Long-term changes of aortic 18F-FDG uptake and calcification in health-screening subjects

Ryu, Yoshiharu; Yoshida, Katsuya; Suzuki, Yoshiyuki; Nakadate, Masashi; Umehara, Isao; Tomita, Makoto; Shibuya, Hitoshi

doi:10.1007/s12149-012-0679-z

Cited by 11 publications

(7 citation statements)

References 21 publications

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“…Multiple regression analysis showed that progression of aortic calcifications was significantly associated with different atherogenic risk factors like age and smoking habit (P<0.001 and 0.0058 respectively) 24 .…”

Section: Discussionmentioning

confidence: 96%

Risk Factors for the Development and Progression of Thoracic Aorta Calcification

et al. 2015

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Background Vascular calcification independently predicts cardiovascular disease (CVD) and computed tomography (CT) is a useful tool to evaluate and quantify not only coronary but also thoracic aortic calcification (TAC). Previous TAC progression reports were limited to dialysis and renal transplant patients. This is the first study to evaluate TAC progression in a large multi-ethnic cohort without clinically evident CVD at entry. Methods Non-contrast enhanced cardiac CT were obtained in 5886 of 6814 MESA participants (mean age 62 years; 48% males; 40% white, 27% Black, 21% Hispanic, 12% Chinese. Baseline and follow-up TAC scores were derived. Results 4308(73%) participants had no detectable baseline TAC. Mean follow-up duration was 2.4±0.8 years, during which 12% developed TAC. The overall incidence rate was 4.8%/year and was greater with age across gender and ethnic groups; TAC incidence was significantly lower in blacks than whites. After adjustment for follow-up duration, regression analyses showed age, systolic blood pressure, antihypertensives, and smoking were associated with incident TAC. 1578(27%) participants had TAC at baseline with a positive association between average annual TAC change and baseline age. While the overall median change was 32.9 (−1.4, 112.2) Agatston units, 27% showed an annual score change of ≥100 and blacks showed the lowest median across ethnic groups; 22.7 (−3, 86.8). Age, systolic BP, lipid-lowering medication, diabetes and smoking were associated with TAC progression. Conclusion In MESA, traditional CV risk factors were related to both TAC incidence and progression. Blacks had the lowest incidence and median change across ethnic groups, consistent with previous findings for coronary calcification.

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Section: Discussionmentioning

confidence: 96%

Risk Factors for the Development and Progression of Thoracic Aorta Calcification

et al. 2015

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“…There are structural and functional differences in the inherent biomechanical properties of the thoracic and abdominal aorta under normal conditions, as demonstrated by others (29,60). With cardiovascular disease and aging, there is also strong evidence to suggest that remodeling is also not uniform (47) and that the abdominal aorta is relatively stiffer compared with the more proximal regions of the aorta (20,22). Regional differences in the diseased aorta maybe due to differential changes in elastin and collagen content (53) and the subsequent impact on the mechanical properties (3).…”

mentioning

confidence: 88%

Opposing changes in thoracic and abdominal aortic biomechanical properties in rodent models of vascular calcification and hypertension

Ameer

Salman

Avolio

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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This study investigated the effects of hypertension on regional aortic biomechanical and structural properties in three rat models of vascular calcification: the hypertensive Lewis polycystic kidney (LPK; n = 13) model of chronic kidney disease, spontaneously hypertensive rats (SHRs; n = 12), and calcification in normotensive Lewis rats induced by vitamin D3 and nicotine (VDN; n = 8). Lewis and Wistar-Kyoto rats were controls. Thoracic and abdominal aortic stiffness parameters were assessed by tensile testing. In models where aortic stiffness differences compared with controls existed in both thoracic and abdominal segments, an additional cohort was quantified by histology for thoracic and abdominal aortic elastin, collagen, and calcification. LPK and VDN animals had higher thoracic breaking strain than control animals (P < 0.01 and P < 0.05, respectively) and lower energy absorption within the tensile curve of the abdominal aorta (P < 0.05). SHRs had a lower abdominal breaking stress than Wistar-Kyoto rats. LPK and VDN rats had more elastic lamellae fractures than control rats (P < 0.001), which were associated with calcium deposition (thoracic R = 0.37, P = 0.048; abdominal: R = 0.40, P = 0.046). LPK rats had higher nuclear density than control rats (P < 0.01), which was also evident in the thoracic but not abdominal aorta of VDN rats (P < 0.01). In LPK and VDN rats, but not in control rats, media thickness and cross-sectional area were at least 1.5-fold greater in thoracic than abdominal regions. The calcification models chronic kidney disease and induced calcification in normotension caused differences in regional aortic stiffness not seen in a genetic form of hypertension. Detrimental abdominal aortic remodeling but lower stiffness in the thoracic aorta with disease indicates possible compensatory mechanisms in the proximal aorta.

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“…Tissue remodeling associated with cardiovascular disease and aging is not uniform along the length of the aorta 40 . The abdominal aorta is relatively stiffer than more proximal sites 41,42 .…”

Section: Resultsmentioning

confidence: 99%

Alterations to adipose tissue morphology during inflammatory arthritis is indicative of vasculopathology in DBA/1 mice

2017

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The physiologic function of adipose tissue is altered by the host's inflammatory response; the implications for maintaining human health and regulating inflammation-associated disease progression are ill defined. However, this cannot be investigated in humans, therefore the use of animal models is required. With the aim to determine morphological and molecular alterations to perivascular and organ-associated adipose tissues during inflammatory arthritis, collagen-induced arthritis (CIA) was established in male DBA/1 mice. Emerging evidence from this study signposts CIA in the DBA/1 mouse as a model that is relevant to study the development and treatment of early cardiovascular pathology associated with inflammatory arthritis. Here, we show global morphological changes in adipose tissue and the thoracic aorta in animals induced with CIA compared with the non-immunized controls. In CIA, we concluded that the increased cell count in PVAT was, at least in part, caused by an ingress and/or expansion of macrophages that had a mixed phenotype. A substantial increase of galectin-3 was expressed in PVAT from mice with CIA. Galectin-3 is elevated in the blood of patients with CVDs, however, it has never before been measured in PVAT in rodents or humans. Here, PVAT-associated galectin-3 is identified as a potential biomarker for detecting early vascular pathology in CIA and a promising candidate for translation to RA.

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Long-term changes of aortic 18F-FDG uptake and calcification in health-screening subjects

Cited by 11 publications

References 21 publications

Risk Factors for the Development and Progression of Thoracic Aorta Calcification

Risk Factors for the Development and Progression of Thoracic Aorta Calcification

Opposing changes in thoracic and abdominal aortic biomechanical properties in rodent models of vascular calcification and hypertension

Alterations to adipose tissue morphology during inflammatory arthritis is indicative of vasculopathology in DBA/1 mice

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