44-51.
9. Fletcher P.J., Pfeffer J.M., Pfeffer M.A.,
Braunwald E. Left ventricular diastolic
pressure-volume relations in rats with healed
myocardial infarction. Effects on systolic
function. Circ. Res. 1981; 49: 618-626.
16. Orenstein T.L., Parker T.G., Butany J.W., Goodman
J.M., Dawood F., Wen W.H., Wee L., Martino T.,
McLaughlin P.R., Liu P.P. Favorable left ventricular
remodeling following large myocardial infarction by
exercise training. J. Clin. Invest. 1995; 96: 858-866.
17. Verdouw P., van den Doel M., Zeeuw S., Duncker
D. Animal models in the study of myocardial ischaemia and ischaemic syndromes. Cardiovasc. Res. 1998;
39:121-135.
10. Pfeffer M. A., Pfeffer J.M., Fishbein
M.C., Fletcher P.J., Spadaro J., Kloner R.A.,
Braunwald E. Myocardial infarct size and
ventricular function in rats. Circ. Res. 1979;
44: 503-512
11. Gaudron P., Eilles C., Kugler I., Ertl G.
Progressive left ventricular dysfunction and
remodeling after
myocardial infarction.
Potential mechanisms and early predictors.
Circulation. 1993; 87: 755-763.
12. Giannuzzi P., Tavazzi L., Temporelli
P. L., Corrá U., Imparato A., Gattone
M., Giordano A., Sala L., Schweiger C.,
Malinverni C., Long-term physical training
and left ventricular remodeling after anterior
myocardial infarction: results of exercise in
33
GOMES, Om - Economic Roller Ventilador for Small Animals
HOW TO DO / Como Fazer
Ventilador Econômico de Roletes para Pequenos Animais
Economic Roller Ventilator for Small Animals
Otoni Moreira Gomes
Abstract
Resumo
A simple and economic model of artificial
ventilator is presented that can be used in
experimental researches in small animals. The
apparatus was obtained from a common roller
pump used in extracorpo¬real circulation, but
with a hole in the rubber (latex) tube for better
control of the inspiration time and volume.
The ventilator was used in tem rats
during one hour of controled respiration, with
good metabolic results (mean: pH 7.38; pO2
134.2; pCO2 35.0 and “BE” - 4.4).
Para uso em pesquisas com pequenos
animais, um modelo simples de ventilador
artificial foi construido empregando-se sistema
de bomba de roletes, comumente usada em
circulação extracorpórea, mas com furo no
tubo de borracha (látex) para melhor controle
do volume e tempo inspiratórios.
O aparelho foi empregado em dez ratos,
durante uma hora de respiração controlada,
com bons resultados metabólicos (pH 7,38;
pO2 134,2; pCO2 35,0 e “BE” - 4,4, em média)
Keywords: Artificial ventilator;
mental surgery.
Palavras-Chave:
cirurgia experimental.
Experi-
Prof. Titular do Departamento de Cirurgia da FM.UFMG; Diretor Científico da
Fundação Cardiovascular São Francisco de Assis Verdade é Jesus. ServCor
Correspondence:
Otoni Moreira Gomes
Rua José do Patrocínio, 522 - Santa Mônica
34
Ventilador
artificial,
INTRODUção
A ventilação artificial para anestesia de
pequenos animais pode constituir dificuldade
especial em centros de pesquisa menos dotados
de recursos econômicos.
O presente trabalho descreve modelo
de respirador artificial de fácil construção e
manuseio1 para uso em pesquisas com pequenos
animais, construído empregando-se sistema
de bomba de roletes2, comumente usada em
circulação extracorpórea, mas com furo no
tubo de borracha (látex) (Figs. 1,2) para melhor
controle do volume e tempo inspiratórios. Em
dez ratos albinos, sem distinção de sexo, com
pesos variáveis entre 280 e 350g. Após anestesia
procedeu-se à traqueotomia e entubação traqueal,
com cânula adaptada para redução do espaço
morto, otimizando a dinâmica de ventilação
(Fig.3).
Após uma hora de respiração controlada
com ventilador de roletes, realizaram-se
toracotomia mediana anterior e punção da aorta
ascendente, obtendo-se amostra de sangue
arterial para controle gasométrico, determinandose os níveis de pH, pCO2, pO2 e “BE” (diferença
de bases).
Concluída a experiência os animais foram
sacrificados por injeção intracardíaca de cloreto
de potássio.
Fig. 2 - Bomba de roletes e tubo de látex com poro de 10mm para
estalecer o volume de ar injetado em cada ciclo respiratório.
Fig. 3 – Cânula traqueal com poro, para redução do espaço morto.
Todos os animais suportaram todo o
período de experiência programado.
pós a toracotomia pôde-se constatar
ex¬pansão cíclica adequada dos pulmões, sem
lesões ou rotura bronquíolo-alveolar (fístulas)
detectáveis à ectoscopia.
O Quadro I mostra os resultados
metabólicos obtidos, podendo-se notar valores
médios satisfatórios com pH de 7,38, pO2 de
134,2 mmHg, pCO2 de 35,0 mmHg e “BE” de 4,4 mEq.de bases).
Quadro I - Avaliação Metabólica dos Animais
Fig. 1 - Ventilador para pequenos animais composto por bomba
de roletes, circuito ou tubos de látex e PVC e adap-tador para
cânula traqueal.
OBS
pH
Nº
pO2
pCO2 “B.E.”
mmHg mmHg mEq/L
1
2
3
4
5
6
7
8
9
10
7,273
7,360
7,780
7,460
7,430
7,040
7,383
7,352
7,357
7,331
83,5
107,7
248,9
60,0
190,0
79,2
183,0
121,9
140,2
127,8
37,5
30,5
5,9
18,8
16,7
112,0
33,0
33,9
31,0
30,9
- 7,8
- 3,8
- 3,5
- 5,0
- 10,2
+ 1,8
- 3,5
- 4,6
- 3,9
- 3,7
Média
7,38
134,2
35,0
- 4,4
35
Comentários
O ventilador com roletes descrito destacase pela simplicidade funcional, pelo baixo custo
e pela facilidade de aquisição, posto que estas
bombas estão muito difundidas.
Entre os dez animais estudados, sete
evoluíram com perfis metabólicos altamente
satisfatórios. Os desvios observados nos ratos de
números 3 e 6 poderiam ser facilmente corrigidos
por variações dos roletes no rato nº 3 e aumento
no nº 6.
Pode-se concluir, com base no estudo
realizado, que o ventilador artificial de roletes,
com o circuito descartável descrito, permite
manutenção respiratória adequada em animais
de pequeno porte.
REFERÊNCIAS
1. Gomes OM, Pitchon M, Filgueiras MP,
Monteiro ELC. Ventilador de roletes, para
pequenos animais. LA Arch. Cardiovasc. Sci.
2002; 3 (2):10-12
2. De Backey, M.E. - Apud in Galletti, P.M.
& Brecher, G.A. Heart-Lung Bypass. Principles
and techniques for extracorporeal circulation.
New York, Grune & Stratton, 1962
36
maia, hcA et al - Esophageal Protection During Atrial Fibrillation Ablation.
UPDATING ARTICLE
ARTIGO DE ATUALIZAÇÃO
Esophageal Protection During Atrial Fibrillation Ablation.
Proteção Esofágica Durante Ablação de Fibrilação Atrial.
Henrique César de Almeida Maia1, Simone Nascimento dos Santos Santos2 ,
Benhur Davi Henz2,Luiz Roberto Leite da Silva2
A series of complications have been
associated with atrial fibrillation ablation, among
them the thromboembolism, the pulmonary vein
stenosis, phrenic nerve injury, cardiac tamponade
and esophageal injuries1-4. The latter is expressed
as esophageal mucosa injury, esophagus
perforation and formation of atrio-esophageal
fistula5-8.
Those two forms of injury have different
prognosis and occurrence, though they have
the same physiopathology and one, the fistula,
results from the other, the esophageal mucosa
injury 7,9.
The occurrence of esophageal mucosa
injury is premature and can be seen by means
of a digestive endoscopy on the first day after the
ablation9 and has an incidence relatively high,
around 35% of the cases in some series10. It can
be asymptomatic or be expressed by symptoms
of dysphagia, pyrosis or retroesternum pain and
generally has benign evolution, with self-solution
on the first four weeks10. The atrio-esophageal
fistula, on the other hand, has an incidence
estimated in 0.1%9, has a later evolution,
higher incidence around the third week after the
postoperative period and it is generally associated
with a high morbidity and mortality secondary to
gaseous embolism and sepsis8.
The physiopathological mechanism of the
esophagus injury has been ascribed to the thermal
injury secondary to the application of energy on
the lower wall of the left atrium during the ablation
procedure, due to a close anatomic relationship
between the left atrium and the esophagus, and
the little thickness of the atrium muscular wall in
that region9,11-15. It corroborates that concept, the
observation, in animal models, of the relationship
between esophageal and transmural injury of the
atrium13.
In this context, it has been proposed that
the esophageal temperature monitoring in regions
near the area where energy is applied during the
atrial fibrillation ablation would result in decreasing
the occurrence of esophageal injury9,17.
In fact, when using a temperature probe in
the esophagus and moving it to the craniocaudal
direction in order to position it as close as
possible to the ablation point and interrupting
the application of energy when the esophageal
temperature reaches 38.5°C, it was possible
to prove the reduction from 36% to 6%9 of
occurrence of esophageal mucosa injury visible
by the high digestive endoscopy.
The premise that the esophageal
temperature monitoring results in a reduction
of the occurrence of the esophageal injury
is reproducible and accepted by most of the
authors9,11-13,16,17. However, papers published
about the theme present several questions to be
considered, among them:
1- Ritmocardio - Serviço de Arritmia e Eletrofisiologia de Brasilia
2- Centro de Fibrilação Atrial do Distrito Federal - Hospital Brasília - Brasília - DF
Correspondence:
Henrique César de Almeida Maia
Ritmocardio - Serviço de Arritmia e Eletrofisiologia de Brasilia
SHLS 716 Ed. Centro Clínico Sul, Torre I - Sala 17.
Brasília – DF, Brasil, CEP: 70390-700 .
37
• The occurrence of esophageal injury
does not increase proportionally to the quantity
of energy applications that result in the increase
of esophageal temperature above 38.5°C9.
• Absence of esophageal temperature
from which occurs larger quantity of esophageal
injury16.
• There is no relationship between the
energy application power and occurrence of
injury9.
• Absence of other factors, regardless the
esophageal temperature, related to the formation
of esophageal injury, such as the use of general
anesthesia and gastric investigation9,16.
The reason for those considerations
seems to result from the limitations inherent
to the method used to monitor the esophageal
temperature. The probe with just one temperature
sensor restrains the observation to a small area
of the esophagus16,18, even to probes with several
sensors is helpful for craniocaudal monitoring,
because the side movement of the probe can
result in the esophagus traction towards the
energy application point and, through that,
generate an iatrogenic injury16. That seems to
be a critical restrain for esophageal temperature
monitoring.
It must be taken into account that the
probes used have a diameter much smaller than
the esophagus lumen and that the esophagus is
mobile in the region it is in contact with the left
atrium. Those factors, associated with the obstacle
for the side movement of the probe, can result in
a fake confidence feeling and energy application
away from the esophageal monitoring probe, but
on the esophagus, once it is not visible in X-rays.
That can explain the residual occurrence of 6%
of injury even when esophageal temperature
monitoring is used.
Finally, the tissue injury during the ablation
is due the temperature the tissue reaches and the
time in which it is kept under such temperature.
Thus, to prevent an esophageal injury during the
ablation, the temperature monitoring procedure
needs to be able to determine the temperature
increase in a very short time, in order to reduce as
much as possible the tissue exposure to heat18.
So, one of the factors to be taken into
account is the response time of the temperature
sensor. Such time depends on the heating thermal
constant (time that the temperature sensor needs
to inform the actual temperature) which can
38
vary from fractions of seconds to more than 10
seconds19. A second factor that determines the
speed the actual temperature recording occurs
is the sensor physical structure. Sensors coated
by thermal-conductive material, such as silicone,
like the esophageal temperature probes used in
cardiac surgeries, are very slow to determine the
temperature changes19.
The highest incidence of injury associated
with the use of general anesthesia during the
procedure seems to be related to the relative
reduction of esophageal movement secondary to
anesthesia. The esophagus motor response to the
thermal stimulus may be responsible for setting
the organ away from the heating point with the
consequent reduction of occurrence of injury16.
The use of a gastric probe during the atrial
fibrillation ablation seems to be related to the
increase of occurrence of injury on the esophageal
mucosa. The explanation for that phenomenon is
the curvature in the lower wall of the atrium due to
the presence of the probe inside the esophagus.
This would result in a better contact of the catheter
with the atrium wall (bigger pressure) increasing
the chance of transmural injury and consequent
esophageal injury16.
A new physiopathological aspect of the
atrio-esophageal fistula has been proposed based
on the observation of esophageal mucosa injury
in animal model that the use of proton pump
blockers avoids the fistula development16. Based
on that observation, it has been proposed that
the evolution from esophageal ulcer to atrioesophageal fistula is associated with the gastric
juice action, due to the gastro-esophageal reflux,
resulting from the periesophageal vagal plexus
during the ablation13. Thus, the preventive use
of hydrogen pump blockers has been proposed
to the preparation of patients to be submitted to
atrial fibrillation ablation16.
Other methods have been proposed to
decrease the occurrence of fistulas. Among them,
the esophagus displacement by the endoscope,
the non performance of injuries on the lower
wall, the power limitation during the application
on the lower wall, among others15,17,20,21. Most of
those approaches result in the limitation of the
number of injuries or the area covered during
the ablation, with the consequent reduction of
successful procedures.
Few trials have evaluated the occurrence
of esophageal injury post atrial fibrillation ablation
based on the visualization through endoscopy19,
almost all papers have used the esophagus
temperature as the evaluation method. That
approach leads to observation error, because
part of the patients in which there is increase of
esophageal temperature does not evolve with
esophageal injury, and the opposite is true as
well. From this concept, the best evaluation of
occurrence of post ablation injury is the direct
observation of injury by digestive endoscopy.
A systematic review and statistical reanalysis of the data from the papers that have
used digestive endoscopy as the criterion to
determine what factors are associated with the
esophageal injury formation has shown that no
method, separately, resulted in an important
reduction of the esophageal injury risk19. That trial
has also shown that the association of esophageal
temperature monitoring, limited to 39°C, with
the use of irrigated catheter and the esophagus
imaging visualization has an excellent negative
correlation with the formation of esophageal
injury (Correlation = 0.93, p=0.002)19. On the
other hand, the use of general anesthesia and the
gastric investigation are correlated with higher
occurrence of injury during the atrial fibrillation
ablation.
A recent trial22 showed that this
association of factors has a direct influence on
the esophageal injury formation. In that trial was
used the intracavitary echocardiogram to guide
the temperature probe to regions close to the
ablation point. Thus, it was possible to move
the probe not only to the craniocaudal direction
but also to the latero-lateral directions, without
iatrogenic displacement of the esophagus, once it
is visible by ultrasound. As a cut limit, it was used
the increase of 1°C in the esophageal temperature
and, as the esophageal probe, an ablation catheter
due to the fast response of the temperature
sensor (low heating thermal constant). That
trail evaluated 43 (forty-three) subjects and no
esophageal injury22 was observed.
Those results support the authors’ opinion
regarding the use of several factors for the
esophageal protection during the atrial fibrillation
ablation, among them the echocardiogram as a
positioning guide for the temperature probe.
REFERENCES
1. Jais P. et al. Phrenic nerve injury after atrial
fibrillation catheter ablation: characterization and
outcome in a multicenter study. J Am Coll Cardiol.
2006; 47, 2498 -2503.
2. Natale A. et al. Pulmonary vein total occlusion
following catheter ablation for atrial fibrillation:
clinical implications after long-term follow-up. J Am
Coll Cardiol.2006; 48, 2493-9.
3. Haissaguerre M. et al. Incidence and prevention
of cardiac tamponade complicating ablation for
atrial fibrillation.
Pacing Clin Electrophysiol. 2005; 28, S106 -9.
4. Morady F. et al. Risk of thromboembolic events
after percutaneous left atrial radiofrequency
ablation of atrial fibrillation.
Circulation.
2006;114,759 -65.
5. Pappone C. et al. Atrio-esophageal fistula as a
complication of percutaneous transcatheter ablation
of atrial fibrillation, Circulation.2004; 109, 27246.
6. Sossa E. et al. Left atrial-esophageal fistula
following radiofrequency catheter ablation of atrial
fibrillation. J Cardiovasc Electrophysiol.2004; 15,
960 -2.
7. Gillinov AM. et al. Esophageal injury during
radiofrequency ablation for atrial fibrillation. J
Thorac Cardiovasc Surg. 2001; 122, 1239-40.
8. Doll N. et al. Esophageal perforation during left
atrial radiofrequency ablation: is the risk too high? J
Thorac Cardiovasc Surg. 2003; 125, 836-42.
9. Reddy VY. et al. Esophageal injury and
temperature monitoring during atrial fibrillation. .
Circ Arrhythmia Electrophysiol.2008; 1, 162-8.
10. Jackman WM. et al. High incidence of
asymptomatic
esophageal
ulceration
after
pulmonary vein antrum isolation in patients with
atrial fibrillation. Heart Rhythm.2007; 14, S61.
11. Hornero F, Berjano EJ. Esophageal temperature
during radiofrequency catheter ablation of left
Atrium: a three-dimensional computer modeling
study. J Cardiovasc Electrophysiol.2006; 17, 40510.
12. Klein G.J. et al. Esophageal temperature
monitoring during radiofrequency ablation of atrial
fibrillation. J Cardiovasc Electrophysiol. 2005; 16,
589 -93.
13. Jackman WM. et al. Canine model of
esophageal injury and left atrial-esophageal fistula
after pulmonary vein isolation. Circulation. 2007;
116(Suppl II), II-490.
14. Hayashida H. et al. Atrial fibrillation ablation with
esophageal cooling with a cooled-water irrigated
39
intraesophageal balloon. J Cardiovasc Electrophysiol. 2007;
18, 145-50.
15. Berjano EJ, Hornero F. A cooled intraesophageal
balloon to prevent thermal injury during endocardial surgical
radiofrequency ablation of the left atrium: a finite element
study. Phys. Med. Biol. 2005; 50, 269 -79.
16. Nakagawa MD. et al. Limitations of Esophageal
Temperature-Monitoring to Prevent Esophageal Injury During
Atrial Fibrillation Ablation Circ Arrhythmia Electrophysiol.
2008; 1, 150-2.
17. Bahnson WM. Strategies to Minimize the Risk of Esophageal
Injury durings Catheter Ablation for Atrial Fibrillation. Pace.
2009; 32(02), 248-60.
18. Cosman ER, Rittman WJ. Physical Aspects of radiofrequency
energy applications. In: HUANG S. K. S. (Ed.). Radiofrequency
Catheter Ablation of Cardiac Arrhythmias. New York, Futura.
1995; p. 13-23.
19. Maia HCA. et al. Avaliação do tempo de resposta dos
sensores empregados na monitorização de temperatura
esofágica durante ablação de fibrilação atrial..Remblampa.
2006; 19(4), 259.
20. Ikeda A. et al. Can cryo-catheter ablation in left atrium
produce esophageal injury? Heart Rhythm. 2008; 15, S68.
21. Jackman WM. et al. Esophageal cooling prevents
esophageal injury during pulmonary vein ablation in a canine
model. Heart Rhythm.2007; 14,S12.
22. Silva LRL. et al. Monitorização da Temperatura Esofágica
Guiada pelo Ecocardiograma Intracardíaco na Prevenção de
Lesão Esofágica Remblampa. 2009; 22(4), 172.
40
maia, hcA et al - Protección Esofágica Durante Ablación de Fibrilación del Atrio.
ARTÍCULO ORIGINAL
UPDATING ARTICLE
Protección Esofágica Durante Ablación de Fibrilación del Atrio.
Benhur Davi Henz2, Luiz Roberto Leite da Silva2
Una serie de complicaciones se han
asociado a la ablación de fibrilación del atrio,
incluso el tromboembolismo, la estenosis de la
vena pulmonar, la lesión del nervio frénico, el
taponamiento cardiaco y las lesiones esofágicas
1-4
.Esta última se manifiesta tanto como lesión en
la mucosa esofágica como por perforación del
esófago y formación de fístula atrio esofágica 5-8.
Eses dos modos de lesión tienen
pronóstico y ocurrencias distintas, aunque tengan
la misma fisiopatología y una, la fístula, se resulte
de la otra, la lesión de la mucosa esofágica 7,9.
La ocurrencia de la lesión de la mucosa
esofágica es precoz y se puede verla a través
de la endoscopia digestiva en el primer día tras
la ablación e incide de manera relativamente
elevada, cerca de un 35% de los casos en algunas
series10. Puede ser asintomático o manifestarse
con síntomas de disfagia, pirosis o dolor
retroesternal y generalmente tienen una evolución
benigno, con auto resolución en las primeras
cuatro semanas10. La fístula atrio esofágica, por el
contrario, tiene incidencia estimada en un 0.1%9,
tiene un desarrollo posterior, mayor incidencia
alrededor de la tercera semana de postoperatorio
y generalmente se asocia a una alta morbilidad
y mortalidad secundaria a la embolia gaseosa y
sepsis8.
El mecanismo fisiopatológico de la lesión
del esófago se ha atribuido a la lesión térmica
secundaria a la aplicación de energía en la
pared posterior del atrio izquierdo durante el
procedimiento de ablación, debido a la relación
íntima anatómica entre el atrio izquierdo y el
esófago, y la pequeña espesura de la pared
muscular del atrio en esa región9,11-15. Apoya ese
concepto de observación, en modelos animales,
de la relación entre lesión esofágica y transmural
del atrio13.
En ese contexto, fue propuso que el
control de la temperatura esofágica en las
regiones cerca del área donde se aplica energía
durante la ablación de la fibrilación del atrio
resultaría en la reducción de la ocurrencia de
lesión esofágica9,17.
De hecho, al utilizar una sonda de
temperatura en el esófago y moverla en el sentido
cráneo caudal hasta ponerla lo más cerca posible
del punto de ablación, haciendo la interrupción
de la aplicación de energía cuando la temperatura
esofágica llega a 38.5º C se ha demostrado
una reducción de un 36% hacia un 6%9 de la
ocurrencia de lesión de la mucosa esofágica
visible a través de una alta endoscopia digestiva.
La premisa que el control de la temperatura
esofágica resulta en una reducción de la
ocurrencia de lesión esofágica es reproducible y
aceptada por la mayoría de los autores 9,11-13,16,17.
Sin embargo, los trabajos publicados sobre el
tema presentan muchas cuestiones a considerar,
incluso:
• La ocurrencia de lesión esofágica no
aumenta de manera proporcional a la cantidad
de aplicaciones de energía que resultaran en el
aumento de la temperatura esofágica superior a
38.5ºC9.
• Falta de una temperatura esofágica
desde la que tiene mayor cantidad de lesión
esofágica16.
• No hay relación entre potencia de la
aplicación de energía y ocurrencia de lesión9.
• Hay otros factores, independientes de la
temperatura esofágica, en relación a la formación
de la lesión esofágica, tales como la utilización de
anestesia general y sonda gástrica9,16.
La razón para estas consideraciones
parece resultar de las limitaciones inherentes al
Correspondencia:
41
método utilizado para controlar la temperatura
del esófago. Las sondas de un sólo sensor
de temperatura limitan la observación a una
pequeña área del esófago16,18, aunque la sonda
con muchos sensores sólo ayudan en el control
cráneo caudal, pues el movimiento lateral de la
sonda puede resultar en la tracción del esófago
hacia cerca del punto de aplicación de energía
y, con eso, generar lesión iatrogénica16. Esa
parece una limitación crítica en el control de la
temperatura del esófago.
Hay que tener en cuenta que las sondas
utilizadas tienen un diámetro menor que el lumen
del esófago y que el esófago en el área que está
en contacto con el atrio izquierdo es móvil.
Estos factores, asociados a la obstrucción del
movimiento lateral de la sonda, pueden resultar
en falso sentido de seguridad y aplicación de
energía lejos de la sonda de control esofágico,
pero sobre el esófago, ya que nos es visible a los
rayos X. Eso puede explicar la ocurrencia residual
de cerca de un 6% de lesión, aunque se utilice
control de temperatura esofágica.
En última instancia, la lesión del tejido
durante la ablación es función de la temperatura
que alcanza el tejido y del tiempo en que se
mantiene en esta temperatura. Luego, para una
eficaz prevención de lesión del esófago durante
la ablación, es necesario que el procedimiento de
control de temperatura esté listo para determinar
el aumento de la temperatura en un corto tiempo,
hasta que reduzca al máximo la exposición del
tejido al calor18.
Luego, uno de los factores que debe
tenerse en cuenta es el tiempo de respuesta del
sensor de temperatura. Ese tiempo depende de
la constante térmica de calentamiento (tiempo de
retraso del sensor de temperatura en informar la
temperatura real) que puede ir desde fracciones
de segundo hasta más que 10 segundos19. Un
segundo factor que determina la velocidad en
que se ocurre el registro real de la temperatura
es la constitución física del sensor. Sensores
involucrados en material de poca conducción
térmica, como la silicona, así como se ocurre en
las sondas de temperatura esofágica utilizadas
durante cirugía cardíaca, son muy lentos al
determinar cambios de temperatura19.
La mayor incidencia de lesión asociada
a la utilización de anestesia general durante el
procedimiento parece relacionarse con la relativa
reducción del movimiento esofágico secundario
a la anestesia. La respuesta motora del esófago
al estímulo térmico puede responsabilizarse
del alejamiento del órgano del punto de
calentamiento con consecuente reducción de la
42
ocurrencia de lesión16.
La utilización de sonda gástrica durante la
ablación de la fibrilación del atrio también parece
relacionarse con el aumento de ocurrencia de
lesión de la mucosa esofágica. La explicación
para ese fenómeno está en la curvatura de la
pared posterior del atrio a causa de la presencia
de la sonda dentro del esófago. Eso resultaría
en un mejor contacto del catéter con la pared
del atrio (mayor presión) con aumento de la
posibilidad de lesión transmural y consecuente
lesión esofágica16.
Un nuevo aspecto de la fisiopatología
de la fístula atrio esofágico se ha propuesto
en la observación de lesión de la mucosa del
esófago en modelo animal que la utilización de
bloqueadores de la bomba de protones evita
el desarrollo de la fístula16. Con base en esa
observación se ha propuesto que la evolución
de la úlcera esofágica para fístula atrio esofágica
se asocia a la acción del jugo gástrico, debido al
reflujo gastroesofágico, resultante de la lesión del
plexo vagal periesofágico durante la ablación13.
Luego, la utilización preventiva de bloqueadores
de la bomba de hidrógeno se ha propuesto en
la preparación de los pacientes sometidos a
ablación de fibrilación del atrio16.
Otros métodos se han propuestos con el
objetivo de reducir la ocurrencia de fístulas. Entre
ellos, el desplazamiento del esófago a través de
un endoscopio, no realizar lesiones en la pared
posterior, la limitación de potencia durante
aplicación en la pared posterior, entre otros15,17,20,21.
Esos abordajes resultan, en la mayor parte, en
limitación del número de lesiones o del área
abarcada durante la ablación, con consecuente
reducción del suceso del procedimiento.
Pocos estudios evaluaran la ocurrencia
de lesión del esófago postoblación de fibrilación
del atrio con base en la visualización a través de
endoscopia, casi todos los trabajos han utilizado
la temperatura del esófago como método de
evaluación.
Ese abordaje conduce a errores de
observación, pues parte de los pacientes en los
cuales se ocurre el aumento de temperatura
esofágica no se evoluciona con lesión de
esófago y el inverso también se hace verdad.
Con base en este concepto, la mejor evaluación
de la ocurrencia de lesión postoblación es la
observación directa de la lesión a través de una
endoscopia digestiva.
Una revisión sistemática y un nuevo análisis
estadísticos de los datos de los trabajos que han
utilizado endoscopia digestiva como criterio para
determinar qué factores se asocian a la formación
de lesión del esófago han demostrado que
ningún método, individualmente, ha resultado
en importante reducción del riesgo de lesión del
esófago19. Este estudio también ha presentado
que al asociar el control de la temperatura
esofágica, con límite en 39ºC, asociado a la
utilización de catéter irrigado y la visualización por
imagen del esófago tienen excelente correlación
negativa con formación de lesión esofágica
(Correlación=0.93, p=0.002)19. De otra manera,
la utilización de anestesia general y sonda gástrica
se correlacionan con mayor ocurrencia de lesión
durante la ablación de fibrilación del atrio.
Un reciente22 trabajo ha demostrado que
al asociar los factores, habrá influencia directa en
la formación de lesión esofágica. En ese trabajo se
ha utilizado el ecocardiograma intracavitario para
llevar la sonda de temperatura a la región cerca
del punto de ablación. De esa manera ha sido
posible mover la sonda no sólo en sentido cráneo
caudal, pero también en sentido latero lateral,
sin desplazamiento iatrogénico del esófago, ya
que se puede verlo a través del ultrasonido. El
aumento de 1ºC ha sido utilizado como límite de
corte en la temperatura esofágica y, como sonda
esofágica, un catéter de ablación por la rápida
respuesta de su sensor de temperatura (baja
constante térmica de calentamiento). En este
estudio han sido evaluados 43 pacientes y no se
ha observado ninguna lesión esofágica22.
Esos resultados sustentan la opinión
de los autores sobre la utilización de muchos
factores en la protección esofágica durante
la ablación de fibrilación del atrio, incluso el
ecocardiograma como guía de posición de la
sonda de temperatura.
of atrial fibrillation, Circulation.2004; 109, 2724-6.
6. Sossa E. et al. Left atrial-esophageal fistula following
radiofrequency catheter ablation of atrial fibrillation. J
Cardiovasc Electrophysiol.2004; 15, 960 -2.
7. Gillinov AM. et al. Esophageal injury during radiofrequency
ablation for atrial fibrillation. J Thorac Cardiovasc Surg. 2001;
122, 1239-40.
8. Doll N. et al. Esophageal perforation during left atrial
radiofrequency ablation: is the risk too high? J Thorac
Cardiovasc Surg. 2003; 125, 836-42.
9. Reddy VY. et al. Esophageal injury and temperature
monitoring during atrial fibrillation. . Circ Arrhythmia
Electrophysiol.2008; 1, 162-8.
10. Jackman WM. et al. High incidence of asymptomatic
esophageal ulceration after pulmonary vein antrum isolation in
patients with atrial fibrillation. Heart Rhythm.2007; 14, S61.
11. Hornero F, Berjano EJ. Esophageal temperature during
radiofrequency catheter ablation of left Atrium: a threedimensional computer modeling study. J Cardiovasc
12. Klein G.J. et al. Esophageal temperature monitoring during
radiofrequency ablation of atrial fibrillation. J Cardiovasc
Electrophysiol. 2005; 16, 589 -93.
13. Jackman WM. et al. Canine model of esophageal injury
and left atrial-esophageal fistula after pulmonary vein isolation.
Circulation. 2007; 116(Suppl II), II-490.
18, 145-50.
2008; 1, 150-2.
2009; 32(02), 248-60.
REFERENCES
2006; 47, 2498 -2503.
Coll Cardiol.2006; 48, 2493-9.
atrial fibrillation. Pacing Clin Electrophysiol. 2005;
28, S106 -9.
after percutaneous left atrial radiofrequency ablation
of atrial fibrillation. Circulation. 2006;114,759 65.
5. Pappone C. et al. Atrio-esophageal fistula as a
complication of percutaneous transcatheter ablation
1995; p. 13-23.
2006; 19(4), 259.
43
maia, hc et al - Proteção Esofágica Durante Ablação de Fibrilação Atrial.
UPDATING ARTICLE
ARTIGO DE ATUALIZAÇÃO
Proteção Esofágica Durante Ablação de Fibrilação Atrial.
Benhur Davi Henz2, Luiz Roberto Leite da Silva2
Uma série de complicações tem sido
associada à ablação de fibrilação atrial, entre
elas o trombo-embolismo, a estenose de
veia pulmonar, a lesão do nervo frênico, o
tamponamento cardíaco e as lesões esofágicas
1-4
. Essa última se manifesta tanto como lesão
da mucosa esofágica quanto por perfuração do
esôfago e formação de fístula átrio-esofágica5-8.
Essas duas formas de lesão têm prognóstico
e ocorrência distintas, embora tenham a mesma
fisiopatologia e uma, a fístula, ser decorrente da
outra, a lesão da mucosa esofágica7,9.
A ocorrência de lesão de mucosa esofágica
é precoce e pode ser vista por endoscopia digestiva
no primeiro dia após a ablação9 e tem incidência
relativamente elevada, cerca de 35% dos casos
em algumas séries10. Pode ser assintomática ou
manifestar-se com sintomas de disfagia, pirose ou
dor retroesternal e têm evolução habitualmente
benigna, com auto-resolução nas primeiras quatro
semanas10. A fístula átrio-esofágica, por outro
lado, têm incidência estimada em 0.1%9, tem
evolução mais tardia, maior incidência por
volta da terceira semana de pós-operatório e é
geralmente associada a uma elevada morbidade
e mortalidade secundária à embolia gasosa e
sepse8.
O mecanismo fisiopatológico da lesão do esôfago
tem sido atribuído a lesão térmica secundária à
aplicação de energia na parede posterior do átrio
esquerdo durante o procedimento de ablação,
devido a íntima relação anatômica entre o átrio
esquerdo e o esôfago, e a pequena espessura
da parede muscular do átrio nessa região9,1115.
Corrobora esse conceito a observação, em
modelos animais, da relação entre lesão esofágica
e transmural do átrio13.
Nesse contexto, foi proposto que a
monitoração da temperatura esofágica nas
regiões próximas à área onde se aplica energia
durante a ablação da fibrilação atrial resultaria em
diminuição da ocorrência de lesão esofágica9,17.
De fato, ao utilizar uma sonda de
temperatura no esôfago e movimentá-la no
sentido crânio-caudal de forma a posicioná-la o
mais próximo possível do ponto de ablação e
interrompendo a aplicação de energia quando a
temperatura esofágica atinge 38.5ºC foi possível
demonstrar diminuição de 36% para 6%9 da
ocorrência de lesão da mucosa esofágica visível
por endoscopia digestiva alta.
O premissa que a monitoração da
temperatura esofágica resulta em decréscimo
da ocorrência de lesão esofágica é reprodutível
e aceita pela maior parte dos autores 9,11-13,16,17. No entanto, os trabalhos publicados sobre
o tema apresentam várias questões a serem
consideradas, entre elas:
• A ocorrência de lesão esofágica não
aumenta proporcionalmente à quantidade de
aplicações de energia que resultaram no aumento
da temperatura esofágica acima de 38.5ºC9.
• Inexistência de uma temperatura
esofágica a partir da qual ocorre maior quantidade
de lesão esofágica16.
• Não há relação entre potência da
aplicação de energia e ocorrência de lesão9.
• Existência de outros fatores, independentes da temperatura esofágica, relacionados à
formação da lesão esofágica como por exemplo
Correspondencia:
44
o uso de anestesia geral e sondagem gástrica9,16.
A razão para essas considerações parece
decorrer das limitações inerentes ao método
utilizado para monitorar a temperatura do
esôfago. As sondas com apenas um sensor de
temperatura limitam a observação a uma pequena
área do esôfago16,18, mesmo as sondas com vários
sensores ajudam apenas na monitoração crâniocaudal, pois a movimentação lateral da sonda
pode resultar em tração do esôfago para próximo
do ponto de aplicação de energia e, com isso,
gerar lesão iatrogênica16.Essa parece ser uma
limitação crítica na monitoração da temperatura
do esôfago.
Deve-se levar em consideração que as
sondas utilizadas têm diâmetro muito menor que o
lúmen do esôfago e que o esôfago na região onde
está em contato com o átrio esquerdo, é móvel.
Esses fatores, associados ao impedimento da
movimentação lateral da sonda, podem resultar
em falsa sensação de segurança e aplicação de
energia longe da sonda de monitoração esofágica,
porém sobre o esôfago, já que ele não é visível aos
raios-x. Isso pode explicar a ocorrência residual
de cerca de 6% de lesão mesmo quando se utiliza
monitoração de temperatura esofágica.
Em última análise, a lesão tecidual
durante a ablação é função da temperatura que
o tecido atinge e do tempo em que ele é mantido
em tal temperatura. Assim, para uma eficiente
prevenção de lesão do esôfago durante a ablação,
é necessário que o procedimento de monitoração
de temperatura seja capaz de determinar o
aumento da temperatura em muito pouco tempo,
de modo a diminuir ao máximo a exposição do
tecido ao calor18.
Assim, um dos fatores a ser levado em
consideração é o tempo de resposta do sensor de
temperatura. Esse tempo depende da constante
térmica de aquecimento (tempo que o sensor de
temperatura demora em informar a temperatura
real) que pode variar de frações de segundo até
mais que 10 segundos19. Um segundo fator que
determina a velocidade com que o registro real
da temperatura ocorre é a constituição física do
sensor. Sensores envoltos em material pouco
termo-condutor, como silicone, tal como ocorre
nas sondas de temperatura esofágica utilizadas
durante cirurgia cardíaca, são muito lentos em
determinar mudanças de temperatura19.
A maior incidência de lesão associada ao
uso de anestesia geral durante o procedimento
parece estar relacionado à relativa diminuição da
movimentação esofágica secundária à anestésia.
A resposta motora do esôfago ao estímulo térmico
pode ser responsável por afastamento do órgão
do ponto de aquecimento com conseqüente
diminuição da ocorrência de lesão16.
O uso de sonda gástrica durante a
ablação da fibrilação atrial também parece estar
relacionada com aumento de ocorrência de
lesão da mucosa esofágica. A explicação para
esse fenômeno está no abaulamento da parede
posterior do átrio pela presença da sonda dentro
do esôfago. Isso resultaria em melhor contato do
cateter com a parede do átrio (maior pressão)
com aumento da chance de lesão transmural e
conseqüente lesão esofágica16.
Um novo aspecto da fisiopatologia da
fístula átrio-esofágica tem sido proposta baseada
na observação de lesão da mucosa do esôfago
em modelo animal que o uso de bloqueadores
da bomba de prótons evita o desenvolvimento
da fístula16. Com base nessa observação tem sido
proposto que a evolução da úlcera esofágica para
fístula átrio-esofágica está associada à ação do
suco gástrico, devido ao refluxo gastro-esofágico,
resultante da lesão do plexo vagal peri-esofágico
durante a ablação13. Assim, o uso preventivo
de bloqueadores da bomba de hidrogênio tem
sido proposto no preparo dos pacientes a serem
submetidos à ablação de fibrilação atrial16.
Outros métodos têm sido propostos no
intuito de diminuir a ocorrência de fístulas. Dentre
eles, o deslocamento do esôfago por endoscópio,
a não realização de lesões na parede posterior, a
limitação de potência durante aplicação na parede
posterior, entre outros15,17,20,21. Essas abordagens
resultam, em sua maioria, em limitação do
número de lesões ou da área abordada durante
a ablação, com conseqüente diminuição do
sucesso do procedimento.
Poucos estudos avaliaram a ocorrência
de lesão do esôfago pós-ablação de fibrilação
atrial tendo por base a sua visualização por
endoscopia19, quase todos os trabalhos utilizaram
como método de avaliação a temperatura
do esôfago. Essa abordagem leva a erro de
observação, pois parte dos pacientes nos quais
ocorrem aumento de temperatura esofágica não
evoluem com lesão de esôfago, sendo o inverso
também verdadeiro. Partindo deste conceito, a
melhor avaliação da ocorrência de lesão pósablação é a observação direta da lesão por
endoscopia digestiva.
Uma revisão sistemática e re-análise
estatística dos dados dos trabalhos que
utilizaram endoscopia digestiva como critério
para determinar quais fatores estão associados
à formação de lesão do esôfago demonstrou
que nenhum método, isoladamente, resultou
em importante diminuição do risco de lesão do
45
esôfago19. Esse estudo também demonstrou que
a associação da monitoração da temperatura
esofágica, com limite em 39ºC, associado ao uso
de cateter irrigado e a visualização por imagem do
esôfago têm excelente correlação negativa com
formação de lesão esofágica (Correlação=0.93,
p=0.002)19. Por outro lado, o uso de anestesia
geral e a sondagem gástrica se correlacionam
com maior ocorrência de lesão durante a ablação
de fibrilação atrial.
Em trabalho recente22 demonstrou que
essa associação de fatores tem influência direta
na formação de lesão esofágica. Nesse trabalho
foi utilizado o ecocardiograma intracavitário para
guiar a sonda de temperatura para as regiões
próximas ao ponto de ablação. Dessa forma foi
possível movimentar a sonda não somente no
sentido crânio-caudal, mas também no sentido
látero-lateral, sem deslocamento iatrogênico do
esôfago, visto que esse é visível pelo ultrassom.
Utilizou-se como limite de corte o aumento de
1ºC na temperatura esofágica e, como sonda
esofágica, um cateter de ablação pela a rápida
resposta do seu sensor de temperatura (baixa
constante térmica de aquecimento). Nesse estudo
foram avaliados 43 pacientes e não se observou
nenhuma lesão esofágica22.
Esses resultados suportam a opinião
dos autores quanto ao uso de vários fatores na
proteção esofágica durante a ablação de fibrilação
atrial entre eles o ecocardiograma como guia de
posicionamento da sonda de temperatura.
REFERÊNCIAS
2006; 47, 2498 -2503.
Coll Cardiol.2006; 48, 2493-9.
atrial fibrillation. Pacing Clin Electrophysiol. 2005;
28, S106 -9.
after percutaneous left atrial radiofrequency ablation
of atrial fibrillation. Circulation. 2006;114,759 65.
5. Pappone C. et al. Atrio-esophageal fistula as
a complication of percutaneous transcatheter
ablation of atrial fibrillation, Circulation.2004;
109, 2724-6.
7. Gillinov AM. et al. Esophageal injury during radiofrequency
ablation for atrial fibrillation. J Thorac Cardiovasc Surg. 2001;
122, 1239-40.
8. Doll N. et al. Esophageal perforation during left atrial
radiofrequency ablation: is the risk too high? J Thorac
Cardiovasc Surg. 2003; 125, 836-42.
9. Reddy VY. et al. Esophageal injury and temperature
monitoring during atrial fibrillation. . Circ Arrhythmia
10. Jackman WM. et al. High incidence of asymptomatic
esophageal ulceration after pulmonary vein antrum isolation in
patients with atrial fibrillation. Heart Rhythm.2007; 14, S61.
11. Hornero F, Berjano EJ. Esophageal temperature during
radiofrequency catheter ablation of left Atrium: a threedimensional computer modeling study. J Cardiovasc
12. Klein G.J. et al. Esophageal temperature monitoring during
radiofrequency ablation of atrial fibrillation. J Cardiovasc
Electrophysiol. 2005; 16, 589 -93.
13. Jackman WM. et al. Canine model of esophageal injury
and left atrial-esophageal fistula after pulmonary vein isolation.
Circulation. 2007; 116(Suppl II), II-490.
18, 145-50.
2008; 1, 150-2.
2009; 32(02), 248-60.
1995; p. 13-23.
2006; 19(4), 259.
6. Sossa E. et al. Left atrial-esophageal fistula
following radiofrequency catheter ablation of atrial
fibrillation. J Cardiovasc Electrophysiol.2004; 15,
960 -2.
46
UPCOMING EVENTS
47
48
49

13 - Cardiovascular Sciences Forum

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