scholarly journals POS0216 GREATER HIGH-DENSITY LIPOPROTEIN LEVELS OVER TIME ARE LINKED TO DECREASED CORONARY PLAQUE FORMATION AND REGRESSION AND STABILIZATION OF HIGH-RISK LESIONS IN RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 325.2-326
Author(s):  
G. Karpouzas ◽  
S. Ormseth ◽  
E. Hernandez ◽  
M. Budoff
Keyword(s):  
Coronary Atherosclerosis ◽  
Density Lipoprotein ◽  
Coronary Plaque ◽  
Plaque Formation ◽  
Prednisone Dose ◽  
Calcified Plaque ◽  
Plaque Regression ◽  
Mixed Plaque ◽  
Over Time

Background:The relationship between serum lipoproteins and cardiovascular disease risk in rheumatoid arthritis (RA) is complex1. Their levels and function may vary based on disease activity and medication use. Beneficial effects on high-density lipoprotein (HDL-C) levels, structure and behavior, in response to treatment have been described. However, the impact of HDL-C levels over time on coronary atherosclerosis progression in RA is unknown.Objectives:We here evaluated the influence of HDL-C levels over time on long-term coronary plaque formation and progression in patients with RA.Methods:One hundred one RA patients without symptoms or history of cardiovascular disease who participated in a computed tomography angiography study of coronary atherosclerosis had repeat assessments after 6.9±0.3 years to evaluate plaque progression. Clinical, laboratory and medication data were recorded at baseline and regular outpatient follow-up visits thereafter. Time-averaged HDL-C was calculated for each patient using available consecutive HDL measurements between baseline and follow-up. Robust logistic regression assessed the association between time-averaged HDL-C and likelihood of new plaque formation in segments without plaque at baseline, and transition of prevalent mixed plaque to calcified plaque. Robust multinomial logistic regression evaluated the effect of time-averaged HDL-C on likelihood of new non-calcified, mixed or calcified plaque formation in segments without plaque (compared to remaining without plaque), and non-calcified plaque regression or transition to mixed or calcified plaque at follow-up (compared to remaining non-calcified). All models accounted for clustering of coronary segments within patients and adjusted for Framingham D’Agostino risk score, proximal segment location, time-averaged CRP, cumulative prednisone dose, bDMARD duration, statin duration, waist-to-height ratio, and time-averaged triglycerides.Results:Participants were mostly female (n=87, 86.1%), with a mean ± standard deviation (SD) age of 51.5±10.3 years and time-averaged HDL-C of 51.7±13.9. Ninety-seven new plaques formed in segments without plaque at baseline; 20 were noncalcified, 21 were mixed, and 56 were calcified. Time-averaged HDL-C had no effect on new total plaque formation (adjusted odds ratio-OR 0.88 [95% CI 0.64-1.21]). However, each 1-SD increase in time-averaged HDL-C associated with a 44% reduced likelihood of new non-calcified plaque formation at follow-up (adjusted OR 0.56 [95% CI 0.35-0.92], Figure 1). In contrast, there was no effect of time-averaged HDL-C on new mixed or calcified plaque formation. Of 98 non-calcified plaques at baseline, 42 did not change at follow-up, 32 regressed (disappeared), 16 transitioned to mixed and 8 to calcified plaques. Each SD increase in time-averaged HDL-C yielded a 2.2-fold greater likelihood of non-calcified plaque regression (adjusted OR 2.21 [95% CI 1.02-4.83]). Sixteen of 52 mixed plaques present at baseline transitioned to more stable calcified lesions, and time-averaged HDL-C (per 1-SD increment) predicted a 3.5-fold increased likelihood of transition of mixed to fully calcified plaque (adjusted OR 3.56 [95% CI 1.25-10.17]).Conclusion:Higher HDL-C over time predicted regression of existing and decreased formation of new higher-risk non-calcified plaque. It also associated with transition of vulnerable mixed plaque to more stable fully calcified plaque. These effects were independent of RA treatment duration, prednisone dose and statin exposure.References:[1]Toms TE et al. Curr Vasc Pharmacol. 2010;8:301–326.Figure 1.Impact of HDL-C over time on coronary plaque progression in RADisclosure of Interests:George Karpouzas Speakers bureau: Sanofi/Genzyme/Regeneron, Consultant of: Sanofi/Genzyme/Regeneron, Grant/research support from: Pfizer, Sarah Ormseth: None declared, Elizabeth Hernandez: None declared, Matthew Budoff: None declared

scholarly journals Pericoronary adipose tissue attenuation in low-risk asymptomatic individuals, sex-differences and association with markers of cardiovascular disease

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
N Shanmuganathan ◽  
R Ramanathan ◽  
D Dey ◽  
M Goeller ◽  
MW Kusk ◽  
...  
Keyword(s):  
Density Lipoprotein ◽  
Coronary Plaque ◽  
Low Risk ◽  
Low Density ◽  
Ct Attenuation ◽  
Calcified Plaque ◽  
Blood Pressures ◽  
Asymptomatic Individuals ◽  
Pai 1

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Pericoronary adipose tissue (PCAT) attenuation by coronary computed tomography angiography (CCTA) is a marker of coronary inflammation and predicts clinical outcomes in symptomatic patients undergoing CCTA. Sex-differences in PCAT CT attenuation among asymptomatic individuals are not previously described. Purpose To evaluate PCAT CT attenuation according to sex and markers of cardiovascular disease (CVD). Methods Cross-sectional cohort study including asymptomatic individuals, 50- or 60-year of age, not taking any medicine and without known CVD or type-2 diabetes. At baseline and 5-year follow-up smoking habits, blood pressures and biochemistry (lipids, CRP, fibrinogen, D-dimer, t-PA, PAI-1, vWF) were recorded and Agatston Score measured. At follow-up, CCTA was achieved. Quantitative coronary plaque analysis was performed and PCAT CT attenuation within a radial distance of 3 mm from the outer vessel wall 10–50 mm distal to the origin of the right coronary artery measured. A validated PCAT CT attenuation threshold (high vs low risk) of -70.1 Hounsfield units was applied. Results Included were 123 participants (60 women). Independent of co-variation, PCAT CT attenuation (median, [IQR]) was lower in women (-71.0, [-77.2- -67.0]) vs men (-64.5, [-69.9- -57.4]), p < 0.001. No associations between PCAT CT attenuation (high vs low) and risk factors of CVD, CAC or coronary plaque volumes were demonstrated (Table). Variations in blood pressures, biochemical markers and CAC over five years were not associated with PCAT CT attenuation. Conclusion In low-risk asymptomatic individuals, PCAT CT attenuation was lower in women compared to men, irrespective of markers of CVD. Table. Patient characteristics stratified by PCAT CT attenuation PCAT CT attenuation ≤ -70.1 HU (n = 49) PCAT CT attenuation > -70.1 HU (n = 74) p-value Risk factors Age65-years55-years 2623 3143 0.32 SexMenWomen 1534 4826 <0.001 TobaccoNeverCurrent/previous 1732 3737 0.10 Systolic BP, mmHgDiastolic BP, mmHgTotal cholesterol, mmol/lLDL-cholesterol, mmol/lHDL-cholesterol, mmol/lTriglycerides, mmol/l 137 (17)76 (10)5.61 (0.92)3.50 (0.93)1.41 (0.30)1.65 (0.99 - 2.22) 136 (16)77 (10)5.42 (0.82)3.30 (0.82)1.45 (0.35)1.35 (1.03 - 2.11) 0.660.590.230.220.570.52 Biochemistry CRP, mg/lFibrinogen, μmol/lD-dimer, mg/lvWFt-PAPAI-1 1.16 (0.99 - 2.22)9.5 (8.5 - 10.7)0.40 (0.30 - 0.49)128 (102 - 154)7.1 (5.8 - 8.8)20.5 (16.2 - 31.8) 0.61 (0.30 - 1.14)9.0 (7.8 - 10.0)0.32 (0.24 - 0.47)116 (92 - 146)6.3 (5.1 - 8.8)20.3 (14.7 - 26.3) <0.010.10<0.050.110.200.34 Coronary plaque data Agatston ScoreTotal plaque volume, mm³NCP volume, mm³CP volume, mm³LD-NCP volume, mm³ 1 (0 - 36)15.7 (0 - 143.3)0 (0 - 128.1)0 (0 - 14.6)0.5 (0 - 18.7) 8 (0 - 115)15.6 (0 - 268.2)13.5 (0 - 220.5)1.7 (0 - 31.7)1.8 (0 - 21.8) 0.300.450.490.360.74 Values are n (%), mean (SD) or median (IQR).Abbreviations: HU =Hounsfield unit; LDL =low-density lipoprotein; HDL =high-density lipoprotein; BP =blood pressure; CRP = c-reactive protein: vWF =von-Willebrand Factor; t-PA =tissue plasminogen activator; PAI-1 =plasminogen activator inhibitor -1; NCP =non-calcified plaque; CP =calcified plaque; LD-NCP =low-density non-calcified plaque.

scholarly journals OP0120 BIOLOGICS MAY PREVENT CARDIOVASCULAR EVENTS IN RHEUMATOID ARTHRITIS BY INHIBITING CORONARY PLAQUE FORMATION AND STABILIZING HIGH-RISK LESIONS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 79.1-80
Author(s):  
G. Karpouzas ◽  
S. Ormseth ◽  
E. Hernandez ◽  
M. Budoff
Keyword(s):  
Rheumatoid Arthritis ◽  
High Risk ◽  
Coronary Plaque ◽  
Plaque Formation ◽  
Cvd Risk ◽  
Calcified Plaque ◽  
Lower Likelihood ◽  
Low Attenuation Plaque

Background:Biologic disease-modifying antirheumatic drugs (bDMARDs) effectively control inflammation and may improve cardiovascular outcomes in Rheumatoid arthritis.Objectives:To evaluate if bDMARDs decrease long-term cardiovascular disease (CVD) risk in rheumatoid arthritis and whether potential benefits might be rendered by impacting coronary plaque formation or progression.Methods:In this single-center observational cohort study, 150 patients underwent computed tomography angiography for evaluation of coronary atherosclerosis (total, non-calcified, mixed/calcified and low-attenuation or high-risk plaque); 101 had repeat assessments within 6.9±0.3 years to evaluate plaque progression. All CVD events were prospectively recorded, including cardiac death, myocardial infarction, unstable angina, revascularization, stroke, claudication, and heart failure hospitalization. The Framingham-D’Agostino score assessed clinical risk. Segment stenosis score (cumulative stenosis) measured plaque burden. The effect of bDMARD treatment on CVD events was assessed using marginal structural models. The inverse probability of treatment and censoring weights were used in a weighted pooled logistic regression with current bDMARD use and time since study entry included in the model to approximate a Cox proportional hazards model allowing for time-varying weights. Robust logistic regression evaluated the effect of bDMARD exposure (>50 percent of follow-up period) on likelihood of new plaque formation or change in plaque composition in per-segment models adjusted for Framingham-D’Agostino score, time between scans, statin duration, cumulative prednisone dose and time-averaged CRP.Results:Sixteen patients incurred 19 CVD events. Current bDMARD use associated with lower CVD risk (OR=0.20 [95%CI=0.05-0.75], p=0.018, Figure 1). However, the effect of bDMARDs was no longer significant when a 6-month exposure extension was applied (OR=0.42 [95% CI 0.13-1.38], p=0.15). The effect of bDMARD use on CVD risk was moderated by non-calcified plaque and low-attenuation plaque presence (Figure 1); specifically, bDMARDs were associated with lower CVD risk only in patients with non-calcified plaque (p=.048) or low-attenuation plaque (p=0.036) at baseline. Per-segment plaque progression analyses showed no main effect of bDMARD exposure on likelihood of new plaque formation (Figure 2). However, bDMARD exposure predicted lower likelihood of new plaque forming in segments without plaque among patients without mixed/calcified plaque in other coronary segments (OR=0.40 [95%CI=0.17-0.93]), but not among those with mixed/calcified plaque elsewhere in their arteries (OR=1.60 [95%CI=0.71-3.62]). Moreover, transition of non-calcified to mixed/calcified plaque associated with bDMARD exposure (OR=4.00 [95%CI=1.05-15.32]). bDMARD use also predicted low-attenuation plaque loss (p=0.042).Figure 1.Effect of bDMARD use on cardiovascular disease risk stratified by coronary plaque presenceFigure 2.Effect of bDMARD exposure on plaque formation and transition from baseline to follow-upConclusion:In rheumatoid arthritis, bDMARD use associated with reduced long-term CVD risk, lower likelihood of new plaque formation in patients with early atherosclerosis, stabilization of high-risk plaque and protective calcification of non-calcified lesions.Disclosure of Interests:George Karpouzas Grant/research support from: Pfizer, Consultant of: Sanofi-Genzyme-Regeneron, Janssen, Speakers bureau: Sanofi-Genzyme-Regeneron, BMS, Sarah Ormseth: None declared, Elizabeth Hernandez: None declared, Matthew Budoff: None declared

Abstract P040: GlycA, a Novel Inflammatory Marker, and Subclinical Coronary Atherosclerosis in the Multicenter AIDS Cohort Study (MACS)

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Oluwaseun E Fashanu ◽  
Martin Tibuakuu ◽  
Di Zhao ◽  
James D Otvos ◽  
Todd T Brown ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Coronary Atherosclerosis ◽  
Inflammatory Marker ◽  
Prevalence Ratio ◽  
Coronary Plaque ◽  
Plaque Burden ◽  
Cvd Risk ◽  
Cross Sectional ◽  
Calcified Plaque ◽  
Mixed Plaque

Background: Inflammation may link HIV infection to cardiovascular disease (CVD). GlycA, a novel nuclear magnetic resonance (NMR) biomarker of systemic inflammation, has been associated with incident CVD events in the general population. The relation between GlycA and the presence, extent and composition of subclinical coronary plaque in men with HIV infection (HIV+) or at risk for HIV (HIV-) is unknown. Methods: This is a cross-sectional analysis of 935 men enrolled in MACS with plasma measurement of GlycA and non-contrast cardiac CT and/or coronary CT angiography. We used multivariable adjusted Poisson and linear regression to assess associations of GlycA with prevalent coronary atherosclerosis and plaque extent, respectively. Results: Mean ± SD age was 54 ± 7 yrs; 31% were black, and 63% HIV+ with 81% having undetectable viral load (VL). GlycA levels were higher in HIV+ compared to HIV- men (397 ± 68 vs 380 ± 60 μmol/L, p=0.0001), and higher for those with detectable VL vs. undetectable (413 ± 79 vs 393 ± 65 μmol/L, p=0.004). After adjusting for demographic and CVD risk factors, every 1 SD increment in GlycA was associated with an increased prevalence of coronary artery calcium (CAC>0) (prevalence ratio: 1.09, 95% CI: 1.03-1.15), coronary stenosis ≥ 50% (1.20, 1.02-1.41), and calcified plaque (1.12, 1.02-1.23); p for all < 0.03. These associations remained significant after adjusting for other inflammatory markers and did not differ by HIV status. Among men with plaque, GlycA was positively associated with the extent of CAC, total plaque and mixed plaque ( Table ). Associations were weaker in HIV+ men for total and mixed plaque (P interaction = 0.003 and 0.03, respectively). GlycA was not associated with non-calcified plaque. Conclusion: HIV+ men have higher levels of GlycA than HIV- men. Higher GlycA is positively and independently associated with subclinical coronary atherosclerosis. Whether modification of GlycA through lifestyle or pharmacotherapy can reduce coronary plaque burden and future CVD events requires further study.

scholarly journals POS0215 DIRECT AND CONDITIONAL EFFECTS OF EPICARDIAL ADIPOSE TISSUE VOLUME ON CORONARY PLAQUE PROGRESSION IN RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 325.1-325
Author(s):  
G. Karpouzas ◽  
S. Ormseth ◽  
E. Hernandez ◽  
M. Budoff
Keyword(s):  
Risk Factors ◽  
Coronary Atherosclerosis ◽  
Coronary Plaque ◽  
Statin Treatment ◽  
Cardiac Risk ◽  
Plaque Formation ◽  
Cardiac Risk Factor ◽  
Cardiac Risk Factors ◽  
Calcified Plaque ◽  
Atherosclerosis Development

Background:Epicardial adipose tissue volume (EATv) predicts coronary atherosclerosis presence, progression and cardiovascular event risk in general patients1,2. Our group recently reported that EATv associated with greater subclinical coronary plaque burden, non-calcified plaque presence and vulnerable plaque characteristics in patients with rheumatoid arthritis (RA). The relationship was stronger in RA patients with lower disease duration, no traditional cardiac risk factors, and who were not obese.Objectives:To evaluate the predictive value of EATv on long-term coronary atherosclerosis development, and moderators of the association between EATv and plaque formation.Methods:This single-center observational cohort study included 100 patients without symptoms or diagnosis of cardiovascular disease who underwent computed tomography angiography for evaluation of EATv and coronary atherosclerosis at baseline and repeat assessments 6.9±0.3 years later to evaluate plaque progression. New plaque formation in segments without plaque at baseline was the main outcome. Robust multivariable logistic regression evaluated the effect of high versus low EATv (based on median) on likelihood of new plaque formation, accounting for clustering of segments within patients. Potential moderator effects of prespecified predictors were also assessed.Results:High EATv (>107 cm3) predicted new plaque formation in segments without baseline plaque (OR 2.77 [95% CI 1.43-5.37], p= 0.003); however, significance was lost in the multivariable model. Importantly, high EATv associated with formation of higher-risk non- and partially calcified plaque after adjusting for Framingham D’Agostino risk score, obesity, segment location, time-averaged CRP, duration of bDMARD and statin treatment and cumulative prednisone dose (adjusted OR 2.57 [95% CI 1.02-6.48], p= 0.045). RA duration (<10 versus >10 years), cardiac risk factor burden (≤1 versus >1), presence of mixed/calcified plaque in other coronary segments at baseline, and statin exposure (≤1 versus >1 year, based on median) moderated the effect of EATv on all new plaque formation (all p for interaction ≤ 0.021). Specifically, high EATv predicted new plaque formation in patients with RA duration <10 years (adjusted OR 5.75 [95% CI 1.77-18.67]), those with ≤1 cardiac risk factors (adjusted OR 3.40 [95% CI 1.46-7.90]), those without calcification at baseline (adjusted OR 2.65 [95% CI 1.11-6.31]) and those with statin treatment <1 year (adjusted OR 3.33 [95% CI 1.13-9.77]). This was not the case for patients with RA >10 years, ≥ 2 cardiac risk factors, calcification at baseline and statin treatment >1 year (figure 1).Conclusion:High baseline EATv independently predicted future higher-risk non-calcified and mixed coronary plaque in RA. Moreover, it conditionally promoted new plaque formation overall in patients with earlier disease, low cardiac risk factor burden, who had little or no atherosclerosis at baseline and who had limited exposure to statin therapy. These findings indicate the need for a larger prospective evaluation of the role of EATv as a biomarker of coronary atherosclerosis development in RA.References:[1]Hwang I-C et al. J Atheroscler Thromb 2017;24:262–74. 2. Ding J et al. Am J Clin Nutr 2009;90:499–504.Figure 1.Moderators of influence of EATv on new coronary plaque formationDisclosure of Interests:George Karpouzas Speakers bureau: Sanofi/ Genzyme/ Regeneron, Consultant of: Sanofi/ Genzyme/ Regeneron, Grant/research support from: Pfizer, Sarah Ormseth: None declared, Elizabeth Hernandez: None declared, Matthew Budoff Consultant of: Pfizer

scholarly journals Multi-trajectories of lipid indices with incident cardiovascular disease, heart failure, and all-cause mortality: 23 years follow-up of two US cohort studies

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Fatemeh Koohi ◽  
Davood Khalili ◽  
Mohammad Ali Mansournia ◽  
Farzad Hadaegh ◽  
Hamid Soori
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Cohort Studies ◽  
Significant Risk ◽  
Density Lipoprotein ◽  
Lipid Levels ◽  
Cvd Risk ◽  
All Cause Mortality ◽  
Over Time

Abstract Background Understanding the distinct patterns (trajectories) of variation in blood lipid levels before diagnosing cardiovascular disease (CVD) might carry important implications for improving disease prevention or treatment. Methods We investigated 14,373 participants (45.5% men) aged 45–84 from two large US prospective cohort studies with a median of 23 years follow-up. First, we jointly estimated developmental trajectories of lipid indices, including low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride (TG) concentrations using group-based multi-trajectory modeling. Then, the association of identified multi-trajectories with incident CVD, heart failure, and all-cause mortality were examined using Cox proportional hazard model. Results Seven distinct multi-trajectories were identified. The majority of participants (approximately 80%) exhibited decreasing LDL-C but rising TG levels and relatively stable HDL-C levels. Compared to the individuals with healthy and stable LDL-C, HDL-C, and TG levels, those in other groups were at significant risk of incident CVD after adjusting for other conventional risk factors. Individuals with the highest but decreasing LDL-C and borderline high and rising TG levels over time were at the highest risk than those in other groups with a 2.22-fold risk of CVD. Also, those with the highest and increased triglyceride levels over time, over optimal and decreasing LDL-C levels, and the lowest HDL-C profile had a nearly 1.84 times CVD risk. Even individuals in the multi-trajectory group with the highest HDL-C, optimal LDL-C, and optimal TG levels had a significant risk (HR, 1.45; 95% CI 1.02–2.08). Furthermore, only those with the highest HDL-C profile increased the risk of heart failure by 1.5-fold (95% CI 1.07–2.06). Conclusions The trajectories and risk of CVD identified in this study demonstrated that despite a decline in LDL-C over time, a significant amount of residual risk for CVD remains. These findings suggest the impact of the increasing trend of TG on CVD risk and emphasize the importance of assessing the lipid levels at each visit and undertaking potential interventions that lower triglyceride concentrations to reduce the residual risk of CVD, even among those with the optimal LDL-C level.

Abstract 2511: Impact of Olmesartan on Progression of Coronary Atherosclerosis; - A Serial Volumetric IVUS Analysis from the OLIVUS Trial -

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Atsushi Hirohata ◽  
Hirosuke Yamaji ◽  
Masaaki Murakami ◽  
Eiki Hirose ◽  
Keisuke Ohkawa ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Stable Angina ◽  
Coronary Atherosclerosis ◽  
Coronary Plaque ◽  
Stable Angina Pectoris ◽  
Plaque Volume ◽  
Receptor Blocking ◽  
Percent Change ◽  
Angiotension Ii

Prior intravascular ultrasound (IVUS) trials suggest slowing of coronary plaque progression with some medicines but have not shown convincing evidence of regression using angiotension-II receptor blocking agents (ARB). A prospective, double-blind, randomized, multicenter trial (Impact of OLmesartan on progression of coronary atherosclerosis; evaluation by IntraVascular UltraSound [OLIVUS]) was performed in 247 stable angina pectoris patients with native coronary artery lesions. When these patients underwent percutaneous coronary intervention for culprit lesions, IVUS was performed in their non-culprit vessels (without angiographically documented coronary stenosis [<50%]). Patients were randomly assigned to receive 20 mg of Olmesartan or control, and treated with a combination of β-blockers, calcium channel blockers, diuretics, nitrates, glycemic control agents and/or statins per physician’s guidance. Patients already on ACE inhibitors or other ARBs were excluded. Serial IVUS examinations (baseline and 14-months follow-up) were performed to assess coronary plaque volume. Volumetric IVUS analyses (mean measured length:41.2 ± 8.7mm) included lumen (LV), plaque (PV), vessel volume (VV), percent plaque volume (% PV), percent change in total PV (PCPV) and percent change in % PV (PC%PV). At baseline, patient characteristics and all IVUS parameters were identical between the two groups. However, follow-up IVUS showed significantly decreased PCPV and PC%PV in the Olmesartan group, despite similar blood pressure (table ). In addition, multivariate analysis identified Olmesartan administration as one of the factors that decreased plaque volume (β-coefficient −0.29 (95%CI, −0.7 to 0.4), p<0.01). These observations suggest a positive role in potential plaque regression through the administration of Olmesartan, an angiotension-II receptor blocking agent, for patients with stable angina pectoris.

scholarly journals Impaired high-density lipoprotein function in patients with heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.E Emmens ◽  
J Congzhuo ◽  
L.L Ng ◽  
A.A Voors ◽  
R.A De Boer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cholesterol Efflux ◽  
Density Lipoprotein ◽  
Funding Source ◽  
Antioxidative Capacity ◽  
Hdl Function ◽  
Hdl Functionality ◽  
Anti Inflammatory ◽  
Over Time

Abstract Background We recently showed that a lower high-density lipoprotein cholesterol (HDL-C) concentration was one of the strongest predictors of death or heart failure (HF) hospitalisation in patients with HF. In a follow-up study, we suggested that this association could be partly explained by HDL proteome composition. However, whether the emerging concept of HDL function contributes to prognosis of HF patients has not been addressed. Methods We measured three key HDL function metrics, namely cholesterol efflux, antioxidative capacity, and anti-inflammatory capacity, at baseline and after 9 months in 446 randomly selected HF patients from BIOSTAT-CHF. Additionally, the relationship between HDL functionality and HDL proteome composition was determined in 86 patients. Results From baseline to 9 months, HDL-C concentrations did not substantially change, but HDL-mediated cholesterol efflux and anti-inflammatory capacity had decreased (both P&lt;0.001). In contrast, antioxidative capacity improved during the 9 months follow-up (P&lt;0.001). Higher HDL-mediated cholesterol efflux was independently associated with lower risk of mortality after adjustment for BIOSTAT risk models and log HDL-C (HR=0.81 [95% CI: 0.71–0.92], P=0.001). Other functionality parameters were not associated with outcome. Several HDL proteins correlated with HDL functionality, mainly with cholesterol efflux, and apolipoprotein A1 emerged as the main protein associated with all three functionality parameters. Conclusions HDL-mediated cholesterol efflux and anti-inflammatory capacity significantly decreased over time in patients with HF. Better baseline cholesterol efflux was prospectively associated with reduced mortality during follow-up independent of HDL-C. Combined these data indicate that HDL function measurements have the potential to provide clinical information beyond static HDL-C concentrations in HF patients. Changes in HDL functionality over time Funding Acknowledgement Type of funding source: Public grant(s) – EU funding. Main funding source(s): European Commission

scholarly journals Metabolically healthy obesity: predictors of transformation to unhealthy phenotype in St Petersburg population (according to the ESSE-RF study)

2021 ◽  
Vol 27 (3) ◽  
pp. 279-290
Author(s):  
M. A. Boyarinova ◽  
O. P. Rotar ◽  
A. M. Erina ◽  
N. A. Paskar ◽  
A. S. Alieva ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Uric Acid ◽  
Waist Circumference ◽  
Low Density Lipoprotein ◽  
Fasting Blood Glucose ◽  
Density Lipoprotein ◽  
Metabolically Healthy Obesity ◽  
Metabolically Healthy ◽  
Over Time

Objective. The purpose of the study was to determine the dynamics of the metabolically healthy obesity (MHO) status according to the Meigs criteria, and to establish the predictors of the transformation of healthy obesity phenotype into an unhealthy (MUHO) one in the population of residents of St Petersburg (Russia) at 6,5-year follow-up. Design and methods. Within the epidemiology study ESSE-RF a random sample of 1600 St Petersburg inhabitants stratified according to gender and age was formed. Examination of participants included anthropometry with measurement of waist circumference and calculation of body mass index (BMI), measurement of blood pressure (BP), fasting blood glucose, insulin (index of insulin resistance was calculated), creatinine, cortisol, lipid spectrum, C-reactive protein, adiponectin, leptin, and uric acid. Meigs MHO criteria (2006) were used in obese subjects (BMI > 30 kg/m²). Obese patients, who were identified as metabolically healthy in 2012–2013, were invited for follow-up in 2018–2019. Results. At the first stage obesity was diagnosed in 430 (26,9 %) participants, according to the BMI, 116 (27,0 %) of them were metabolically healthy according to the Meigs criteria. At follow-up, 44,4% individuals with the MHO phenotype transformed to the MUHO category on average after 6,5 years. Individuals who retained the MHO phenotype over time had significantly lower baseline systolic BP and diastolic BP levels, more favorable lipid levels and lower levels of uric acid, insulin, and index of insulin resistance. Glucose increase by every 0,5 mmol/l and higher was associated with elevated probability of transformation MHO to MUHO phenotype by 10,9 times (adjusted for sex and age). Conclusions. Significantly higher levels of BP, insulin resistance, low density lipoprotein and uric acid at baseline, as well as an increase in glucose levels over time, were associated with the transformation of the metabolically healthy to the unhealthy phenotype in obese individuals at 6,5-year follow-up. In all individuals with the MHO phenotype, there was a significant increase in waist circumference over time, accompanied by an increase in BMI only in those who transformed into the MUHO status.

scholarly journals Usefulness of MCP-1 Chemokine in the Monitoring of Patients with Coronary Artery Disease Subjected to Intensive Dietary Intervention: A Pilot Study

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3047
Author(s):  
Magdalena Makarewicz-Wujec ◽  
Jan Henzel ◽  
Cezary Kępka ◽  
Mariusz Kruk ◽  
Łukasz Wardziak ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Dietary Intervention ◽  
Coronary Plaque ◽  
Control Group ◽  
Dash Diet ◽  
Plaque Component ◽  
Calcified Plaque ◽  
Atheroma Volume ◽  
Artery Disease

Monocyte chemotactic protein-1 (MCP-1) plays an important role in the entire atherosclerotic process, from atherogenesis to destabilisation of the atherosclerotic plaque. The purpose of this study is to evaluate the effect of the dietary approaches to stop hypertension (DASH) diet in patients with coronary artery disease on the MCP-1 plasma concentration and to evaluate the potential usefulness of this chemokine as a marker of change in the volume and composition of coronary plaque. Material and method. As part of the dietary intervention to stop coronary atherosclerosis in computed tomography (DISCO-CT) study, patients were randomised to an intervention group (n = 40) in which the DASH diet was introduced, and to a control group (n = 39) with no dietary intervention. In the DASH group, dietary counselling was provided at all follow-up visits within 12 months of the follow-up period. MCP-1 plasma concentration was determined using enzyme-linked immunosorbent assay (ELISA). Coronary plaque analysis was performed using a semi-automated plaque analysis software system (QAngioCT, Medis, the Netherlands). Results. In the DASH group, MCP-1 plasma concentration significantly decreased by 34.1 pg/mL (p = 0.01), while in the control group, the change in MPC-1 was not significant. Significant inverse correlations were revealed for the change in MCP-1 plasma concentration and change in the consumption of vitamin C and dietary fibre both in the DASH (r = −0.519, p = 0.0005; r = −0.353, p = 0.025, respectively) and in the control group (r = −0.488 p = 0.001; r = −0.502, p = 0.001, respectively). In patients with the highest decrease in percent atheroma volume (PAV), a significant positive correlation was observed between the change in MCP-1 plasma concentration and changes in PAV (r = 0.428, p = 0.033) and calcified plaque component (r = 0.468, p = 0.018), while the change in noncalcified plaque component correlated inversely with change in MCP1 (r = −0.459, p = 0.021). Conclusion. Dietary intervention based on the DASH diet model reduces the MCP-1plasma concentration, mostly due to an increased intake of plant-derived, fibre-rich foods and antioxidants. The change in MCP-1 plasma concentration seems to reflect changes in the atheroma volume and proportions between the calcified and non-calcified plaque elements.

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