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The Metabolic Activity of the Spleen and Bone Marrow in Patients with Acute
Myocardial Infarction Evaluated by 18F-FDG PET Imaging
Kim et al.: Activation of the spleen and bone marrow in AMI
Eung Ju Kim, MD, PhD;1 Sungeun Kim, MD, PhD;2
Hong Seog Seo, MD, PhD;1 Dong Oh Kang, MD1
1Cardiovascular Center, Division of Cardiology, Department of Internal Medicine;
2Nuclear Medicine, Korea University Guro Hospital, Korea University College of Medicine,
Seoul, Korea
Correspondence to Hong Seog Seo, MD, PhD Division of Cardiology, Department of Internal Medicine, Korea University Guro Hospital, Korea University College of Medicine, 80 Guro-dong, Guro-gu, Seoul 152-703, Korea Tel: 82-2-2626-3018, Fax: 82-2-863-1109 Email: [email protected]
DOI: 10.1161/CIRCIMAGING.113.001093
Journal Subject Codes: [4] Etiology: acute myocardial infarction; [32] Diagnostic testing:
nuclear cardiology and PET; [134] Atherosclerosis: pathophysiology
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Abstract
Background—Atherosclerosis is considered to be an inflammatory disease associated with the
activation of hematopoietic and immune-related organs such as the bone marrow (BM) and
spleen. We evaluated the metabolic activity of those organs and of the carotid artery with 18F-
FDG PET in patients with coronary artery disease, including acute myocardial infarction (AMI).
Methods and Results—Whole-body combined 18F-FDG PET/CT was performed in 32 patients
with AMI, 33 patients with chronic stable angina, and 25 control subjects. The mean standard
uptake value (SUV) was calculated in the regions of interest in the spleen and the BM of lumbar
vertebrae. The target-to-background ratio (TBR) of the SUVs of the carotid artery and jugular
vein was also calculated. In patients with AMI, the SUVs of the BM (1.67±0.16) and spleen
(2.57±0.39), as well as the TBR of the carotid artery (2.13±0.42), were significantly higher than
the corresponding values of patients with angina (1.22±0.62; 2.03±0.35; 1.36±0.37, all p<0.001)
and controls (0.80±0.44; 1.54±0.26; 1.22±0.22, all p<0.001) independent of traditional
cardiovascular risk factors and high-sensitivity CRP (hsCRP). In all groups combined, the TBR
of the carotid artery was significantly associated with the SUVs of the BM (r=0.535, p<0.001),
spleen (r=0.663, p<0.001), and hsCRP (r=0.465, p<0.001).
Conclusions—The metabolic activity of the BM and spleen as well as of the carotid artery was
highest in patients with AMI, intermediate in patients with angina, and lowest in control subjects.
The activation of the BM and spleen was significantly associated with inflammatory activity of
the carotid artery.
Keywords: spleen, bone marrow, coronary artery disease, positron emission tomography
Basic biological and clinical research supports the role of inflammation in the initiation, growth,
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and rupture of atherosclerotic plaques.1 At every stage of atherosclerosis, monocyte-derived
macrophages are the principal mediators of inflammation.2, 3 Recent studies lend some clarity to
the role of inflammation in driving the atherogenic response to hypercholesterolemia and suggest
that this process is initiated in the bone marrow (BM) and spleen.4-6 In response to
hypercholesterolemia, both the BM and spleen overproduce inflammatory monocytes that enter
the circulation, accumulate in lesions, and differentiate into macrophages.7
Acute myocardial ischemic injury8 and infarction (AMI)9 activate the sympathetic
nervous system and trigger a cascade of hematopoietic stem and progenitor cell (HSPC)
proliferation in the BM and emigration to the spleen, as well as peripheral monocytosis.7 In this
process, the spleen acts as an extramedullary hematopoietic reservoir producing inflammatory
monocytes that aggravate atherosclerosis.8 Thus, this inflammatory linkage between the BM,
spleen and blood following an acute cardiac event may intensify the chronic inflammatory
process involved in atherosclerosis, independently from the primary myocardial wound site.7
This mechanism of systemic inflammation in atherosclerotic disease initiated by the BM and
spleen has been studied in animal models, but not in humans with coronary artery disease (CAD).
Activated inflammatory cells express high levels of glucose transporters and accumulate
18F-fluorodeoxyglucose (18F-FDG).10, 11 For this reason, 18F-FDG positron emission tomography
(PET) is a useful noninvasive imaging technique to evaluate the inflammatory status of
atherosclerotic plaques12_ENREF_11 and periodontal disease.13_ENREF_16 Theoretically, the
metabolic activity of the BM and spleen can be also evaluated by PET using 18F-FDG.10, 11
This study has 3 objectives: (1) to determine whether the metabolic activation of the BM
and spleen is associated with AMI; (2) whether the degree of metabolic activation of these
organs is associated with inflammatory activity at carotid plaques remote from the coronary
enitor cell ((((HSPCC) ) ) ) ) ) )
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arteries, and (3) whether the activity in the BM and spleen is higher in patients with chronic
stable angina (CSA) than in control subjects. We measured 18F-FDG uptake in the spleen, BM,
and carotid artery using whole-body 18F-FDG-PET/computed tomography (CT) in patients with
AMI, CSA, and control subjects without a history of CAD.
Methods
Study Subjects
Between June 2008 and March 2009, we prospectively recruited patients at Korea University
Guro Hospital who were diagnosed with AMI or CSA. AMI was defined as typical changes in
biochemical markers of myocardial necrosis along with at least 1 of the following: ischemic
symptoms, electrocardiographic changes indicative of new ischemia, development of pathologic
Q waves, or imaging evidence of new loss of viable myocardium or new regional wall motion
abnormalities.14 CSA was defined as the presence of stable anginal symptoms for at least 6
months with at least 50% luminal narrowing in at least 1 major coronary artery on angiography.
Criteria for exclusion from the control group were a history of cardiovascular disease
(myocardial infarction, unstable angina, stroke, or cardiovascular revascularization), greater than
stage 1 hypertension (resting blood pressure 160/100 mmHg), uncontrolled diabetes mellitus
(glycated hemoglobin >9%), malignancy, or severe renal or hepatic disease. Subjects with a
history of an inflammatory condition, or those taking inflammation-modulating medications
within the prior 6 months, were excluded from the study. All participants provided written
informed consent and the Korea University Institutional Review Board approved this study
protocol.
The following clinical and demographic parameters were recorded: age, sex, body mass
index, waist circumference, the presence of hypertension (defined as those taking
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th at least 50% llluminal ll narrowing g in at least 1 majojj r corororooonnnaryy aaaaarrtrrr ery y on anggiogg
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antihypertensive medications or 2 blood pressure recordings over 140/90 mmHg), the presence
of diabetes mellitus (defined as those undergoing treatment with diet and/or medications or a
fasting serum glucose >126 mg/dl), and dyslipidemia (defined as those taking lipid-lowering
medications or a fasting serum total cholesterol 240 mg/dl, triglycerides 200 mg/dl, high
density lipoprotein cholesterol <40 mg/dl, or low density lipoprotein cholesterol 160 mg/dl).
Cardiac troponin T and creatine kinase-MB fraction (CK-MB) were measured using
electrochemiluminescence immunoassays on the Elecsys 2010 analyzer (Roche Diagnostics,
Indianapolis, Inidiana, USA). Concentrations of troponin T >0.1 ng/mL and CK-MB >6.73
ng/mL in men or >3.77 ng/mL in women were used as cutoff values to diagnose AMI based on
the manufacturer’s instructions.
18F-FDG- PET/CT Imaging
18F-PET/CT was performed using the Gemini TF 16-Slice PET/CT scanner (Philips Medical
Systems, Cleveland, Ohio, USA). Patients diagnosed with AMI, all of whom were successfully
treated by primary percutaneous coronary intervention, underwent PET/CT within 10 days of the
event when they were clinically stable (mean: 6.3 days; range: 1-10). The TF scanner is a new
high-performance, time-of-flight-capable, fully 3-dimensional PET scanner that uses lutetium-
yttrium oxyorthosilicate crystals.15 After at least 12 hours of fasting, FDG (5.19 MBq/kg) was
injected intravenously, after which patients rested in a quiet room for 60 minutes. In diabetic
patients, who may have a different blood clearance from nondiabetic patients, we determined
blood glucose level before 18F-FDG administration and changed the PET schedule if it exceeded
180 mg/dl to reduce the metabolic effect on FDG uptake. Whole-body PET images (from below
the cerebellum to the inguinal region) were acquired for 10 minutes (1 minute per bed position).
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Analysis of Positron Emission Tomography Images
PET images were analyzed on a dedicated workstation (Extended Brilliance Workspace 3.5;
Philips). Right carotid FDG uptake was measured along the length of the right carotid vessel,
starting at the bifurcation and extending inferiorly and superiorly every 4 mm for a total of 8
consecutive PET/CT images for each subject. Arterial FDG uptake was quantified in the region
of interest (ROI) around each artery on every slice of the co-registered transaxial fusion PET/CT
images. The highest standard uptake values (SUVs) of the ROIs of all 8 slices within the right
carotid artery were averaged together for each subject. Next, the arterial SUV was divided by the
blood-pool SUV measured from the jugular vein for normalization. In this way, the arterial
target-to-background ratio (TBR) was calculated for each subject. 18F-FDG uptake was measured
in the spleen by placing an ROI around the organ on all transaxial slices. The highest SUVs from
all transaxial slices were recorded and their average was used as the mean SUV for the entire
organ. BM 18F-FDG uptake was calculated under CT-guided anatomical reference from the third
to fifth lumbar vertebrae,16 and the average of the highest SUVs was used as the mean SUV for
analysis. To determine the variability of the mean SUV measurements, images from 20 subjects
were analyzed twice, several weeks apart, by 2 readers who were unaware of the subjects’
clinical histories. The intra- and inter-observer correlation coefficient values of the mean SUV
measurements were greater than 0.9.
Statistical Analysis
Baseline characteristics of the participants were analyzed according to the 3 main study groups.
Frequencies and proportions were reported for categorical variables, and either mean ± standard
deviation or median with interquartile range were reported for continuous variables based on
normality of distribution. The Pearson chi-squared test, Fisher’s exact test, one-way analysis of
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variance (ANOVA), and the Kruskal-Wallis test were used to compare variables between groups.
Subsequent comparisons were performed by Bonferroni’s post-hoc test, or the Mann-Whitney U-
test or Fisher’s exact test with Bonferroni corrected p values. The SUVs of the BM and spleen
and the TBRs of the carotid artery were compared between the 3 groups using analysis of
covariance (ANCOVA) with Bonferroni multiple comparisons, in which the possible
confounding effects of sex, waist circumference, hypertension, diabetes, dyslipidemia, smoking,
statin use, and high-sensitivity C-reactive protein (hsCRP) were taken into account by including
them in the model as covariates. Spearman correlation analysis was performed to identify the
relationship between 18F-FDG uptake in multiple organs and hsCRP. Multiple linear regression
analyses using the TBR of the carotid artery as a dependent variable were also performed to
investigate whether there was an independent relationship between 18F-FDG uptake in each
organ and uptake in the carotid artery. Data were analyzed using SPSS for Windows version 20.0
(SPSS, Chicago, IL, USA). P-values less than 0.05 were considered statistically significant.
Results
Clinical and laboratory characteristics
The subjects included 51 men (56.7%) and 39 women (43.3%). Women comprised the majority
of the control group, while men comprised the majority of the CSA and AMI groups. The mean
age of subjects was 57.7±10.1 years, and did not differ significantly between groups. Compared
to the control group, most of the traditional cardiovascular risk factors, such as hypertension,
diabetes, dyslipidemia, and smoking, were more prevalent in the CSA and AMI groups. The
prevalence of those risk factors was not significantly different between the CAD groups.
Subjects taking statins comprised nearly a third of total subjects in both CAD groups upon initial
presentation. There were significant stepwise increases in white blood cell count and hsCRP
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from the control group to the AMI group (Table 1).
Comparison of FDG uptake in the bone marrow, spleen, and carotid artery between groups
The mean maximum SUV levels in the spleen and BM were incrementally and significantly
higher in the AMI and CSA groups compared to the control group (Table 1, Figure 1A, Figure
2A, and Figure 2B). The AMI group had higher carotid artery TBRs than did the CSA and
control groups (Table 1, Figure 1B, and Figure 2C). Although the carotid artery TBR of the CSA
and control groups did not differ significantly (Table 1 and Figure 2C), it reached statistical
significance after adjusting for sex, waist circumference, hypertension, diabetes, dyslipidemia,
smoking, statin use, and hsCRP in ANCOVA analysis (for the carotid artery TBR, AMI vs. CSA
group, p<0.001; CSA vs. control group, p=0.038). The SUVs of the spleen and BM were also
significantly different between groups after the same adjustments (for spleen SUV, AMI vs. CSA
group, p<0.001; CSA vs. control group, p<0.001, for BM SUV, AMI vs. CSA group, p=0.003;
CSA vs. control group, p=0.017).
Correlation between high-sensitivity C-reactive protein and FDG uptake in the bone marrow,
spleen, and carotid artery
The TBR of the carotid artery and SUVs of the BM and spleen correlated significantly with each
other in study subjects overall. Without adjustment, the TBR of the carotid artery was most
highly correlated with the SUV of the spleen. HsCRP was also significantly correlated with FDG
uptake in the BM, spleen, and carotid artery (Table 2). In the AMI group, there was no
correlation between peak serum CK-MB and troponin-T levels and FDG uptake in the BM,
spleen, or carotid artery (data not shown).
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Relationship between carotid artery target-to-background ratio and bone marrow FDG uptake,
spleen FDG uptake, and high-sensitivity C-reactive protein
Multiple linear regression analysis of the overall study population, which included age, sex,
waist circumference, hypertension, diabetes, dyslipidemia, smoking, and statin use as covariates,
revealed an independent relationship between carotid artery TBR, the SUVs of the spleen and
BM, and hsCRP. The SUVs of the spleen and BM were significantly associated with carotid
artery TBR even after further adjustment for hsCRP. In contrast, hsCRP did not maintain a
significant association with carotid artery TBR when the SUV of the BM or spleen was entered
into the model as an independent variable (Table 3).
Discussion
This study revealed significant associations between CAD, the metabolic activity of the spleen
and BM, and the inflammatory activity of the carotid artery independent of traditional
cardiovascular risk factors and hsCRP level. Those activities were highest in patients with AMI,
intermediate in patients with CSA, and lowest in the control group. The 18F-FDG uptake in the
carotid artery was significantly associated with the metabolic activity of the spleen and BM as
well as with hsCRP level.
Most studies that support the association between inflammation and CAD have been
based on epidemiologic analysis of circulating biomarkers17-19 and animal experiments.20-23
Recent studies have identified that the role of the spleen and BM in chronic and acute
inflammation in atherosclerotic disease. In chronic inflammation of atherosclerosis, both the BM
and spleen are involved. HSPCs progressively relocate from the BM to the splenic red pulp,
where they clonally expand with granulocyte macrophage colony-stimulating factor and
interleukin-3 and differentiate into inflammatory monocytes.5 Monocytes born in the spleen
BM or sppppppleen wwasasasasasasas e
and the inflammatory activity of the carotid artery independent of trad
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intravasate, circulate, and accumulate into atherosclerotic lesions in murine models.5_ENREF_24
Our findings are consistent with this knowledge, in that significantly higher activity was found in
the BM, spleen, and carotid artery in the CSA group than in the control group.
Using 18F-FDG PET, Assmus et al. found significantly higher metabolic activity in the
BM and significantly larger populations of hematopoietic CD34+ and CD133+ cells in BM
aspirates from patients within 7 days after AMI than in patients with chronic post-ischemic heart
failure.24 The same authors reported that AMI induced by ligating a coronary artery or
application of other stressors can activate stem cells in the BM in non-atherosclerotic mice.24 It
has also been reported that acute ischemic myocardial injury triggers emergency hematopoiesis
in the BM and spleen,7 and that AMI liberates HSPCs from BM niches via signals from the
sympathetic nervous system.9_ENREF_25 The progenitors then seed the spleen and yield a
sustained boost in monocyte production to meet demand in the infarcted myocardium.7, 9 This
process, however, may have unintended consequences, such as acceleration of underlying
atherosclerosis triggering reinfarction or stroke.7, 9 Dutta et al. found that in ApoE-/- mice, AMI
accelerates underlying aortic atherosclerosis.9
In light of these findings, our AMI group indeed demonstrated higher metabolic activity
in the spleen and BM than the CSA group. The greater inflammatory activity in the carotid
arteries of the AMI group compared to the CSA group may be evidence of this damaging
accumulation of monocytes in atherosclerotic lesions. Moreover, we found that the metabolic
activity of the carotid artery was closely associated with that of the spleen and BM as well as
with the level of hsCRP in the overall patient population. These findings suggest that the
inflammatory status of atherosclerosis is influenced by systemic inflammation modulated by the
spleen and BM.
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Metabolic activation of the major organs that harbor inflammatory cells such as the
spleen,8 or that participate in inflammatory cell production, such as the BM and spleen,5, 9 has
been revealed using 18F-FDG-PET in a variety of systemic conditions, including infection,25
cancer,16 connective tissue diseases26 and systemic autoimmune disorders.27 However, few
studies have demonstrated the metabolic activation of the BM and spleen in humans with CAD.
To the best of our knowledge, this is the first in vivo human study showing the metabolic activity
of the spleen and BM in patients with CAD using a molecular imaging tool.
In our study, the metabolic activity of the spleen and BM was high in patients with AMI
even after a mean of 6.3 days from the event. Inflammatory monocytes, which have been found
to be chronically expanded in the blood pool of atherosclerotic apoE-/- mice, impair infarct
healing through prolonged presence in the infarct and deregulated resolution of inflammation.28
This result suggests that patients with AMI who have underlying inflammation associated with
atherosclerosis may have prolonged activation of the organs involved in inflammation. Further
studies are needed to determine the time period during which activation of the spleen and BM
persists after AMI in humans.
Our study has several limitations. First, its cross-sectional design, small sample size, and
significant differences between subjects and controls may have introduced various levels of bias.
Although we attempted to adjust for these differences and the small sample size, our model may
not be sufficiently powered to support the results. Second, we did not perform coronary
angiography in the control group to confirm the presence of coronary atherosclerosis and this
may have affected our results. Third, we did not perform histopathological analysis of tissue
samples from the spleen or BM. However, it is already known that 18F-FDG accumulates in
tissue macrophages and its intensity correlates with the staining density of tissue macrophages in
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corresponding histological sections of specimens.10, 11 Fourth, the patients with AMI may have
had elevated levels of catecholamines and endogenous steroids associated with stress in addition
to their underlying inflammatory state. However, we were not able to control for all factors
affecting glucose metabolism and FDG uptake, including levels of insulin, catecholamines,
steroids, and other substrates in plasma, which may have affected our results. Fifth, we did not
control for other factors affecting systemic inflammation, such as life style habits, low-grade
chronic infections, and genetic predisposition. Finally, we did not measure the biomarkers of
HSPC in the BM or monocyte subsets in the peripheral blood. In short, this study was not
designed to definitively prove an etiological hypothesis, but was an observational study designed
to measure metabolic activity of the spleen and BM in patients with CAD as an indirect probe
into a previously established condition.
In conclusion, the metabolic activity of the BM and spleen as well as of the carotid artery
was highest in patients with AMI, intermediate in patients with CSA, and lowest in controls. The
relationship between those parameters and CAD status was independent of traditional
cardiovascular risk factors. Activation of the BM and spleen was closely associated with the
activity in the carotid artery. Our results offer insights into risk stratification, monitoring of
therapy, and physiological changes in the early stages of atherosclerosis, when intervention may
be most effective.
Sources of Funding
This study was partly supported by the Korea Institute of Science and Technology Institutional
Program (Project No. 2E24080); a grant from the Korean Health Technology R&D Project of the
Ministry for Health, Welfare & Family Affairs of the Republic of Korea (A070001); and a grant
from the Korea University-Korea Institute of Science and Technology (KU-KIST) Graduate
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School Converging Science and Technology(R1106223).
Disclosures
None.
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Table 1. Baseline characteristics of study subjects. AMI (n=32) CSA (n=33) Control (n = 25) p-value
Age, yrs 56.9±11.6a 61.2±11.5a 57.1±7.5a 0.206
Men 21 (65.6)a 24 (72.7)a 6 (24.0) <0.001
BMI (kg/m2) 24.6±2.6a,b 26.0±4.0b 23.5±2.9a 0.022 WC (cm) 83.4±16.3 92.3±11.4 80.9±7.5 <0.001 Hypertension 15 (46.9)a 19 (57.6)a 1 (4.0) <0.001
Diabetes 13 (40.6)a 13 (39.4) a 2 (8.0) 0.013
Dyslipidemia 19 (59.4)a 16 (48.5)a 2 (8.0) <0.001
Smoking 13 (40.6)a 13 (39.4)a 2 (8.0) 0.013
Statin use 9 (28.1)a 11 (33.3)a 0 (0) 0.006
Total cholesterol, mg/dL 187±44 a 156±35 189±25 a 0.001
Triglycerides, mg/dL 137±142 a, b 160±100 a 87±44 b 0.009
88 (58-168) 113 (85-254) 68 (56-122)
HDL-cholesterol, mg/dL 45±12 a 49±15 a 59±16 0.001
LDL-cholesterol, mg/dL 124±42 a 92±30 115±24 a 0.001
HbA1c, % 6.9±2.1a 7.0±1.6a 5.7±0.4 0.001
6.1 (5.7-7.8) 6.6 (5.7-7.5) 5.6 (5.4-5.9)
WBC, x103/uL 10.9±3.3 6.5±1.2 5.0±1.3 <0.001
10.6 (8.4-12.6) 6.5 (5.5-7.7) 5.0 (3.9-6.3) hsCRP, mg/L 3.48±3.10 1.53±1.55 0.55±0.57 <0.001 1.88 (1.05-5.97) 1.16 (0.32-2.49) 0.41 (0.17-0.82) peak CK-MB, ng/mL 145.6±127.3 - - - peak troponin-T, ng/mL 3.66±4.64 - - -
TBR
Carotid artery 2.13±0.42 1.36±0.37a 1.16±0.09a <0.001
SUV Spleen 2.57±0.39 2.03±0.35 1.54±0.26 <0.001 Bone marrow 1.67±0.16 1.22±0.62 0.80±0.44 <0.001
Data are expressed as mean ± SD; median with interquartile range in parenthesis; or number with percentage in parentheses. P-values represent overall differences across groups as determined by ANOVA or the Kruskal-Wallis test for continuous variables and Pearson’s chi-squared test or Fisher’s exact test for categorical variables. a,b The same letters indicate no statistical significance based on Bonferroni’s post-hoc test, or the Mann-Whitney U-test and, or separate Pearson’s chi-squared test or Fisher’s exact test with Bonferroni corrected p values. AMI, acute myocardial infarction; BMI, body mass index; CSA, chronic stable angina; HDL, high density lipoprotein; hsCRP, high sensitivity C-reactive protein; LDL, low density lipoprotein; SUV, standard uptake value; TBR, target-to-background ratio; WBC, white blood cell; WC, waist circumference.
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Table 2. Spearman correlation analysis between hsCRP level and FDG uptake in the carotid artery, spleen, and BM in the overall study population.
SUV of BM SUV of Spleen hsCRP
TBR of Carotid artery 0.535* 0.663* 0.465*SUV of BM - 0.637* 0.525*SUV of Spleen 0.637* - 0.458*
* p<0.001 BM, bone marrow; hsCRP, high sensitivity C-reactive protein; SUV, standard uptake value; TBR, target-to-background ratio.
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Table 3. Multiple linear regression analysis using the carotid artery TBR as a dependent variable.
p R2 R2adjusted
SUV, bone marrow* 0.438 <0.001 0.329 0.245
SUV, bone marrow † 0.395 <0.001 0.378 0.288
SUV, spleen* 0.688 <0.001 0.461 0.394
SUV, spleen † 0.644 <0.001 0.486 0.412
hsCRP* 0.011 0.040 0.192 0.088 *The association with the carotid artery TBR after adjustment for age, sex, waist circumference, hypertension, diabetes, dyslipidemia, smoking, and statin use. †The association with the carotid artery TBR after adjustment for the above covariates and hsCRP. R2
adjusted = 1 – (1- R2)(N-1)/(N-P-1), where R2= sample R-square, p=number of predictors, N=total sample size.
hsCRP, high sensitivity C-reactive protein; SUV, standard uptake value; TBR, target-to-background ratio.
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Figure Legends
Figure 1. A. Representative examples of maximum-intensity-projection 18F-FDG PET images
showing highly increased uptake and moderately increased uptake throughout the bone marrow
and spleen in patients with acute myocardial infarction (AMI) and chronic stable angina (CSA),
respectively. B. Axial fusion images at the carotid artery level from the same scan showing
diffuse intense uptake of 18F-FDG in the carotid arteries of patients with AMI (arrow) and
moderate uptake in patients with CSA.
Figure 2. Mean differences in spleen SUV (A), BM SUV (B), and the carotid artery TBR (C)
between the 3 study groups. Error bars show 95% confidence intervals of means.
AMI, acute myocardial infarction; BM, bone marrow; CSA, chronic stable angina; SUV,
standard uptake value; TBR, target-to-background ratio.
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Eung Ju Kim, Sungeun Kim, Hong Seog Seo and Dong Oh KangF-FDG PET Imaging18Infarction Evaluated by
The Metabolic Activity of the Spleen and Bone Marrow in Patients with Acute Myocardial
Print ISSN: 1941-9651. Online ISSN: 1942-0080 Copyright © 2014 American Heart Association, Inc. All rights reserved.
TX 75231is published by the American Heart Association, 7272 Greenville Avenue, Dallas,Circulation: Cardiovascular Imaging
published online January 31, 2014;Circ Cardiovasc Imaging.
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