Shields, Kelly
(2012)
Perivascular Adipose Tissue of the Descending Thoracic Aorta, Vascular Calcification, and Systemic Lupus Erythematosus.
Master's Thesis, University of Pittsburgh.
(Unpublished)
Abstract
Aims: Women with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular disease (CVD). Traditional CVD and disease related risk factors have been implicated, but do not fully account for this increased risk. Visceral adipose is most strongly associated with vascular dysfunction and metabolic disorder than other adipose regions. Perivascular adipose tissue (PVAT) is a visceral adipose depot in close proximity to blood vessels, which may have more direct influence over vascular function and progression of CVD. We hypothesized that SLE patients have increased PVAT surrounding the descending thoracic aorta than healthy control subjects. For both SLE and control subjects, we examined the relation between PVAT and vascular calcification of the aorta (AC) and coronary arteries (CAC).
Methods: Using EBT, we quantified the PVAT of the descending thoracic aortic PVAT in SLE (n=135) and age/race matched controls (n=152). Participants were non-diabetic and free of CVD. CAC and AC were quantified using Agatston scores and the PVAT was quantified using standard attenuation values for adipose tissue (–190 to –30 HU) on commercially available software. The total PVAT volume (tPVAT) was calculated by summing the areas and multiplying by the length of the participant’s aorta.
Results: The SLE women were more likely to be hypertensive (p<0.0001) and had a larger waist to hip ratio (p=0.001) than controls reflecting a different adipose distribution. The SLE group had a greater tPVAT than the control group (p=0.0071) despite no differences in BMI (p=0.26), or metabolic syndrome (MS, p=0.17). Total PVAT remained associated with SLE after adjusting for CVD risk factors including BMI (1.025[1.0-1.1], p=0.022), but was attenuated to non-significance with inflammatory factors (p=0.34). In a logistic regression analysis, tPVAT was associated with AC (1.073[1.043- 1.103],p<0.0001), which remained significant after adjustment for CVD and inflammatory factors including BMI (p<0.0007) and MS (p<0.0004). The tPVAT association with CAC (1.051[1.03-1.07],p<0.0001) was non-significant with BMI (p>0.075) and attenuated with MS (p<0.047) when adjusted for CVD or inflammatory factors.
Conclusions: Total PVAT is greater in clinically CVD-free SLE versus control participants and is associated with AC independent of overall adiposity. This work contributes to the field of public health elucidating the mechanisms of CVD progression through PVAT in SLE patients and ultimately in the general population.
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Details
Item Type: |
University of Pittsburgh ETD
|
Status: |
Unpublished |
Creators/Authors: |
|
ETD Committee: |
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Date: |
30 January 2012 |
Date Type: |
Completion |
Defense Date: |
1 December 2011 |
Approval Date: |
30 January 2012 |
Submission Date: |
15 December 2011 |
Access Restriction: |
No restriction; Release the ETD for access worldwide immediately. |
Number of Pages: |
65 |
Institution: |
University of Pittsburgh |
Schools and Programs: |
School of Public Health > Epidemiology |
Degree: |
MS - Master of Science |
Thesis Type: |
Master's Thesis |
Refereed: |
Yes |
Uncontrolled Keywords: |
Systemic Lupus Erythematosus, Cardiovascular Disease, Adipose, Perivascular Adipose Tissue, Vascular Calcification, Coronary Artery Calcification, Aortic Calcification |
Date Deposited: |
30 Jan 2012 19:01 |
Last Modified: |
19 Dec 2016 14:38 |
URI: |
http://d-scholarship.pitt.edu/id/eprint/10821 |
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