Journal of Vascular Surgery
Volume 48, Issue 2 , Pages 417-423, August 2008

Increased 18F-fluorodeoxyglucose uptake in abdominal aortic aneurysms in positron emission/computed tomography is associated with inflammation, aortic wall instability, and acute symptoms

  • Christian Reeps, MD

      Affiliations

    • Department of Vascular Surgery, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany
    • Corresponding Author InformationReprint requests: Christian Reeps, MD, Abteilung für Gefäβchirurgie, Klinikum rechts der Isar der Technischen Universität München, Ismaninger Str 22, 81675 München, Germany.
    • ,
  • Markus Essler, MD

      Affiliations

    • Department of Nuclear Medicine, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany
    • ,
  • Jaroslav Pelisek, PhD

      Affiliations

    • Department of Vascular Surgery, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany
    • ,
  • Stefan Seidl, MD

      Affiliations

    • Institute of Pathology and Pathologic Anatomy, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany.
    • ,
  • Hans-Henning Eckstein, MD

      Affiliations

    • Department of Vascular Surgery, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany
    • ,
  • Bernd-Joachim Krause, MD

      Affiliations

    • Department of Nuclear Medicine, University Hospital rechts der Isar, Technical University of Munich, Munich, Germany

Received 27 November 2007; accepted 16 March 2008. published online 24 June 2008.

Article Outline

Objective

With the established computed tomographic (CT)- morphologic parameters, only the relative, but not the individual rupture risk of abdominal aortic aneurysm (AAA), can be determined. So far, increased aortic 18F-fluorodeoxyglucose (FDG) metabolism measured by positron emission tomography (PET) has been reported in AAA with increased rupture risk. The aim of the study was to analyze the histopathologic changes in AAA wall correlated with increased FDG uptake for further implications on aortic wall stability and AAA rupture risk.

Methods

Fifteen patients with asymptomatic (n = 12) and symptomatic (n = 3) AAA underwent FDG-PET/CT, followed by open AAA repair. FDG-PET/CT was used for precise localization of maximum FDG uptake, and the maximum standard uptake values (SUVmax) were calculated. Biopsies of the AAA wall were operatively collected from areas with maximum FDG uptake, immunohistologically stained, and semiquantitatively analyzed for inflammatory infiltrates, vascular smooth muscle cells (VSMC), matrix metalloproteinase (MMP)-2 and -9 expression, as well as for elastin and collagenous fibers.

Results

Symptomatic AAA showed significantly increased FDG uptake compared with asymptomatic AAA (SUVmax, 3.5 ± 0.6 vs 7.5 ± 3; P < .001). Thus, increased FDG uptake was correlated with higher densities of inflammatory infiltrates (r = +0.87, P < .01) and macrophage and T-cell infiltrations (r = +0.95, P < .01 and r = +0.66, P < .05), with higher MMP-9 expressions (r = +0.86; P < .01), and with reduction of collagen fiber (r = –0.76; P < .01) and VSMCs (r = –0.71; P < .01). Consecutive correlations were found for total inflammatory infiltrates, T lymphocytes, and macrophages with MMP-9 expression (r = +0.79, +0.79 and +0.74; P < .01). Moreover, MMP-9 expression was correlated with decreasing collagen fiber content (r = –0.53, P < .05) and VSMC density (r = –0.57, P < .05).

Conclusions

Maximum aortic FDG uptake correlated significantly with inflammation, followed by increased MMP expression and histopathologic characteristics of aneurysm wall instability and clinical symptoms. Therefore, FDG-PET/CT might be a new diagnostic technique to study AAA disease in vivo and may contribute to improve prediction of individual AAA rupture risk.

Clinical Relevance

With the established CT morphologic parameters, the exact rupture risk of individual abdominal aortic aneurysm (AAA) cannot be determined. Regarding AAA formation and rupture, metabolic processes that weaken the aortic wall, such as chronic inflammation and proteolysis, have a pivotal role. This pilot study demonstrated that increased metabolism in the AAA wall can be visualized by 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET)/computed tomography (CT). Furthermore, aortic FDG uptake correlated with inflammation, histopathologic characteristics of aneurysm wall instability, and clinical symptoms. Therefore, after further investigation FDG-PET/CT might be a new diagnostic technique to assess AAA wall stability in vivo and consequently may contribute to improved prediction of individual AAA rupture risk.

 

Rupture of abdominal aortic aneurysm (AAA) is fatal in 70% to 90% and is the 13th leading cause of death in Western societies.1, 2 As a consequence, precise prediction of AAA rupture risk is essential. With the current, well-established CT morphologic parameters, such as maximum aortic diameter, aneurysm shape, AAA expansion, and computed wall stress, only the relative—but not the individual rupture risk—can be determined.3 Hence, AAA rupture may occur unexpectedly in aneurysms that are smaller than the critical diameter limits, whereas many large aneurysms may remain stable throughout patient's lifetime, without prophylactic surgery.

In current pathologic concepts, metabolic processes such as chronic inflammation and proteolysis play a pivotal role in AAA formation and rupture.4, 5, 6 With 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET), increased metabolism can be visualized in vivo and has been previously described in aortic infection, arteritis, inflammatory AAA, and casuistically in AAA with increased rupture risk (ie, symptomatic AAA).7, 8 However, the histopathologic changes in AAA wall associated with increased FDG uptake and their putative impact on aortic wall stability still remain unclear.

In this pilot study we analyzed operatively retrieved samples from sites with maximum FDG uptake in AAA vessel wall in symptomatic and asymptomatic AAA accurately localized by FDG-PET/CT. The intensity of FDG uptake was correlated with semiquantitatively evaluated main determinants of aortic wall integrity and metabolism such as inflammatory cell infiltration, matrix metalloproteinase (MMP)-2 and -9 activity, and elastin and collagen fiber content.

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Materials and methods 

Patients 

The cohort comprised 15 patients (13 men, 2 women) with a mean age of 69 ± 5 years (range, 61-77 years) with asymptomatic (n = 12) and symptomatic (n = 3) AAA. These patients had specific abdominal pain and underwent FDG-PET/CT, followed immediately by prophylactic or urgent conventional open aneurysm repair. Surgery was performed in isolated AAA in 13 and in thoracoabdominal AA (TAAA) with infrarenal descending disease in two. In these two patients the region of interest was limited to the abdominal part of the aorta. In addition, 24 age-matched control patients without aortic aneurysm disease were analyzed for aortic tracer uptake. Exclusion criteria were chronic renal failure (serum creatinine >1.8 mg/dL), acute congestive heart failure, known intolerance against CT- iodinated contrast media, or elevated blood glucose level (>130 mg/dL).

The study was conducted with the approval of our Institutional Review Board, and we obtained informed consent from all the subjects before their participation in the study.

Protocol for FDG-PET/CT 

Patients were instructed to fast for at least 6 hours before the PET/CT examination. After a bolus of 370 MBq was FDG injected into a peripheral vein (uptake time, 90 minutes) a low-dose CT scan (Siemens Biograph Sensation 16, Erlangen, Germany; 120 kV, 20 mAs) was obtained at first for attenuation correction of PET emission data, followed by routine diagnostic native and contrast-enhanced thoracoabdominal multi-slice CT with intravenous injection of 100 mL contrast medium (Imeron 300, Byk-Gulden, Konstanz, Germany; flow, 4 mL/s over the cubital vein; table speed, 12 mm/s, 5-mm-slice thickness reconstruction). The data were processed on a Volume Wizard workstation (Siemens Medical Solutions, Erlangen, Germany), slices were indexed at 3 mm, and three-dimensional multiplanar reconstructions of the aorta and side branches were obtained. Immediately after the CT scanning, PET emission images were acquired for 3 minutes for each bed position. The emission data were consecutively reconstructed with measured attenuation correction based on the low-dose CT transmission data.

Image analysis 

All FDG-PET/CT scans were preoperatively visually analyzed by a nuclear medicine physician and a vascular surgeon on a Syngo workstation (Siemens Medical Solutions). The superimposed CT and PET images were assessed for aneurysm morphology and distribution of FDG tracer uptake. Areas with maximum focal FDG uptake were visually detected, and the maximum standard uptake value (SUVmax) in each aneurysm was obtained by computational analyses using the True D software (Siemens Medical Solutions). These areas were mapped precisely for later intraoperative identification. For mapping, distances to the renal arteries and the aortic bifurcation were assessed, and the localization in the cross-sectional plane was defined clockwise.

Tissue collection and immunohistochemistry 

For analyses of histopathologic changes at sites of maximum focal intramural glucose metabolism, corresponding AAA vessel wall specimens were operatively retrieved from all patients during conventional AAA repair. Histologic specimens were then dissected of luminal thrombus and peripheral tissue, fixed in 4% paraformaldehyde, and embedded in paraffin. Sections were routinely stained with hematoxylin-eosin and elastin van Gieson to assess the overall tissue architecture, infiltrates, elastin, and collagen. For immunohistochemistry, paraffin sections were dewaxed in xylene and rehydrated through graded ethanol (100% to 70%) to water.

Primary antibody solution was added for 1 hour at room temperature. MMP-2 epitope was detected using mouse monoclonal antibody (Ab-4, clone A-Gel VC2; Lab Vision, Fremont, Calif) and MMP-9 by epitope-specific rabbit antibody (Lab Vision). Colocalization studies were done for macrophages (mouse monoclonal anti-human CD68, clone KP1; DakoCytomation, Hamburg, Germany), vascular smooth muscle cells (VSMC, antihuman smooth muscle actin [SMA], clone HHF3S; DakoCytomation), endothelial cells (antihuman von Willebrand factor VIII, clone F8/86; DakoCytomation), and lymphocytes (polyclonal rabbit antihuman CD3; DakoCytomation). After the primary antibody incubation, visualization was performed using ChemMate Detection Kit (LSAB, DakoCytomation) according to the manufacturer's instructions. All sections were evaluated by three experienced observers blinded to FDG-PET/CT results and to each other.

According to the inhomogeneous and accentuated distribution of histopathologic patterns, semiquantitative analyses were performed to describe the predominant histologic characteristics in the entire sample. Specimens were evaluated by using a score of 0 to 6+, with 0 indicating no, 1+ indicating weakly positive, 2+ indicating more positive, 3+ indicating intermediate positive, 4+ indicating markedly positive, 5+ indicating strongly positive, and 6+ indicating massive positive staining.

Statistical analysis 

For statistical analyses, the nonparametric Kruskal-Wallis and Mann-Whitney test were used to describe differences in subgroups because parameters were not normally distributed. For correlation analyses, the Pearson product-moment correlation coefficient was applied. Values of P < .05 were considered significant. SUV values are shown as mean ± standard deviation.

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Results 

Patients 

The study comprised 15 patients (13 men, 2 women) with a mean age of 69 ± 5 years (range, 61-77 years). The AAAs were asymptomatic in 12 (11 men, 1 woman; mean age of 70 ± 5 years; range, 61-77 years) and symptomatic in three (2 men, 1 woman; mean age of 68 ± 5 years; range, 64-74 years). Symptomatic patients presented with aneurysm-specific abdominal pain. Two patients had TAAAs and 13 had AAAs. The mean maximum infrarenal cross-sectional aortic diameter was 59 ± 12 mm (range, 50-72 mm) in symptomatic patients and 54 ± 8 mm (range, 45 for women to 72 mm) in asymptomatic patients. History of aneurysm expansion could be assessed reliably in seven patients. Of those, three AAAs were stable with an annual growth rate <0.3 cm and 4 AAAs were progressive (>0.6 cm). No patient had an inflammatory or mycotic AAA by intraoperative inspection during surgery. Further patient characteristics for comorbidities and oral medication are reported in the Table.

Table. Demographic data
VariableSymptomatic AAAAsymptomatic AAA
Patient, No.312
Age, mean ± SD, years68 ± 568 ± 5
Sex, F/M1/21/11
Disease, AAA/TAA2/11/11
Max diameter, mean ± SD mm59 ± 1154 ± 8
Antiplatelet therapy, yes/no2/111/1
NSAR, yes/noNone1/0
Statin, yes/noNone6/6
β-Blocker, yes/no1/27/5
Nicotine abuse, yes/no2/110/2
Diabetes, yes/no1/25/7
Arterial hypertension, yes/no3/011/2
Coronary heart disease, yes/no1/27/5
Renal insufficiency,a yes/noNone1/11
Elevated WBC (>9.0 G/L) yes/no1/22/10
Elevated CRP (>0.5 mg/dL) yes/no1/22/10

AAA, Abdominal aortic aneurysm; CRP, complement-reactive protein; NSAR, nonsteroidal antirheumatics; TAA, thoracoabdominal aortic aneurysm; WBC, white blood cell count.

aDefined as serum creatinine level >1.3 mg/dL.

Tracer signal intensity vs clinical characteristics 

In the age-matched control group of 24 patients without aortic aneurysm disease, the mean maximum infrarenal aortic FDG uptake (SUVmax) was 3.0 ± 0.5 (range, 2.4-3.9). In comparison, the 12 asymptomatic AAA patients showed significantly (P < .05) increased mean SUVmax levels of 3.5 ± 0.6 (range, 2.7-4.3). The three symptomatic AAA patients had significantly higher focal FDG tracer enhancement (mean SUVmax, 7.5 ± 0.3; range, 4.8-9.1) compared with asymptomatic AAA patients (P < .001; Fig 1 and Fig 2).

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  • Fig 1. 

    An 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography of abdominal aortic aneurysm (AAA) vessel wall at maximum focal FDG uptake in a 66-year-old woman with a symptomatic AAA (maximum diameter, 50 mm; maximum standard uptake value, 9.1). Panel a, coronal section. Panel b, transversal section; arrow, effusive aortic FDG uptake with spillover effect.

  • View full-size image.
  • Fig 2. 

    Average maximum standard uptake values (SUVmax) of the control group compared with patients with asymptomatic and symptomatic abdominal aortic aneurysms (AAAs). Both, asymptomatic and symptomatic patients showed significant increase in uptake values compared with controls, with highest SUVmax levels in the symptomatic AAAs.

History of AAA progression could reliably be ascertained in seven of 15 patients. Three AAAs were stable (annual AAA growth rate ≤0.3 cm), and four AAAs were instable with rapid annual expansion of >0.6 cm; thus, no significant correlation between maximum FDG uptake and annual aneurysm growth rate was observed (P = .15). Moreover, no association was found between SUVmax with maximum cross-sectional infrarenal AAA diameter in the 15 symptomatic or asymptomatic patients.

Tracer signal intensity vs histopathologic characteristics 

In addition to the clinical course, the preoperatively obtained SUVmax values were compared with corresponding histologic specimens taken from areas with maximum focal FDG uptake in the aneurysm vessel wall. Aneurysm wall biopsy specimens were stained and semiquantitatively assessed for inflammatory infiltrates, MMP-2 and MMP-9 activities, and collagen and elastin fiber content. No sex-specific or age-dependent differences were found.

The total amount of inflammatory cells in the AAA vessel wall was evaluated by conventional hematoxylin-eosin staining. Furthermore, inflammatory cell subpopulations were specified by CD3 (T-lymphocytes) and CD68 (macrophages) immunostaining. Thereby increasing SUVmax levels were significantly associated with increasing medial inflammatory cell infiltrates (r = +0.87, P < .01). Increased SUVmax was significantly correlated with higher densities of CD68-positive cells (macrophages, r = +0.95, P < .01) and with cells positive for CD3 (T lymphocytes, r = +0.66, P < .05; Fig 3 a, c, d and 4, A) Qualitatively, lower FDG uptake was associated with macrophage and foam cell accumulation adjacent to atheroma, whereas higher FDG uptake was related to distinct medial inflammatory infiltrates. Symptomatic AAA with SUVmax levels >5 showed massive transmural CD68-positive cell infiltration (Fig 3, c) Thereby histopathology showed typical characteristics of chronic inflammation but no patterns indicating bacterial infection. Similarly, histologic slides were assessed for MMP-2 and MMP-9 expression and rated semiquantitatively. In correlation with the intensified FDG uptake, an inconstant but significant increase of MMP-9 expression was evident (r = +0.86; P < .01). In two of three symptomatic patients with the highest FDG uptake, surpassing MMP-9 activity was obvious. In contrast, no significant correlation was seen between FDG uptake and MMP-2 tissue staining (Fig 3, e, f and Fig 4, B).

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  • Fig 3. 

    Histologic results to the corresponding 18F-fluorodeoxyglucose uptake of positron emission tomography/computed tomography from Fig 1. Panel a, Hematoxylin and eosin staining; arrow, inflammatory infiltrates. Panel b, Elastin von Gieson staining; arrows, collagen (red) and elastin (black) fibers in the tunica media; Panel c, CD68 antibody staining (brown); arrow designates CD68-positive cells with dens transmural infiltration; Panel d, CD3 antibody staining (brown); arrow designates CD3-positive cells; Panels e and f, Matrix metalloproteinase (MMP) -2, MMP-9 antibody staining (brown); arrow designates positive cells); Panel g, Smooth muscle actin antibody staining (red); arrow designates rarified smooth muscle actin–positive cells. Original magnification, 50×.

  • View full-size image.
  • Fig 4. 

    Scatter plot of maximum standard values (SUVmax) of fluorodeoxyglucose F18 uptake compared with (A) inflammatory cell infiltrate, (B) matrix metalloproteinase (MMP)-2 and -9 activities, and (C) content of elastin, collagen, and vascular smooth muscle cells (VSMC) in the corresponding area of abdominal aortic aneurysm (AAA) vessel wall. Cell densities were semiquantitatively determined and scored from 0 to 6+. Increasing SUVmax correlated significantly with higher densities of (A) inflammatory infiltrates and (B) MMP-2 or MMP-9. C, Negative correlation was found for collagen and VSMCs but not for elastin.

Tracer signal intensity and AAA wall constituents 

Paired histologic slides of sites with maximum FDG uptake were stained using elastin van Gieson and with antibodies against α-SMA. The slides were evaluated for elastic and collagen fiber content and quality or VSMCs quantity. All analyzed samples demonstrated characteristics of extensive elastin and advanced collagen fiber degradation and disruption. Furthermore, aneurysm wall biopsy specimens showed significant negative correlation of collagen fiber (r = –0.76; P < .01) and VSMC (r = –0.71; P < .01) content compared with increasing SUVmax. Elastin quantity did not correlate significantly with SUVmax (Fig 3, b and Fig 4, C); thus, all wall specimens showed only low residual elastin fiber content.

Correlation of histopathologic characteristics 

In addition to tracer signal intensity correlations with the underlying histology, the correlation of inflammatory infiltrates with MMP-expressions and AAA wall constituents was also analyzed. Strong significant correlations were obvious for total inflammatory infiltrate, CD3 (T-lymphocytes), and CD68-positive cells (macrophages) with MMP-9 (r = +0.79, +0.79, and +0.74; P < .01) but not for MMP-2. Furthermore, significant negative correlation was found for MMP-9 expression with collagen fiber content (r = –0.53, P < .05) and VSMC density (r = –0.57, P < .05). In contrast, no significant correlation was seen between AAA wall constituents and MMP-2 tissue expressions.

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Discussion 

This pilot study analyzed the putative role of metabolic imaging in AAA by FDG-PET/CT. The combined anatomic and metabolic information of FDG-PET/CT imaging allowed an exact localization of areas with maximum FDG uptake in the aneurysm wall. In consequence, FDG-PET/CT–guided intraoperative biopsy collection out of these areas was enabled and for the first time in AAA, to our knowledge, maximum tracer signal intensity could be compared with the degree of histopathologic changes within the aneurysm vessel wall.

In context with clinical presentation, the study demonstrates that symptomatic AAA exhibited highly increased FDG uptake compared with asymptomatic AAA and healthy controls. Asymptomatic AAAs showed also significantly increased maximum focal FDG uptake compared with age-matched controls. This observation is in agreement with current pathologic concepts describing aneurysm formation and rupture as an active metabolic process4, 5 with focal accentuation.9 Interestingly, tracer uptake was independent from vessel diameter and AAA expansion. This observation is partly in accordance with a previous report describing strong FDG signalling in PET for symptomatic AAA but also in rapidly expanding AAA.8 This discrepancy may be explained by the small study population and the current status of AAA progression. Frequently in AAA, episodes of rapid expansion are followed by periods of stasis,10 with presumably lower detectable metabolic activity.

Furthermore, FDG-uptake signal intensity was correlated with the underlying histopathology. Such semiquantitative correlation of FDG uptake with the degree of tissue alterations has already been described for several inflammatory diseases,11, 12 but not so far in AAA. In general semiquantitative evaluation of histology seems imprecise, but most of the aortic wall specimens showed inhomogeneous and accentuated distribution of the main pathologic characteristics. We therefore used semiquantitative visual evaluation to describe the predominant characteristic changes in the entire specimen.

Our preliminary results demonstrated that low SUVmax levels of asymptomatic AAA were correlated with macrophage infiltration adjacent to atherosclerotic lesions with low density. In contrast, effusive FDG accumulation was strictly associated with massive transmural macrophage, T-cell infiltration, and clinical symptoms. These results confirm previous casuistic reports identifying macrophages as a main cellular source of FDG glucose hypermetabolism in the aortic wall in atherosclerosis and inflammatory vessel disease.13, 14

Apart from VSMCs, inflammatory infiltrates such as macrophages are the main sources of MMPs in AAAs, and focal proteolytic MMP hyperactivity may lead to AAA rupture at relatively low levels of intraluminal pressure.15 Especially, MMP-9 and MMP-2 were frequently associated with aneurysm growth and rupture.16, 17 In our experiments, increasing FDG uptake was significantly correlated only with MMP-9 expression and inflammatory reaction predominantly in symptomatic AAAs, whereas MMP-2 activity was independent of SUVmax. These results are in accordance with the recent findings evincing an elevated MMP-9 level but not MMP-2 expression at rupture sites of AAAs.9, 18

Furthermore, reciprocal to the increased tracer activity, a significant reduction of resident α-SMA-positive mesenchymal cells was observed. Hence, VSMCs seem unlikely to be responsible for relevant FDG turnover or MMP expression in symptomatic AAAs. These results are consistent with histopathologic studies in AAAs that describe inflammatory infiltration accompanied by VSMC reduction with impaired repair and maintenance of extracellular matrix proteins.19, 20

The extracellular matrix proteins elastin and collagen, the substrates of MMP proteolytic activity, are the main determinants of aortic vessel wall stability. During the progression of an AAA, the elastin content decreases whereas the collagen I and III concentration increases,21, 22 which is responsible for most of the tensile wall strength.23 Consistent with these observations, the ripe AAAs histologically analyzed in this study revealed already an extensive degree of degradation and reduction of elastin fibers, and the reduction of elastin fibers was extensive and similar in all specimens. Therefore, no significant correlation of elastin content with SUVmax could be reached. In contrast, the collagen fiber content and quality correlated negatively with increasing FDG uptake, in particular in symptomatic AAAs, indicating an area with minor AAA wall strength prone to rupture.

The main limitation of this pilot study is the small study population with undersized subgroups, in particular, of the rare symptomatic patients. Consequently, statistical analyses should be treated carefully. This study should demonstrate only preliminary but encouraging results, the methodic approach, and clinical applicability of FDG-PET/CT in patients with AAA. Moreover, to improve specificity of the FDG signal, intraindividual correlation of histologic specimens from areas with minimum and maximum FDG uptake should be performed in future studies.

A further limitation is that the accuracy of FDG-PET/CT imaging may be limited by the partial volume effect observed in small or thin targets like aortic wall. Furthermore, spillover of activity from the vessel lumen may hamper exact quantification of the SUV in the vessel wall (ie, accuracy of signal measurement could be influenced by differences in either activity or volume). The precision of the results can be further improved by partial volume effect correction as intended and described recently for brain or lung imaging.24, 25

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Conclusion 

FDG-PET/CT allowed a reliable preoperative localization of areas with focally increased FDG uptake within the aneurysm wall. Thereby, FDG accumulated in the vessel wall of asymptomatic and symptomatic AAA. In symptomatic AAAs, FDG uptake values were significantly higher compared with asymptomatic AAAs. Furthermore, we found significant correlation of FDG signal intensity with tissue inflammation. In addition, increased macrophage and T-cell accumulation was correlated with increased MMP-9 activity, followed by collagen degradation in areas with intense focal FDG uptake, supporting the current hypothesis that inflammatory changes are more pronounced in symptomatic compared with asymptomatic AAAs.4, 5 The correlation of focal FDG uptake in PET/CT with morphologic and biochemical changes assessed by histology in the specimen in our study therefore provided a more detailed insight in the pathophysiology of AAAs in vivo. As a consequence, FDG-PET/CT imaging might be a new approach to identify AAAs at risk before acute aneurysm onset.

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Author contributions 


Conception and design: CR, ME, HE, JP, SS, BJ

Analysis and interpretation: CR, ME, JP

Data collection: CR, ME, JP, SS,

Writing the article: CR, ME

Critical revision of the article: HE, JP, SS, BJ

Final approval of the article: HE, SS, BJ

Statistical analysis: CR, ME, JP

Obtained funding: HE

Overall responsibility: BJ

CR and ME contributed equally to this article

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We thank Dr Peter Heider for his active assistance in specimen collection and for his competent scientific advice. Furthermore, we thank Renate Hegenloh for her excellent technical support in the histological and immunohistochemical staining.

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 Competition of interest: none.

PII: S0741-5214(08)00509-0

doi:10.1016/j.jvs.2008.03.059

Journal of Vascular Surgery
Volume 48, Issue 2 , Pages 417-423, August 2008

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