|Home | About | Journals | Submit | Contact Us | Français|
Although the precise mechanisms underlying the pathogenesis of abdominal aortic aneurysm (AAA) remain unclear, aortic wall inflammation has been implicated in AAA development. Several studies have reported the use of 18fluoro-deoxyglucose (18F-FDG)/positron emission tomography (PET) to assess the nature of AAA.
We present a case of 77-year-old Japanese male with juxta-anastomotic AAA who was followed up with multiple 18F-FDG-PET/CT scans over 7 years. The scans revealed chronological changes in aortic wall inflammation leading to progress and eventual rupture.
This case supports a notion that aortic wall inflammation plays a role in AAA progression and rupture.
Abdominal aortic aneurysm (AAA) is a degenerative disease of the aorta, occurring primarily in the elderly. The aneurysmal wall comprises intimal atherosclerosis, disruption of elastic media, and inflammatory cell infiltration in the adventitial layer. Although the underlying mechanisms remain to be elucidated, aortic inflammation, particularly at the adventitial layer, is suggested to be the important pathogenesis of AAA.1–3 We previously reported that adventitial mast cells play a role in the development of AAA, and we showed that mast cells stimulate the synthesis of matrix metalloproteinase (MMP)-9 in macrophages, leading to the degradation of extracellular matrix in aortic wall.4
As the aneurysm grows, the rupture rate increases.1 Patients are regularly followed up with computed tomography (CT); however, vulnerability of aneurysmal wall cannot be adequately evaluated using CT scans. Other studies, as well as our previous study, have shown that 18fluoro-deoxyglucose (18F-FDG) positron emission tomography (PET) imaging may be an alternative method to assess the nature of AAA wall5–10; we found that the amount of 18F-FDG uptake is associated with MMP-9 activity.10 Here, we present a case of a patient with juxta-anastomotic AAA who was followed up with multiple 18F-FDG-PET/CT scans, which revealed chronological changes in aortic wall inflammation leading to progress and eventual rupture.
In 2004, a 77-year-old Japanese man with a vascular prosthesis (open repair) for infrarenal abdominal aortic aneurysm, received in 2001, was admitted to our hospital for evaluation of a re-dilating abdominal aorta (41×42 mm in maximal diameter) at just below the bifurcation of the renal arteries and anastomosis. He never stopped smoking since the previous surgery, and he was on antihypertensive drugs (amlodipine 5 mg/day and losartan 50 mg/day). He refused the re-operation; thus, we decided to follow-up with CT on a regular basis. In 2007, he was re-admitted to our hospital because of acute pneumonia. On admission, we performed 18F-FDG-PET/CT for the first time to exclude the possible coexistence of lung cancer. Whole body PET/CT images were obtained 60 minutes after injection of 200 MBq FDG using the 3-dimensional method. We reconstructed all PET images using iterative algorithms (Fourier rebinning plus attenuation-weighted ordered-subset expectation maximization, 2 iterations, 8 subsets, 5-mm Gaussian filter) with CT-based attenuation correction, as previously described.11 Then, the data were further reconstructed with a 256×256 matrix and 3-mm-thick slices using the ESOFT4.5 workstation (Siemens/CTI, Knoxville, TN). A volume of interest (VOI) of the AAA was manually drawn on the 3-dimensional whole body images encompassing the entire lesion. The maximum VOI was defined as the maximum standardized uptake value (SUVmax). To monitor the lesion quantitatively, SUVmax of the aneurysm was recorded in each study. Figure Figure1A1A (October 2007) showed that the maximum size of the aneurysm was 44×53 mm and SUVmax was 3.92. In 2009, the patient complained of hoarseness and underwent laryngeal microsurgery for squamous cell carcinoma of the vocal cords. We performed 18F-FDG-PET/CT to evaluate metastases preoperatively and determined that the maximal aneurysm diameter was 49×52 mm with SUVmax of 3.68 (Figure (Figure1B;1B; November 2009). Thereafter, he agreed to join our research program (permission number 985, University of Miyazaki) for follow-up evaluation of the aneurysm with 18F-FDG-PET/CT under administration of amlodipine 5 mg/day, losartan 50 mg/day, and mast cell stabilizer tranilast 300 mg/day (the product is not labeled for use) on the following dates: April 2012 (Figure (Figure1C;1C; 55×62 mm in maximal diameter; SUVmax=4.25); December 2012 (Figure (Figure1D;1D; 58×61 mm; SUVmax=5.14); and January 2014 (Figure (Figure1E;1E; 65×82 mm, SUVmax=5.18). Figure Figure22 summarizes the chronological changes of SUVmax over 7 years. Nine months after the last scan, he was brought to the emergency room due to syncope accompanied by massive upper gastrointestinal bleeding. A CT scan suggested further growth of the aneurysm (70×83 mm) with an aortojejunal fistula. He died the following day.
This patient provided written informed consent to participate in the study, and his family approved the publication of this case details. This study was approved by the Human Investigation Review Committee of the University of Miyazaki (No. 985) and conformed to the principles outlined in the Declaration of Helsinki (2013).
This report describes the clinical course of a juxta-anastomotic AAA during progression and eventual rupture, as assessed by multiple 18F-FDG-PET/CT scans over the 7-year follow-up period. To the best of our knowledge, this is the first case to follow the AAA size and its nature by 18F-FDG-PET/CT scan for a long period. In addition, these images support the mechanistic insight into the significant role of glycolytic activity in chronological progression and rupture of the aneurysmal wall.10,12,13 The first 3 scans revealed high focal 18F-FDG uptake along with the implanted graft in the neck over 5 years. The fourth scan showed that the most intensified site shifted to the bottom of the aneurysm sac, and the final scan before the rupture and patient's death indicated that it extended to the entire aneurysmal wall. We previously reported that the 18F-FDG-PET signal was correlated with the expression of glucose transporter-3, which is mainly distributed in macrophages, and the activity of MMP-9 in human AAA.10 The multiple 18F-FDG-PET/CT scans suggest that the extent of inflammation of the aneurysmal wall was not uniform and that the maximal inflammatory site varied over time. We speculate that the high focal 18F-FDG uptake might have reflected ongoing extracellular matrix degradation, leading to the continued enlargement of the aneurysm and the resultant rupture. Future studies are designed to image 18F-FDG-PET/CT scan to assess if any medical treatment affects the aortic inflammation and the resultant expansion.
This case supports that active inflammation is associated with the progression and rupture of AAA, and that multiple periodic 18F-FDG-PET/CT scans indicate sequential changes in size and potential active inflammation of the aneurysmal wall.
The authors would like to thank Enago (www.enago.jp) for the English language review.
Abbreviations: 18F-FDG = 18fluoro-deoxyglucose, AAA = abdominal aortic aneurysm, CT = computed tomography, MMP = matrix metalloproteinase, PET = positron emission tomography, SUVmax = maximum standardized uptake value, VOI = volume of interest.
This study was supported by grants-in-aid for Scientific Research (C) (23591052 to T.T.) from the Ministry of Education, Culture, Sport, Science and Technology, Japan. The authors have no conflicts of interest to disclose.