1014 Spiral imaging at 3 T for the measurement of endothelial-dependent coronary arterial function

Prolonged sitting contributes to cardiovascular disease (CVD) risk. The underlying mechanisms are unknown but may include changes in arterial function and vasoactive mediators. We examined the effects of prolonged unbroken sitting, relative to regular active interruptions to sitting time, on arterial function in adults at increased CVD risk. In a randomized crossover trial, 19 sedentary overweight/obese adults (mean ± SD age 57 ± 12 yr) completed 2 laboratory-based conditions: 5 h uninterrupted sitting (SIT) and 5 h sitting interrupted every 30 min by 3 min of simple resistance activities (SRA). Femoral artery function [flow-mediated dilation (FMD)], blood flow, and shear rate were measured at 0 h, 30 min, 1 h, 2 h, and 5 h. Brachial FMD was assessed at 0 and 5 h. Plasma was collected hourly for measurement of endothelin-1 (ET-1), nitrates/nitrites, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1). There was a significant decline in femoral artery FMD, averaged over 5 h in the SIT condition, relative to SRA ( P < 0.001). Plasma ET-1 total area under the curve over 5 h increased in the SIT condition compared with SRA ( P = 0.006). There was no significant difference between conditions in femoral or brachial shear rate, brachial FMD, nitrates/nitrites, VCAM-1, or ICAM-1 ( P > 0.05 for all). Five hours of prolonged sitting, relative to regular interruptions to sitting time, impaired femoral artery vasodilator function and increased circulating ET-1 in overweight/obese adults. There is the need to build on this evidence beyond acute observations to better understand the potential longer-term vascular-related consequences of prolonged sitting. NEW & NOTEWORTHY This is the first study to examine the effect of prolonged sitting on arterial function in adults at increased cardiovascular disease risk. We have shown that 5 h of prolonged sitting, relative to regular interruptions to sitting time, impaired femoral artery vasodilator function and increased circulating endothelin-1 in overweight/obese adults. There is now the need to build on this evidence beyond acute observations to better understand the potential longer-term vascular-related consequences of prolonged sitting.

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Abstract: 132 ARTERIAL FUNCTION IN PATIENTS WITH INHERITED DYSLIPIDEMIAS

Atherosclerosis Supplements ◽

10.1016/s1567-5688(09)70246-6 ◽

2009 ◽

Vol 10 (2) ◽

pp. e242

Author(s):

C Masoura ◽

C Pitsavos ◽

I Skoumas ◽

K Aznaouridis ◽

C Vlachopoulos ◽

...

Keyword(s):

Arterial Function

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Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose-mediated deleterious effect

European Journal of Heart Failure ◽

10.1016/s1388-9842(03)00006-0 ◽

2003 ◽

Vol 5 (3) ◽

pp. 271-279 ◽

Cited By ~ 19

Author(s):

Christophe Meune ◽

Isabelle Mahé ◽

Jean-Jacques Mourad ◽

Alain Cohen-Solal ◽

Bernard Levy ◽

...

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Ace Inhibitors ◽

Deleterious Effect ◽

Arterial Function

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7.1 THE DETRIMENTAL EFFECTS OF LIVE FIREFIGHTING ON ARTERIAL FUNCTION IN FIREFIGHTERS

Artery Research ◽

10.1016/j.artres.2016.10.047 ◽

2016 ◽

Vol 16 (C) ◽

pp. 62

Author(s):

Alexander Rosenberg ◽

Kanokwan Bunsawat ◽

Tommy Wee ◽

Tracy Baynard ◽

Gavin Horn ◽

...

Keyword(s):

Arterial Function

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RADIAL ARTERIAL FUNCTION FOLLOWING PERCUTANEOUS CANNULATION WITH 18??? AND 20-GAUGE CATHETERS

Survey of Anesthesiology ◽

10.1097/00132586-197804000-00015 ◽

1978 ◽

Vol 22 (2) ◽

pp. 134

Author(s):

R. F. BEDFORD

Keyword(s):

Arterial Function ◽

Percutaneous Cannulation

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Methotrexate, blood pressure and markers of arterial function in patients with rheumatoid arthritis: a repeated cross-sectional study

Therapeutic Advances in Musculoskeletal Disease ◽

10.1177/1759720x17719850 ◽

2017 ◽

Vol 9 (9) ◽

pp. 213-229 ◽

Cited By ~ 15

Author(s):

Arduino A. Mangoni ◽

Leena R. Baghdadi ◽

E. Michael Shanahan ◽

Michael D. Wiese ◽

Sara Tommasi ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Blood Pressure ◽

Cardiovascular Risk ◽

Disease Activity Score ◽

Augmentation Index ◽

Cross Sectional Study ◽

Joint Disease ◽

Group Differences ◽

Cross Sectional ◽

Arterial Function

Background: Methotrexate (MTX) treatment in rheumatoid arthritis (RA) has been associated with lower cardiovascular risk compared to other disease-modifying antirheumatic drugs (DMARDs). We sought to identify whether the MTX-associated cardioprotection involves changes in blood pressure (BP) and/or arterial function. Methods: Clinic and 24-hour peripheral and central systolic and diastolic BP (SBP and DBP), augmentation index (AIx), pulse wave velocity (PWV) and plasma asymmetric dimethylarginine (ADMA) were assessed in RA patients on stable treatment with either MTX ± other DMARDs (MTX group, n = 56, age 61 ± 13 years, 70% females) or other DMARDs (non-MTX group, n = 30, age 63 ± 12 years, 76% females). Measurements were performed at baseline and after 8 months. Results: After adjusting for visit, age, gender, body mass index, folic acid use and 28-joint disease activity score, the MTX group had significantly lower clinic peripheral SBP (−7.7 mmHg, 95% CI −13.2 to −2.3, p = 0.006) and DBP (−6.1 mmHg, 95% CI −9.8 to −2.4, p = 0.001) and clinic central SBP (−7.8 mmHg, 95% CI −13.1 to −2.6, p = 0.003) and DBP (−5.4 mmHg, 95% CI −9.1 to −1.6, p = 0.005) versus the non-MTX group. Furthermore, the MTX group had significantly lower 24-hour peripheral and central SBP and DBP and PWV versus the non-MTX group ( p < 0.01 for all comparisons). By contrast, there were no significant between-group differences in AIx and ADMA. Conclusions: RA patients on MTX treatment had significantly lower clinic and 24-hour peripheral and central BP compared to those who did not take MTX. The lower BP with MTX may be related to differences in PWV, but not in AIx or ADMA concentrations. Further longitudinal studies including randomized controlled trials are warranted to confirm these findings, to identify other possible mechanisms responsible for the effects of MTX on BP and PWV, and to establish whether these effects might account for the reduced cardiovascular risk with MTX.

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