Circulating levels of Amyloid Beta 1-40 are associated with the rate of progression of atherosclerosis in menopause

Maturitas ◽  
2021 ◽  
Vol 152 ◽  
pp. 95
Author(s):  
Eleni Armeni ◽  
Dimitrios Delialis ◽  
Georgios Georgiopoulos ◽  
Simon Tual-Chalot ◽  
Nikolaos Vlachogiannis ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Rate Of Progression ◽  
Circulating Levels ◽  
Progression Of Atherosclerosis

The rate of progression of atherosclerosis in menopause is associated with levels of circulating amyloid beta 1-40

2021 ◽  
Author(s):  
Eleni Armeni ◽  
Dimitrios Delialis ◽  
Georgios Georgiopoulos ◽  
Simon Tual-Chalot ◽  
Nikolaos Vlachogiannis ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Rate Of Progression ◽  
Progression Of Atherosclerosis

Levels of circulating amyloid beta 1-40 are associated with the rate of progression of atherosclerosis in menopause

2021 ◽  
Author(s):  
Eleni Armeni ◽  
Stavroula Paschou ◽  
Dimitrios Delialis ◽  
Georgios Georgiopoulos ◽  
Panagiota Chatzivasileiou ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Rate Of Progression ◽  
Progression Of Atherosclerosis

P2541Plasma levels of amyloid beta 1-40 are associated with the rate of progression of carotid subclinical atherosclerosis in postmenopausal women

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Delialis ◽  
G Georgiopoulos ◽  
K Sopova ◽  
I Kanakakis ◽  
C Kontogiannis ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Postmenopausal Women ◽  
Amyloid Beta ◽  
Linear Mixed Model ◽  
Subclinical Atherosclerosis ◽  
Repeated Measurements ◽  
Model Assessment ◽  
Clinical Value ◽  
Rate Of Progression

Abstract Background There is increasingly recognized undetected residual cardiovascular (CV) risk in postmenopausal women, suggesting the need for new risk biomarkers in this population. We have previously shown that amyloid-beta (1–40) (Aβ1–40), a proinflammatory and pro-atherosclerotic peptide, is associated with concurrent subclinical cardiovascular disease (CVD) in the general population and with major adverse cardiac events in patients with established cardiac disease. However, the clinical value of Aβ1–40 in menopause or whether this peptide is linked with an increased rate of progression of atherosclerotic disease is unknown. Purpose To examine the association of Aβ1–40 levels with the rate of progression of carotid intima-media thickness (IMT) in postmenopausal women. Methods In the settings of a Menopause Clinic, postmenopausal women (n=140) without clinically overt CVD or diabetes were consecutively recruited and re-evaluated after a median follow-up period of 24 months. IMT in the carotid arteries was measured by ultrasonography. The average of maximal IMT (mean cIMT) measured at both left and right common carotid, carotid bulb (cb)and internal carotid (ic) artery were used as the main end-point of the analysis. Aβ1–40 was measured in plasma samples at baseline and follow up. Fasting insulin resistance was assessed using the homeostasis model assessment of insulin resistance (HOMA-IR). Results Women with increased plasma levels Aβ1–40 in the highest tertile presented the highest probability to have increased mean cIMT (adjusted OR=2.97, 95% CI 1.18–7.52, p=0.021) independently of age, smoke, hypertension, and hyperlipidemia. After adjustment for HOMA-IR, this association remained significant. Similarly, Aβ1–40 levels were associated with increased mean cb and icIMT (adjusted OR=3.34 for highest versus lower tertile, 95% CI 1.27–8.81, p=0.015). Mean cIMT significantly increased across the follow up period (0.73mm (0.065–0.08) to 0.77mm (0.07–0.089), median increase rate per year 0.024mm, p<0.001). By multi-level linear mixed model analysis, changes in Aβ1–40 levels were associated with increased rate of progression of mean cIMT (4.1% increase per 1-SD increase, p<0.001) after adjustment for differences in follow-up duration and age, hypertension, hyperlipidemia, and smoking. When repeated measurements of HOMA-IR were also considered, this association did not materially change (p=0.021). Similarly, longitudinal changes in Aβ1–40 correlated with the progression of mean cb and icIMT (3.9% increase per 1-SD increase, p=0.001), independently of time to re-evaluation and cardiovascular risk factors. Conclusion Aβ1–40 is an independent predictor of the rate of progression of subclinical carotid atherosclerosis in menopausal women. This finding supports the clinical value of Aβ1–40 in menopause and warrants further investigation for its prognostic role in this population.

4.P.41 Histo-morphometric studies of aortic lipid streaks in young males from populations with different rate of progression of atherosclerosis

1997 ◽  
Vol 134 (1-2) ◽  
pp. 304 ◽  
Author(s):  
V.S. Zhdanov ◽  
N.H. Sternby ◽  
I.P. Drobkova ◽  
I.E. Galakhov ◽  
V.P. Alexeev
Keyword(s):  
Young Males ◽  
Rate Of Progression ◽  
Progression Of Atherosclerosis

4.P.29 Histo-morphometric studies of aortic fatty streaks in young males from populations with different rate of progression of atherosclerosis

1997 ◽  
Vol 134 (1-2) ◽  
pp. 301-302
Author(s):  
V.S. Zhdanov ◽  
N.H. Sternby ◽  
L.P. Drobkova ◽  
I.E. Galakhov ◽  
V.P. Alexeev
Keyword(s):  
Young Males ◽  
Rate Of Progression ◽  
Progression Of Atherosclerosis

scholarly journals Calcium Channel Blockers, Progression to Dementia, and Effects on Amyloid Beta Peptide Production

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Mark A. Lovell ◽  
Erin Abner ◽  
Richard Kryscio ◽  
Liou Xu ◽  
Shuling X. Fister ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Calcium Channel ◽  
Amyloid Beta ◽  
Calcium Channel Blockers ◽  
Antihypertensive Drugs ◽  
Epidemiologic Studies ◽  
Amyloid Beta Peptide ◽  
Channel Blockers ◽  
Beta Peptide ◽  
Rate Of Progression

Previous epidemiologic studies suggest that antihypertensive drugs may be protective against cognitive decline. To determine if subjects enrolled in the University of Kentucky longitudinal aging study who used antihypertensive drugs showed diminished progression to dementia, we used a 3-parameter logistic regression model to compare the rate of progression to dementia for subjects who used any of the five common categories of antihypertensive drugs to those with similar demographic characteristics but who did not use antihypertensives. Regression modeling showed that subjects who used calcium channel blockers (CCBs) but not the other classes of antihypertensives showed a significant decrease in the rate of progression to dementia. Significantly, use of CCBs ameliorated the negative effects of the presence of APOE-4 alleles on cognitive decline. To determine if CCBs could minimize amyloid beta peptide (Aβ1–42) production, H4 neuroglioma cultures transfected to overexpress APP were treated with various CCBs and Aβ1–42levels and levels of proteins involved in Aβproduction were quantified. Results show that treatment with nifedipine led to a significant decrease in levels of Aβ1–42, with no significant decrease in cell viability. Collectively, these data suggest that use of CCBs significantly diminishes the rate of progression to dementia and may minimize formation of Aβ1–42.

scholarly journals The Deleterious Influence of Tenofovir-Based Therapies on the Progression of Atherosclerosis in HIV-Infected Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Gerard Aragonès ◽  
Pedro Pardo-Reche ◽  
Laura Fernández-Sender ◽  
Anna Rull ◽  
Raúl Beltrán-Debón ◽  
...  
Keyword(s):  
Subclinical Atherosclerosis ◽  
Plasma Concentrations ◽  
Hdl Cholesterol ◽  
Lower Plasma ◽  
Expression Levels ◽  
Inflammatory Biomarker ◽  
Atherosclerosis Progression ◽  
Cholesterol Levels ◽  
Circulating Levels ◽  
Progression Of Atherosclerosis

We investigated the potential differential effects of antiretroviral therapies on unbalanced chemokine homeostasis and on the progression of atherosclerosis in HIV-infected patients. A two-year prospective study was performed in 67 consecutive HIV-infected patients initiating antiretroviral therapy with abacavir/lamivudine or tenofovir/emtricitabine. Circulating levels of inflammatory biomarkers, progression of subclinical atherosclerosis and expression levels of selected chemokines genes in circulating leukocytes were assessed. Control subjects showed significantly lower plasma concentrations of CRP, tPA, IL-6, and MCP-1 than HIV-infected patients at a baseline. After two years of followup, the observed decreases in plasma inflammatory biomarker levels were only significant for MCP-1, tPA, and IL-6. The decrease in plasma MCP-1 concentration was associated with the progression of atherosclerosis, and this effect was negligible only in patients receiving TDF-based therapy. Multivariate analysis confirmed that treatment with TDF was positively and significantly associated with a higher likelihood of subclinical atherosclerosis progression. However, the expression levels of selected genes in blood cells only showed associations with the viral load and total and HDL-cholesterol levels. Current antiretroviral treatments may partially attenuate the influence of HIV infection on certain inflammatory pathways, though patients receiving TDF therapy must be carefully monitored with respect to the presence and/or progression of atherosclerosis.

Nitric oxide deficiency in chronic kidney disease

2008 ◽  
Vol 294 (1) ◽  
pp. F1-F9 ◽  
Author(s):  
Chris Baylis
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Metabolic Pathways ◽  
Cardiovascular Complications ◽  
No Production ◽  
Nos Inhibitors ◽  
Rate Of Progression ◽  
Nitric Oxide Deficiency ◽  
Circulating Levels

The overall production of nitric oxide (NO) is decreased in chronic kidney disease (CKD) which contributes to cardiovascular events and further progression of kidney damage. There are many likely causes of NO deficiency in CKD and the areas surveyed in this review are: 1. Limitations on substrate (l-Arginine) availability, probably due to impaired renal l-Arginine biosynthesis, decreased transport of l-Arginine into endothelial cells and possible competition between NOS and competing metabolic pathways, such as arginase. 2. Increased circulating levels of endogenous NO synthase (NOS) inhibitors, in particular asymmetric dimethylarginine (ADMA). Increased methylation of proteins and their subsequent breakdown to release free ADMA may contribute but the major culprit is probably reduced ADMA catabolism by the enzymes dimethylarginine dimethylaminohydrolases. 3. Reduced renal cortex abundance of the neuronal NOS (nNOS)α protein correlates with injury while increasing nNOSβ abundance may provide a compensatory, protective response. Interventions that can restore NO production by targeting these various pathways are likely to reduce the cardiovascular complications of CKD as well as slowing the rate of progression.

scholarly journals Association of FGF-2 Concentrations with Atheroma Progression in Chronic Kidney Disease Patients

2018 ◽  
Vol 13 (4) ◽  
pp. 577-584 ◽  
Author(s):  
Milica Bozic ◽  
Angels Betriu ◽  
Marcelino Bermudez-Lopez ◽  
Alberto Ortiz ◽  
Elvira Fernandez ◽  
...  
Keyword(s):  
Lower Risk ◽  
Cardiovascular Events ◽  
Reference Group ◽  
Fibroblast Growth Factor 2 ◽  
Multivariable Logistic Regression Analysis ◽  
Ckd Stage ◽  
Rate Of Progression ◽  
Atheroma Plaque ◽  
Progression Of Atherosclerosis

Background and objectivesAtherosclerosis is highly prevalent in CKD. The rate of progression of atherosclerosis is associated with cardiovascular events. Fibroblast growth factor 2 (FGF-2) is a member of the FGF family with potentially both protective and deleterious effects in the development of atherosclerosis. The role of circulating FGF-2 levels in the progression of atherosclerosis in CKD is unknown.Design, setting, participants, & measurementsWe used a multicenter, prospective, observational cohorts study of 481 patients with CKD. We determined the presence of atheroma plaque in ten arterial territories by carotid and femoral ultrasounds. Progression of atheromatosis was defined as an increase in the number of territories with plaque after 24 months. Plasma levels of FGF-2 were measured by multiplex analysis. A multivariable logistic regression analysis was performed to determine whether plasma FGF-2 levels were associated with atheromatosis progression.ResultsAverage age of the population was 61 years. The percentage of patients in each CKD stage was 51% in stage 3, 41% in stages 4–5, and 8% in dialysis. A total of 335 patients (70%) showed plaque at baseline. Atheromatosis progressed in 289 patients (67%). FGF-2 levels were similar between patients with or without plaque at baseline (79 versus 88 pg/ml), but lower in patients with atheromatosis progression after 2 years (78 versus 98 pg/ml; P<0.01). In adjusted analyses, higher plasma FGF-2 was associated with lower risk of atheromatosis progression (odds ratio [OR], 0.86; 95% confidence interval [95% CI], 0.76 to 0.96; per 50 pg/ml increment). Analysis of FGF-2 in tertiles showed that atheroma progression was observed for 102 participants in the lowest tertile of FGF-2 (reference group), 86 participants in the middle tertile of FGF-2 (adjusted OR, 0.70; 95% CI, 0.40 to 1.20), and 74 participants in the lowest tertile of FGF-2 (adjusted OR, 0.48; 95% CI, 0.28 to 0.82).ConclusionsLow FGF-2 levels are independently associated with atheromatosis progression in CKD.

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