Chronic unilateral arm lymphedema correlates with increased intima-media thickness in the brachial artery

VASA ◽  
2021 ◽  
Author(s):  
Victoria Klüsch ◽  
Erin C. Boyle ◽  
Saad Rustum ◽  
Maximilian Franz ◽  
Tjoung-Won Park-Simon ◽  
...  
Keyword(s):  
Arterial Wall ◽  
Lymphatic Vessels ◽  
Atherosclerotic Lesion ◽  
Intima Media Thickness ◽  
Cholesterol Transport ◽  
Contralateral Limb ◽  
Arm Lymphedema ◽  
Human Arteries ◽  
Clinical Experiment ◽  
Atherosclerotic Lesion Formation

Summary: Drainage of the arterial wall via adventitial lymphatic vessels has been shown to play a pivotal role for vessel wall homeostasis. Also, retrograde cholesterol transport is ensured via this route, but no studies exist to demonstrate that lymphatic stasis would represent a mechanism to initiate atherosclerotic lesion formation in human arteries. To test this hypothesis, we embarked on a simple clinical experiment, assessing wall thickness in limb arteries with lymphedema after surgical intervention, with the contralateral limb serving as control. Using ultrasound imaging, the differential thickness was assessed separately for the three arterial wall layers. The potential of disease progression by lymphostasis was addressed by depiction of longitudinal results according to the time after lymph dissection.

Pneumococcal vaccination decreases atherosclerotic lesion formation: molecular mimicry between Streptococcus pneumoniae and oxidized LDL

10.1038/nm876 ◽  
2003 ◽  
Vol 9 (6) ◽  
pp. 736-743 ◽  
Author(s):  
Christoph J Binder ◽  
Sohvi Hörkkö ◽  
Asheesh Dewan ◽  
Mi-Kyung Chang ◽  
Emily P Kieu ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Molecular Mimicry ◽  
Oxidized Ldl ◽  
Pneumococcal Vaccination ◽  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Atherosclerotic Lesion Formation

Heme Oxygenase-1 Inhibits Atherosclerotic Lesion Formation in LDL-Receptor Knockout Mice

2001 ◽  
Vol 88 (5) ◽  
pp. 506-512 ◽  
Author(s):  
Kazunobu Ishikawa ◽  
Daisuke Sugawara ◽  
Xu-ping Wang ◽  
Kazunori Suzuki ◽  
Hiroyuki Itabe ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Knockout Mice ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Heme Oxygenase 1 ◽  
Lesion Formation ◽  
Ldl Receptor Knockout Mice ◽  
Atherosclerotic Lesion Formation

scholarly journals Linking cardiorespiratory fitness classification criteria to early subclinical atherosclerosis in children

2015 ◽  
Vol 40 (4) ◽  
pp. 386-392 ◽  
Author(s):  
Xavier Melo ◽  
Helena Santa-Clara ◽  
Diana A. Santos ◽  
Nuno M. Pimenta ◽  
Cláudia S. Minderico ◽  
...  
Keyword(s):  
Cardiorespiratory Fitness ◽  
Arterial Wall ◽  
Operating Characteristic ◽  
Screening Tool ◽  
Subclinical Atherosclerosis ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
High Resolution Ultrasonography

It is unclear if cardiorespiratory fitness (CRF) can be used as a screening tool for premature changes in carotid intima-media thickness (cIMT) in paediatric populations. The purpose of this cross-sectional study was 3-fold: (i) to determine if CRF can be used to screen increased cIMT; (ii) to determine an optimal CRF cut-off to predict increased cIMT; and (iii) to evaluate its ability to predict increased cIMT among children in comparison with existent CRF cut-offs. cIMT was assessed with high-resolution ultrasonography and CRF was determined using a maximal cycle test. Receiver operating characteristic analyses were conducted in boys (n = 211) and girls (n = 202) aged 11–12 years to define the optimal sex-specific CRF cut-off to classify increased cIMT (≥75th percentile). Logistic regression was used to examine the association between the CRF cut-offs with the risk of having an increased cIMT. The optimal CRF cut-offs to predict increased cIMT were 45.81 and 34.46 mL·kg−1·min−1 for boys and girls, respectively. The odds-ratios for having increased cIMT among children who were unfit was up to 2.8 times the odds among those who were fit (95% confidence interval: 1.40–5.53). Considering current CRF cut-offs, only those suggested by Adegboye et al. 2011. (Br. J. Sports Med. 45(9): 722–728) and Boddy et al. 2012 (PLoS One, 7(9): e45755) were significant in predicting increased cIMT. In conclusion, CRF cut-offs (boys: ≤ 45.8; girls: ≤ 34.5 mL·kg−1·min−1) are associated with thickening of the arterial wall in 11- to 12-year-old children. Low CRF is an important cardiovascular risk factor in children and our data highlight the importance of obtaining an adequate CRF.

scholarly journals The onset of atherosclerotic lesion formation in hypercholesterolemic rabbits is delayed by iron depletion

FEBS Letters ◽  
1999 ◽  
Vol 459 (2) ◽  
pp. 218-222 ◽  
Author(s):  
Durairaj Ponraj ◽  
Jagoda Makjanic ◽  
Patricia S.P Thong ◽  
Benny K.H Tan ◽  
Frank Watt
Keyword(s):  
Atherosclerotic Lesion ◽  
Lesion Formation ◽  
Iron Depletion ◽  
Atherosclerotic Lesion Formation

scholarly journals Gasdermin D mediates inflammation-induced defects in reverse cholesterol transport and promotes atherosclerosis.

2021 ◽  
Author(s):  
Emmanuel Opoku ◽  
Cynthia Alicia Traughber ◽  
David Zhang ◽  
Amanda J Iacano ◽  
Mariam Khan ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Reverse Cholesterol Transport ◽  
Foam Cell ◽  
Atherosclerotic Lesion ◽  
Foam Cell Formation ◽  
Cholesterol Transport ◽  
Inflammasome Activation ◽  
Lesion Area ◽  
Direct Role

Nlrp3 inflammasome is activated in advanced human atherosclerotic plaques. Gasdermin D (GsdmD) serves as a final executor of Nlrp3 inflammasome activity, by generating membrane pores for the release of mature Interleukin-1beta (IL-b). Inflammation dampens reverse cholesterol transport (RCT) and promotes atherogenesis, while anti-IL-1b; antibodies were shown to reduce cardiovascular disease in humans. Though Nlrp3/IL-1b; nexus is an emerging atherogenic pathway, the direct role of GsdmD in atherosclerosis is not yet clear. Here, we used in-vivo Nlrp3 inflammasome activation to show that the GsdmD-/- mice release ~80% less IL-1b; vs WT mice. The GsdmD-/- macrophages were more resistant to Nlrp3 inflammasome mediated reduction in cholesterol efflux, showing ~26% decrease vs. ~60% reduction in WT macrophages. GsdmD expression in macrophages exacerbated foam cell formation in an IL-1b; dependent fashion. The GsdmD-/- mice were resistance to Nlrp3 inflammasome mediated defect in RCT, with ~32% reduction in plasma RCT vs. ~ 57% reduction in WT mice, ~ 17% reduction in RCT to liver vs. 42% in WT mice, and ~ 37% decrease in RCT to feces vs. ~ 61% in WT mice. The LDLr anti-sense oligonucleotides (ASO) induced hyperlipidemic mouse model showed role of GsdmD in promoting atherosclerosis. The GsdmD-/- mice exhibit ~42% decreased atherosclerotic lesion area in females and ~33% decreased lesion area in males vs. WT mice. The atherosclerotic plaque-bearing WT mice showed the presence of cleaved N-terminal fragment of GsdmD, indicating cleavage of GsdmD during atherosclerosis. Our data show that GsdmD mediates inflammation-induced defect in RCT and promotes atherosclerosis.

Comparison of Statistical Methods for Assessing Spatial Correlations Between Maps of Different Arterial Properties

2015 ◽  
Vol 137 (10) ◽  
Author(s):  
Ethan M. Rowland ◽  
Yumnah Mohamied ◽  
K. Yean Chooi ◽  
Emma L. Bailey ◽  
Peter D. Weinberg
Keyword(s):  
Wavelet Transforms ◽  
Degrees Of Freedom ◽  
Arterial Wall ◽  
Atherosclerotic Lesion ◽  
Null Distribution ◽  
Correlation Coefficients ◽  
Spatial Correlations ◽  
Aggregated Data ◽  
Anatomical Correlation ◽  
Lesion Frequency

Assessing the anatomical correlation of atherosclerosis with biomechanical localizing factors is hindered by spatial autocorrelation (SA), wherein neighboring arterial regions tend to have similar properties rather than being independent, and by the use of aggregated data, which artificially inflates correlation coefficients. Resampling data at lower resolution or reducing degrees-of-freedom in significance tests negated effects of SA but only in artificial situations where it occurred at a single length scale. Using Fourier or wavelet transforms to generate autocorrelation-preserving surrogate datasets, and thus to compute the null distribution, avoided this problem. Bootstrap methods additionally circumvented the errors caused by aggregating data. The bootstrap technique showed that wall shear stress (WSS) was significantly correlated with atherosclerotic lesion frequency and endothelial nuclear elongation, but not with the permeability of the arterial wall to albumin, in immature rabbits.

Abstract 83: Bone Marrow Derived Cells Do Not Mediate Reductions in Cholesterol, Atherosclerosis and Adiposity in Microsomal Prostaglindin E Synthase 1 Deficient Mice Fed High Fat Diets Enriched in Cholesterol

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Sarah Srodulski ◽  
Victoria L King
Keyword(s):  
Bone Marrow ◽  
Weight Gain ◽  
Marrow Cell ◽  
Atherosclerotic Lesion ◽  
Chimeric Mice ◽  
High Fat ◽  
Lesion Formation ◽  
Bone Marrow Derived Cells ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Formation

Microsomal prostaglandin E 2 synthase-1 (mPGES-1) catalyzes the conversion of COX-2 generated PGH 2 to PGE 2 and is the predominate source of PGE 2 during and inflammatory response. We and others have demonstrated that mPGES-1 deficiency attenuates atherosclerosis in mice on a mixed background. The present study investigated the effect of mPGES-1 deficiency on atherosclerosis in C57BL/6 low density lipoprotein receptor deficient (LDLr-/-) mice. mPGES-1 deficiency attenuated atherosclerosis in LDLr-/- mice fed either a low fat (LF) (P = 0.02) or high fat (HF) (P = 0.0026) diet enriched with cholesterol, or a western diet (P = 0.02) for 17 weeks. mPGES-1 deficiency attenuated weight gain and cholesterol concentrations in mice fed a western (P = 0.004 and P < 0.05; respectively) or HF diet (P = 0.01 and P = 0.012, respectively). However, body weight and cholesterol concentrations were not different in mice fed the LF diet. These data suggest that different mechanisms mediate the reduction in atherosclerosis in mPGES-1 deficient mice fed LF and HF diets. To determine if mPGES-1 deficiency in macrophages contributed to the reduction in atherosclerosis in mice fed HF diets, 4 groups of chimeric mice were generated. Four weeks post bone marrow cell transplant (BMT) mice were fed a western diet. BMT attenuated weight gain in all groups of chimeric mice; however, weight gain was not different between any of the groups. BMT decreased atherosclerotic lesion formation 10 fold in all groups of mice. Neither bone marrow cell specific deficiency of mPGES-1 (KO>WT) or mPGES-1 specific expression in bone marrow derived cells (WT>KO) had an effect on lesion formation compared to WT>WT or KO>KO mice. Cholesterol concentrations were decreased in KO>KO and WT>KO mice compared to WT>WT (P < 0.01) and KO>WT (P< 0.05) mice. These data suggest that mPGES-1 expression in bone marrow derived cells does not contribute to the development of atherosclerosis. Moreover, these data suggest that prostanoids may play a role in hepatic cholesterol homeostasis in mice fed HF diets enriched in cholesterol thereby contributing to atherosclerotic lesion formation. Moreover, these data provide further evidence that prostanoids play a role in regulating the accumulation of diet-induced adiposity.

Abstract 3710: Estrogen Does not Account for Accelerated Atherosclerosis in LDLr−/− Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Victoria L King ◽  
Nicholas Hatch ◽  
Xuan Zhang ◽  
Lisa R Tannock
Keyword(s):  
Body Weight Gain ◽  
Atherosclerotic Lesion ◽  
Young Female ◽  
Lesion Formation ◽  
Accelerated Atherosclerosis ◽  
Female Mice ◽  
Ldl Particles ◽  
Gender Specific Differences ◽  
Event Rates ◽  
Atherosclerotic Lesion Formation

Clinical studies demonstrate less atherosclerosis in pre-menopausal women compared to age-matched men, but an equalization in atherosclerosis burden and cardiovascular event rates between genders following menopause. Conversely, using the LDLR−/− mouse model we and others have previously demonstrated that young female mice develop accelerated atherosclerosis compared to age matched males. Whether this difference is due to sex hormones or differences in metabolic factors is not clear. To determine if estrogen mediated the alterations in atherosclerosis in the female mice, female mice were ovariectomized (Ovx). Ovx mice had a marked reduction in uterus weight (Sham: 86 ± 1 vs Ovx: 26 ± 1mg, P < 0.001) and both Ovx females and males had greater body weight gain when fed a lard-enriched diet (10% kcal from fat, D12451 , Research Diets) for 17 weeks compared to sham females. Ovariectomy resulted in an increase in fasting glucose concentrations, which was comparable to males. Cholesterol and triglyceride concentrations were higher in both sham and Ovx females compared to males; primarily distributed in increased VLDL and LDL particles. Interestingly, ovariectomy had no significant effect on extent of atherosclerotic lesion formation in female mice and the extent of atherosclerotic lesion area in both female groups was significantly increased compared to male mice. These data suggest that gender specific differences in lipids and atherosclerotic lesion formation in female LDL-R deficient mice fed a diet enriched in lard are not mediated by estrogen.

Abstract 56: Macrophage Reverse Cholesterol Transport in Mice Relies on The Lymphatic Vasculature

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Catherine Martel ◽  
Wenjun Li ◽  
Brian Fulp ◽  
Andrew Platt ◽  
Emmanuel L Gautier ◽  
...  
Keyword(s):  
Reverse Cholesterol Transport ◽  
Aortic Wall ◽  
Lymphatic Vessels ◽  
Lymphatic Drainage ◽  
Fecal Excretion ◽  
Lymphatic Transport ◽  
Cholesterol Transport ◽  
Transport Function ◽  
Peripheral Tissues ◽  
Lymphatic Vasculature

Reverse cholesterol transport (RCT) refers to mobilization of cholesterol on HDL particles (HDL-C) from extravascular tissues to plasma, ultimately for fecal excretion. Little is known about how HDL-C leaves peripheral tissues to reach plasma. We first used two models of disrupted lymphatic drainage from skin -one surgical and the other genetic- to quantitatively track RCT following injection of [3H]cholesterol-loaded macrophages upstream of blocked or absent lymphatic vessels. Macrophage RCT was markedly impaired in both models, even at sites with a leaky vasculature. Inhibited RCT was downstream of cholesterol efflux from macrophages, since macrophage efflux of a fluorescent cholesterol analogue (BODIPY-cholesterol) was not altered by impaired lymphatic drainage. We next addressed whether RCT was mediated by lymphatic vessels from the aortic wall by loading the aorta of donor atherosclerotic apoE-/- mice with [2H]6-labeled cholesterol and surgically transplanting these aortas into recipient apoE-/- mice that were treated with anti-VEGFR3 mAb to block lymphatic regrowth or with control mAb to allow such regrowth. [2H]-Cholesterol was retained in aortas of anti-VEGFR3 treated mice. Thus, the lymphatic vessel route is critical for RCT from multiple tissues, including the aortic wall. Therefore, supporting lymphatic transport function may facilitate cholesterol clearance in therapies aimed at reversing atherosclerosis.

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