Left Atrial Epicardial Adiposity and Atrial Fibrillation

Transcription

Omar Batal, MD, Paul Schoenhagen, MD, Mingyuan Shao, MS, Ala Eddin Ayyad, MD,
David R. Van Wagoner, PhD, Sandra S. Halliburton, PhD,
Patrick J. Tchou, MD, and Mina K. Chung, MD
From the departments of: General Internal Medicine, Cleveland Clinic, Cleveland, Ohio, USA
(O.B., AE.A.), Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, USA (P.S., M.S.,
Downloaded from http://circep.ahajournals.org/ by guest on November 18, 2016
D.VW., P.T., M.C.), and Department of Diagnostic Radiology, Cleveland Clinic, Cleveland,
Ohio, USA (P.S., S.H.)
d
dence
Address correspondence
to:
Mina K. Chung, M.D
D
Department of Cardiovascular
iovascular Medicine
Heart and Vascular Institute
Cleveland Clinic
9500 Euclid Avenue, Desk J2-2,
Cleveland, OH 44195
Phone: 216-444-2290
FAX: 216-636-6951
Email: [email protected]
Journal Subject Codes: [5] Arrhythmias, clinical electrophysiology, drugs; [30] CT and MRI;
[113] Obesity; [114] Pericardial disease
Abstract
Background: Atrial fibrillation (AF) has been linked to inflammatory factors and obesity.
Epicardial fat is a source of several inflammatory mediators related to the development of CAD.
We hypothesized that peri-atrial fat may have a similar role in the development of AF.
Methods and Results: Left atrium (LA) epicardial fat pad thickness was measured in
consecutive cardiac CT angiograms performed for CAD or AF. Patients were grouped by AF
burden: No (N=73), Paroxysmal (60), or Persistent (36) AF. In a short axis view at the mid LA,
peri-atrial epicardial fat thickness was measured at the esophagus (LA-ESO), main pulmonary
artery and thoracic aorta; retrosternal fat was measured in axial view (right coro
coronary
ostium
ronn
ro
level). LA-area was determined in the 4-chamber view. LA-ESO fatt was
was thicker
thi
hick
cker
ck
e in patients with
persistent AF versus paroxysmal
was larger in
arox mal AF (p=0.011)
( 0.011) or no AF (p=0.003). LA-area wa
patients with persistent
(p<0.001).
LA-ESO
e AF than paroxysmal AF (p=0.004) or without AF (p<0.0
ent
0
was a significant predictor
LA area (odds
e
edictor
of AF burden even after adjusting for age, BMI and L
ratio 5.30, 95%CI 1.39-20.24, p=0.015). A propensity score-adjusted multivariable logistic
regression that included age, BMI, LA area and comorbidities was also performed and the
relationship remained statistically significant (p=0.008).
Conclusions: Increased posterior LA fat thickness appears to be associated with AF burden
independent of age, BMI, or LA-area. Further studies are necessary to examine cause and effect,
and if inflammatory, paracrine mediators explain this association.
Key words: Atrial fibrillation, inflammation, obesity, pericardium, tomography
2
Abbreviations:
AF: atrial fibrillation
BMI: Body Mass Index
CABG: Coronary Artery Bypass Grafting
CAD: Coronary Artery Disease
CHF: Congestive Heart Failure
CKD: Chronic kidney disease
CRP: C-reactive protein
CT: Computed tomography
DM: Diabetes mellitus
ESO: Esophagus
HPL: Hyperlipidemia
ia
HTN: Hypertension
LA: Left atrium
PA: Main pulmonary artery
PVI: Pulmonary vein isolation
RS: Retrosternal
TA: Thoracic aorta
3
Background:
Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice (1)
and is associated with increased morbidity and mortality (2). While AF pathophysiology is
complex, increasing evidence supports mechanistic links between inflammation and AF. AF has
been associated with inflammatory conditions that involve the heart such as pericarditis and
myocarditis (3, 4). The incidence of AF after coronary artery bypass grafting (CABG) is
increased, with a peak frequency coincident with peak postoperative C-reactive protein (CRP)
levels (5). In addition, CRP appears to be higher in patients with non-postoperative AF and is
associated with AF duration and persistence (6-8). Higher levels
the future
eve
vels
ls of
of CRP
CRP predict
p
development of AF in patients without prior history of AF (9).
atrial biopsies from
(9) Furthermore,
F h
atr
patients with AF have
inflammation
plays
v shown evidence of inflammatory cells, suggesting that inf
ve
f
a role in the pathogenesis
nesis of AF (10-11).
A relationship
inflammation, and
ip has been described between obesity,
y, epi/pericardial
p p
fa , in
fat,
coronary atherosclerosis. Perivascular adipocytes secrete inflammatory cytokines, and the extent
of epicardial fat is associated with the severity of coronary artery disease (CAD) (12-16).
Obesity is a risk factor for AF (17) and has been associated with pericardial fat (13), but the
potential relationship of peri-atrial epicardial fat and AF has not been previously described. We
sought to test the hypothesis that peri-atrial epicardial fat is associated with AF.
Methods:
Patient Population
4
We analyzed data from 169 consecutive patients, who underwent consecutive cardiac
computed tomography (CT) angiograms between January and May 2008, for evaluation of AF or
CAD. Subjects were identified from a cardiovascular CT registry. CT studies obtained for AF
were performed in evaluation for AF catheter ablation (pulmonary vein isolation, [PVI]).
Typically candidates for PVI at our institution are patients who have symptomatic AF despite
medical therapy. The study was approved by the Institutional Review Board with waiver of
consent for medical records review and performed according to institutional guidelines.
Data retrospectively collected from patient medical records included age, sex, body mass
index (BMI) (Kg/m2), comorbidities (hypertension [HTN], hyperlipidemi
hyperlipidemia
ia [HPL], diabetes
mellitus [DM], chronic kidney disease [CKD], CAD, congestive hea
heart
art fa
ffailure
ilur
il
uree [C
ur
[[CHF],
C
and thyroid
disease), history of AF,
burden
A AF burden, treatment by PVI. CAD, CHF and AF burd
d were defined
as per published guidelines
u
uidelines
(18-20). Patients were categorized according to their highest AF
burden (no history of
o AF, paroxysmal AF, and persistent AF). Paroxysmal AF
F was defined as
recurring AF terminating in 7 days or less. Persistent AF indicated a history of AF sustaining
beyond 7 days.
Imaging Protocol
Patients with known AF (N=95) were evaluated with cardiac CT angiography for PVI.
Multi-detector row CT technology was employed (Definition, Siemens Medical Solutions,
Erlangen, Germany or Brilliance 64, Philips Medical Systems, Cleveland, Ohio). The specific
imaging protocol for the clinically indicated scans was adapted to minimize radiation exposure
for each patient while insuring acceptable image quality. Electrocardiogram-referenced scans
were performed following intravenous administration of contrast material. Because pulmonary
vein assessment was the primary clinical goal, 1.5 mm thick images were reconstructed. Patients
5
evaluated for CAD (N=74) were imaged using the same scanner models. Again, the specific
imaging protocol was adapted for each patient and the electrocardiogram-referenced scan
performed following the intravenous administration of contrast material. For evaluation of the
coronary arteries, 0.75 mm thick slices were reconstructed.
For optimal visualization of
coronary anatomy, patients were pre-medicated with sublingual nitroglycerin and intravenous
beta-adrenergic blocker for coronary dilatation and heart rate control, respectively.
Image Analysis:
Using a standard clinical workstation (Leonardo, Siemens), advanced 3-dimensional offline post-processing was performed. The 3-dimensional CT dataset
to obtain
aset was reconstructed
recon
onns
standard cardiac views as used in echocardiography. We first reco
reconstructed
standard 2- and 4ons
nstr
truc
tr
ucte
uc
tedd st
te
sta
chamber views. LA size was determined by manually tracing the LA borders in
i the 4-chamber
view (making sure too exclude the pulmonary veins) and using computer softwa
software
a that calculates
the outlined area. The
perpendicular
h short axis view was reconstructed as a plane perpendicula
he
a to the long axis
of these two views at the level of the mid LA (Figure 1). In this short axis view, the peri-atrial
epicardial fat thickness was measured (in cm) as the shortest distance between the mid left
atrium (LA) wall and three anatomical landmarks: esophagus (LA-ESO), main pulmonary artery
(LA-PA), and descending thoracic aorta (LA-TA) [Figures 2 and 3]. These measurements were
prospectively determined, based on preliminary reviews of representative CT scans before
starting the study, which showed the esophagus, pulmonary artery and thoracic aorta were
readily identifiable anatomic structures which could be used to measure LA epicardial fat.
Retrosternal fat thickness (RS) was measured at the level of the right coronary artery (RCA)
ostium (Figure 4) in the axial view. RS fat was measured based on similar measurements of
epicardial fat thickness used in previous echocardiographic studies evaluating the association of
6
epicardial fat and CAD (14). Measurements were made utilizing digital calipers by a single
investigator (O.B.) with an intra-observer reproducibility of 0.957 (95% CI 0.909-0.979, intraclass correlation, same below) on measurements of epicardial fat and 0.984 (95% CI 0.9370.996) on measurements of LA-area. In a sample of 30 randomly selected patients, the interobserver reliability was 0.948 (95% CI 0.912-0.969) on measurements of epicardial fat and 0.978
(95% CI 0.954-0.990) on measurements of LA-area (by O.B. and P.S.). AF status was blinded to
the investigators at the time of epicardial fat measurements.
Statistical Methods:
AF burden was analyzed by grade (no AF=0, paroxysmal=1,
persistent=2).
Continuous
mal 1, persisten
ent
en
variables were compared using one-way analysis of variance and
were
reported
as mean ±
ndd w
eree re
er
repo
p
standard deviation iff normally distributed, or they were compared
Kruskal-Wallis
test and
d using Kruska
a
were reported as median
± interquartile range if not normally distributed. Pe
e
edian
Pearson
e
chi-square
analysis was used to compare categorical variables. Bonferroni adjustme
adjustment
e for multiple
comparisons was applied following the overall 3 group comparisons.
Univariable and multivariable ordinal logistic regression models were constructed to test
the association between peri-atrial LA-ESO fat thickness and AF burden. In the multivariable
model the covariates were age, BMI and LA area. The proportional odds assumption was tested.
Propensity scores were estimated by running logistic regression using the 75 percentile of LAESO as the response variable and age, BMI, LA area, and patient characteristics (gender,
hypertension, hyperlipidemia, diabetes mellitus, CAD, congestive heart failure, and
hypothyroidism) as the covariates. A propensity score-adjusted multivariable logistic regression
was then performed to adjust for imbalances of the registry data.
7
Missing data of LA-ESO and BMI were imputed using overall mean imputation, and the
imputed data were used to run logistic regressions as a supplement to the analyses of the original
data. Statistical testing was 2-sided and results were considered statistically significant at the
level of p<0.05, or at p<0.015 after the Bonferroni correction. All analyses were conducted using
SAS 9.1.3 (SAS Institute, Cary, NC).
Results:
Patient characteristics
Patient characteristics of the entire study are summarized iin
Table
n Ta
T
blle 1. Th
Thee mean age of the
169 patients included in this study was 54.6 ± 13.2 years (range 15-8
15-82
years);
-822 ye
-8
year
ars)
ar
s);; 334.9% of patients
s)
were female. The mean
ean body mass index (BMI) was 29.2 ± 6.1 Kg/m2. In this sstudy population,
73 (43.2%) patientss did not have AF, 60 (35.5%) had paroxysmal AF, andd 36(21.3%) had
persistent AF. Comorbid
o
orbid
conditions included CAD (15.4%), HTN (42.9%), HPL
HP
P (41.6%), DM
(7.1%), CHF (5.8%), CKD (1.9%) and thyroid disease (12.3%).
Characteristics by AF burden
As shown in Table 1, patients without AF were younger than patients with paroxysmal
AF (p=0.001) and persistent AF (p=0.007), respectively. The BMI of patients without AF
(p=0.311) or with paroxysmal AF (p=0.018) and patients with persistent AF was not
significantly different at the 0.015 significance level. The trend of a greater prevalence of CAD
in patients without AF (vs. paroxysmal AF p=0.019; vs. persistent AF p=0.003) likely reflected
the initial indications for CT angiography. Patients specifically evaluated for CAD had a higher
pretest probability of having CAD than patients who had the cardiac CT prior to PVI.
Differences in other comorbid factors were not statistically significant.
8
Peri-atrial and retrosternal fat and LA-area versus AF burden
Peri-atrial and retrosternal fat measurements by AF burden are summarized in Table 2.
Patients with persistent AF had a significantly thicker LA-ESO fat pad as compared to patients
with no AF (p=0.003) or with paroxysmal AF (p=0.011). A stepwise trend toward increasing
LA-ESO thickness was observed in patients with increasing AF burden and is depicted in figure
5.
The thickness of the retrosternal fat pad (RS) at the level of the RCA takeoff was
compared according to AF burden (table 2). RS fat pad thickness was not associated with AF
burden.
LA-Area was found to be larger in patients with persistent
tentt AF than
tha
hann in
in paroxysmal AF
(p=0.004) or in patients
ents without AF (p<0.001). This is shown in table 2.
Regression analysis::
The association between AF burden by grade (no AF=0, paroxysmal=1, persistent=2) and
peri-atrial LA-ESO fat thickness was assessed by ordinal logistic regression. Univariately, LAESO was a significant predictor of AF burden (odds ratio 6.06 [associated with a 1 cm increase
in LA-ESO], 95% confidence interval [CI] 1.90-19.25; p=0.002). After adjusting for age, BMI
and LA area, the association remained significant (odds ratio 5.30, 95% CI 1.39-20.24; p=0.015).
The assumption of proportional odds was satisfied. Given that it was a registry study of
imbalanced data, propensity scores were estimated in a logistic regression model by setting 75%
percentile of LA-ESO as the outcome variable and age, BMI, LA area, and patient characteristics
(gender, hypertension, hyperlipidemia, diabetes mellitus, CAD, congestive heart failure, and
9
hypothyroidism) as the covariates. A propensity score-adjusted multivariable logistic regression
was then performed. The obtained odds ratio was 6.17 (95% CI 1.60-23.85; p=0.008).
To offset missing data of LA-ESO and BMI in the small sample size, overall mean
imputation was applied to get a complete set of data. For adjusted ordinal logistic regression,
with the overall mean imputation the odds ratio turned out to be 5.09 (95% CI 1.51-17.19;
p=0.009).
Discussion:
In an imaging analysis of 169 patients with cardiac CT,
direct,
T, we found a ssignificant,
i
relationship between AF burden and the thickness of the posterior
or peri-atrial
per
erier
i attri
irial
al ffat
at pad between the
esophagus and the left
significant
l atrium. Furthermore, this relationship remained statistically
statistt
after adjusting for BMI,
M age, LA-area, and propensity score.
MI,
AF has been associated with obesity (17), as well as elevated C-reactive protein levels (59), a measure of systemic inflammation. Left atrial biopsies from patients with lone AF have
shown inflammatory cells (10). Obesity has been related to pericardial fat deposits (13). A
similar relationship between obesity, epicardial fat, and inflammation has been described for
coronary artery disease. It is increasingly recognized that distinct fat depots (such as
subcutaneous and visceral fat depots) differ in metabolic activity and in the pro-inflammatory
mediators secreted (21). Epicardial adipose tissue is a form of visceral adipose tissue located
between the myocardium and the parietal pericardium that shares a common embryonic origin
with intra-abdominal adiposity, a fat depot believed to play a role in metabolic syndrome (15,
21-23). Epicardial fat is a source of several inflammatory mediators, including interleukin-1E,
interleukin-6, tumor necrosis factor-D, and monocyte chemoattractant protein-1.
10
Paracrine
interactions of these cytokines and mediators contribute to peri-vascular inflammation and the
development of CAD (12-16, 21-23). As left atrial biopsies from patients with AF have shown
evidence of inflammatory cells in the atrial tissue, and a local inflammatory response may have a
role in the development of AF (11), we hypothesized that peri-atrial fat may be associated with
AF, perhaps as a promoter of AF persistence or reflective of the inflammatory changes
associated with AF.
It is interesting that only the LA-ESO (esophageal) peri-atrial fat was found to be
associated with AF burden in our study. Triggers that contribute to the initiation of AF are
located in the pulmonary vein ostia (24). The esophagus follows a course alon
along
ng tthe posterior wall
of the left atria and is in close anatomical proximity to the pulmonary
monaary vein
vei
einn ostia
osti
os
ti (25-26). Local
inflammatory mediators
produced by the peri-atrial epicardial fat in the LA po
posterior
wall may
a
ators
o
promote the activation
of ectopic foci in the pulmonary vein ostia. Moreover,
posterior
a
ation
Morr
pericardiectomy during
cardiac surgery has been associated with reduction in ppostoperative AF
r
ring
(27-30). This may in part be due to removal of the posterior esophageal pericardial fat pad.
While epicardial adipose tissue is considered to be pro-inflammatory and is associated
with metabolic syndrome and CAD, not all epicardial fat pads are similar. The heart is reported
to have mainly 3 epicardial fat pads with parasympathetic ganglia: a fat pad on the anterior
surface of the atria located between the aorta and the right pulmonary artery, a fat pad between
the inferior vena-cava and left atrium, and one between the superior vena-cava and right atrium
(31). Reports about the impact of surgical preservation of the anterior fat pad between the aorta
and right pulmonary artery on post-operative AF have had conflicting results (31). Epicardial fat
pad ablation in canine models did not suppress AF inducibility in the long term (32).
Nevertheless, in this study, only LA-ESO, which has not been characterized as having abundant
11
parasympathetic ganglia, was significantly associated with AF. Of interest, the LA-TA, LA-PA,
and RS fat pads were not associated with AF in our study population and rather appear to
decrease in size with AF burden, but this did not achieve statistical significance. It is possible
that, in a larger study, the trend toward thicker non-posterior fat pads in the no AF group might
reach statistical significance or correlate with the higher prevalence of CAD in the no AF group.
CAD has been associated with epicardial fat, and the non-posterior fat pads are likely in closer
proximity to the coronary arteries, rather than the pulmonary veins.
Histological analysis and molecular identification of inflammatory markers may be
necessary in future studies to better explain this association and
whether targeting
d to determinee w
left atrial adiposity is rational as a therapeutic goal. Preliminary data
taa ssuggest
ugge
ug
gest
ge
st a rrole for statins in
the primary and secondary
anti-inflammatory
effects (33o
ondary
prevention of AF, possibly due to their anti-inflamma
a
34). Although speculative,
it is possible that patients with more posterior peri-atrial
fat, such as
u
ulative,
peri-aa
patients with persistent
t
tent
AF, might derive more benefit from anti-inflammatory
y therapy to help
reduce AF burden.
Limitations: The AF and no AF groups may not represent all patients with and without AF. AF
patients in this study were younger than the typical AF population which may lead to a lower
prevalence of certain age-associated medical conditions such as HTN. This may limit the
applicability of our results to all AF patients. Similarly, patients in the no AF group were
generally referred for evaluation for CAD and thus had a larger prevalence of CAD and
associated medical conditions. This may have contributed to the trend toward thicker nonposterior left atrial fat thicknesses observed in the no AF group, as previous literature suggests a
relationship between coronary atherosclerotic disease and pericardial fat. Optimally, a matched
control without AF and without CAD should be used; however, this would require a prospective
12
enrollment of such patients in a controlled trial. Nonetheless, propensity score-adjusted logistic
regression was performed to adjust for imbalances of the registry data.
Although blinding was potentially limited by differences in slice thickness, and labeling
for studies that assessed CAD, the CT reading was blinded to AF status. Although thickness of
peri-atrial fat along the atrial wall is variable (25-26), the mid LA was used as a landmark to
measure peri-atrial fat using the shortest distance to the esophagus, pulmonary artery, and
thoracic aorta. A similar method was also applied to retrosternal fat measurements, using the
ostium of the right coronary artery as the landmark.
Our method of quantifying fat has limitations as it is unclear iff th
tthe epicardial fat
thicknesses based on a short axis view at the mid left atrium is representative
r pr
re
pres
essen
enta
tatti
ta
tiv of overall LA
epicardial fat. A better
been
t assessment of peri-atrial and retrosternal fat may have be
ter
e possible if an
automated method to
While
t measure the peri-atrial fat volume were available. Wh
h such analytic
approaches have been
e described to analyze epicardial fat surrounding the entire hheart (12-13), we
en
are currently unaware of software allowing limited assessment of peri-atrial fat burden. Future
software development may allow future studies to include volumetric assessments of peri-atrial
fat. Nevertheless, given the possible specific significance found in this study of LA-ESO fat, the
posteriorly located fat pad located near the pulmonary veins where AF triggers are located, focal
fat quantification may continue to be of interest, in addition to global periatrial fat volumes.
Volumetric assessments may also overcome variability in posterior LA fat measurements that
may be related to dynamic changes in esophageal movement relative to the posterior LA wall.
Implications: In our study, we investigated whether or not LA epicardial fat is associated with
atrial fibrillation. Our study suggests that the thickness of the posterior epicardial fat pad
between the LA and the esophagus (LA-ESO), which can easily be measured using cardiac CT,
13
is associated with an increased AF burden independent of the known AF risk factors of age,
BMI, and LA size. This may be explained in part by its proximity to the pulmonary vein ostia
which have known contributions to AF pathogenesis. These findings have potential implications
for better understanding of AF pathogenesis. Inflammation and inflammatory states have been
not only associated with AF duration and persistence, but also with the future development of AF
in patients without prior history of AF. While further studies are needed to determine the
inflammatory role of the posterior LA epicardial fat pad and its cause/ effect relationship with
AF, measurement of LA-ESO thickness during cardiac CT may prove to have a similar role as
other routinely measured inflammatory markers in relation to AF.
F.
Conclusion:
Increased posterior left atrial-esophageal fat pad thickness appears to be associated with
increased AF persistence,
t
tence,
independent of age, BMI, and LA-area. This first study
studd to describe an
association between LA pericardial fat and AF is hypothesis generating but does not define
causal connections. Future investigations are needed to further clarify the role of LA pericardial
fat in AF and to study the potential inflammatory role of posterior peri-atrial adiposity at a
microscopic and molecular level.
Funding Sources: This work was supported by NIH/NHLBI grant R01 HL090620 (MKC,
DRV); Leducq Foundation 07-CVD 03 (DRV); Atrial Fibrillation Innovation Center, State of
Ohio (MKC, DRV). The content is solely the responsibility of the authors and does not reflect
the views of the funding agencies.
Conflict of Interest Disclosures: None
14
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20
Table 1: Patient characteristics and biomarkers by AF burden
Total population
No AF
Paroxysmal AF
Persistent AF
N (%)
169
73 (43.2)
60 (35.5)
36(21.3)
Age, years, mean ± SD †
54.6 ± 13.2
50.1 ± 12.8
58.1 ± 12.4
58.0 ± 12.9
Female, N (%)
59 (34.9)
30 (41.1)
18 (30.0)
11 (30.6)
BMI, kg/m2, mean ± SD (N)
29.2 ± 6.1 (140)
29.2 ± 5.9 (47)
27.8 ± 6.1 (59)
31.4 ± 6.0 (34)
CAD†
26 (15.4)
19 (26.0)
6 (10.0)
1 (2.8)
HTN
66 (42.9)
23 (39.7)
25 (41.7)
18 (50.0)
HPL
64 (41.6)
20 (34.5)
26 ((43.3)
43.3
43
.3))
.3
18 (50.0)
DM
11 (7.1)
5 (8.6)
6 (10.0)
0
CHF
9 (5.8)
2 (3.4)
4 (6.7)
3 (8.3)
CKD
3 (1.9)
1 (1.7)
2 (3.3)
0
Hypothyroidism
16 (10.4)
5 (8.6)
7 (11.7)
4 (11.1)
Hyperthyroidism
3 (1.9)
0
2 (3.3)
1 (2.8)
Comorbidities, N (%) ‡
SD= standard deviation, AF= atrial fibrillation , BMI= body mass index, CAD= coronary artery disease, CHF=
congestive heart failure, CKD= chronic kidney disease, DM= diabetes mellitus, HPL= hyperlipidemia, HTN=
hypertension.
†p<0.015 when comparing age of no AF vs paroxysmal AF (p=0.001) and no AF vs persistent AF (p=0.007), and
prevalence of CAD in no AF vs persistent AF (p=0.003). All other comparisons had p>0.015. Bonferroni adjustment
was applied in the multiple comparisons.
‡
15 patients had incomplete documentation of their past medical history in their medical records (excluding AF or
CAD which were available in the CT report) and were treated as missing in terms of comorbidities.
21
Table 2: Left atrial size, Peri-atrial and retrosternal fat thickness
Total population
No AF
Paroxysmal AF
Persistent AF
LA-PA, cm, median (IQR) (N)
0.65 (0.44, 0.94) (157)
0.68 (0.44, 0.94) (68)
0.66 (0.45, 0.96) (56)
0.55 (0.41, 0.72) (33)
LA-ESO, cm, median (IQR) (N) †
0.40 (0.25, 0.59) (139)
0.34 (0.21, 0.52) (56)
0.39 (0.27, 0.54) (55)
0.56 (0.40, 0.69) (28)
LA-TA, cm, median (IQR) (N)
0.58 (0.39, 0.90) (148)
0.53 (0.39, 0.95) (62)
0.59 (0.41, 0.89) (55)
0.61 (0.39, 0.74) (31)
Retro-sternal fat, cm, mean ± SD (N)
0.70 ± 0.42 (164)
0.78 ± 0.49 (72)
0.3
3 (57)
0.64 ± 0.
0.32
0.64 ± 0.36 (35)
LA-Area, cm2, mean ± SD (N) †
21.2 ± 6.76 (169)
18.6 ± 4.45 (73)
21.6 ± 6.9
6.97 (60)
25.8 ± 7.77 (36)
Peri-atrial fat thickness (cm)
AF= atrial fibrillation, LA-ESO= epicardial fat located between mid left atrium and esophagus, LA-PA= epicardial fat located between mid left atrium and
pulmonary artery, LA-TA= epicardial fat located between mid left atrium and thoracic aorta, RS= retrosternal fat at the level of RCA ostium, IQR= interquartile
range, SD= standard deviation.
† p<0.015 when comparing LA-ESO in no AF vs persistent AF (p=0.003) and paroxysmal AF vs persistent AF (p=0.011), and LA-Area in no AF vs persistent
AF (p<0.001) and paroxysmal AF vs persistent AF (p=0.004). All other comparisons had p>0.015. Bonferroni adjustment was applied in the multiple
comparisons.
Figure Legend:
Figure 1: Reconstruction of the short axis view
Standard 2-(right upper figure) and 4-chamber (left lower figure) views are constructed first. The
short axis view (left upper figure) was reconstructed as a plane perpendicular to the long axis of
these two views at the level of the mid left atrium as indicated by the red line.
Figure 2: The heart in the short axis view at the level of the mid LA
In this view, the thickness of the epicardial fat can be demonstrated between the LA and three
anatomical landmarks: esophagus, main pulmonary artery and descending thoracic aorta. Actual
cation.
measurements were taken after window optimization for each location.
PA=main pulmonary artery, LA =left atrium, ASC AO =ascending aorta, DES
S AO
O=
=descending
d scen
de
endi
en
ding
di
ng aorta, ESO
=esophagus, LA-PA=peri-atrial
LAESO=
ri-atrial epicardial fat located between mid left atrium and pulmonary artery,
a
peri-atrial epicardial fatt located between mid left atrium and esophagus, LA-TA=peri-atrial epicardial
fat located
epicc
between mid left atrium and
a thoracic aorta
Orientation Cube: A=anterior,
F=feet L=left
n
nterior,
Figure 3: Magnified short-axis view of the peri-atrial fat pad between the esophagus and mid LA
demonstrating measurement of the LA-ESO fat pad thickness.
There are 5 different layers identifiable starting from the left atrial cavity to the esophageal
lumen in order: the left atrial cavity with radiocontrast is most radiodense, a thin LA wall that is
less radiodense than the LA cavity, a relatively radiolucent layer of epicardial fat, the esophageal
muscle wall, and the esophageal lumen with the radiodensity of air.
DES AO=descending aorta, ESO =esophagus, LA =left atrium, LA-ESO=peri-atrial epicardial fat located between
mid left atrium and esophagus
Orientation Cube: A=anterior, L=left, F=feet
Figure 4: The heart in the axial view at the level of the RCA ostium
Measurement of the retrosternal fat (RS) was determined in this view as the shortest distance
(indicated by the white double arrow) between the ventricular wall and the parietal pericardium
at the level of the RCA ostium (indicated by the anteriorly directed retrosternal white arrow).
Orientation Cube: F=feet
Figure 5: Relationship of mean epicardial fat thickness between the esophagus and the mid-left
atrium and atrial fibrillation burden
There is a trend towards increasing epicardial fat thickness between the esophagus and the midDownloaded from http://circep.ahajournals.org/ by guest on November 18, 2016
left atrium (LA-ESO) in patients with higher burden of atrial fibrillation (AF). Patients with
persistent atrial fibrillation have a significantly thicker mean LA-ESO fat ppad than patients with
no AF or with paroxysmal AF.
24
Omar Batal, Paul Schoenhagen, Mingyuan Shao, AlaEddin Ayyad, David R. VanWagoner, Sandra S.
Halliburton, Patrick J. Tchou and Mina K. Chung
Circ Arrhythm Electrophysiol. published online May 26, 2010;
Circulation: Arrhythmia and Electrophysiology is published by the American Heart Association, 7272 Greenville Avenue,
Dallas, TX 75231
Copyright © 2010 American Heart Association, Inc. All rights reserved.
Print ISSN: 1941-3149. Online ISSN: 1941-3084
The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://circep.ahajournals.org/content/early/2010/05/26/CIRCEP.110.957241
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in
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Left Atrial Epicardial Adiposity and Atrial Fibrillation

Transcription

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