Subclinical Carotid Atherosclerosis Research Articles

Comprehensive metabolomics profiling reveals common metabolic alterations underlying the four major non-communicable diseases in treated HIV infection.

BackgroundHIV infection and normal aging share immune and inflammatory changes that result in premature aging and non-communicable diseases (NCDs), but the exact pathophysiology is not yet uncovered. We identified the common metabolic pathways underlying various NCDs in treated HIV infection.MethodsWe performed untargeted metabolomics including 87 HIV-negative (–) normal controls (NCs), 87 HIV-positive (+) NCs, and 148 HIV+ subjects with only one type of NCDs, namely, subclinical carotid atherosclerosis, neurocognitive impairment (NCI), liver fibrosis (LF) and renal impairment. All HIV+ subjects were virally suppressed.ResultsHIV+ patients presented widespread alterations in cellular metabolism compared to HIV– NCs. Glycerophospholipid (GPL) metabolism was the only one disturbed pathway presented in comparisons including HIV– NCs across age groups, HIV+ NCs across age groups, HIV+ NCs vs HIV– NCs and each of HIV+ NCDs vs HIV+ NCs. D-glutamine and D-glutamate metabolism and alanine-aspartate-glutamate metabolism were presented in comparisons between HIV+ NCs vs HIV– NCs, HIV+ LF or HIV+ NCI vs HIV+ NCs. Consistently, subsequent analysis identified a metabolomic fingerprint specific for HIV+ NCDs, containing 42 metabolites whose relative abundance showed either an upward (mainly GPL-derived lipid mediators) or a downward trend (mainly plasmalogen phosphatidylcholines, plasmalogen phosphatidylethanolamines, and glutamine) from HIV– NCs to HIV+ NCs and then HIV+ NCDs, reflecting a trend of increased oxidative stress.InterpretationGPL metabolism emerges as the common metabolic disturbance linking HIV to NCDs, followed by glutamine and glutamate metabolism. Together, our data point to the aforementioned metabolisms and related metabolites as potential key targets in studying pathophysiology of NCDs in HIV infection and developing therapeutic interventions.FundingChina National Science and Technology Major Projects on Infectious Diseases, National Natural Science Foundation of China, Yi-wu Institute of Fudan University, and Shanghai Municipal Health and Family Planning Commission.

Naïve hepatitis B e antigen-negative chronic hepatitis B patients are at risk of carotid atherosclerosis: A prospective study.

BACKGROUNDThere is an increased risk of atherosclerosis in patients with chronic hepatitis C or human immunodeficiency virus, but there is scarce data on hepatitis B virus infection. The hypothesis of this study is that hepatitis B virus infection increases the risk of carotid plaques and subclinical atherosclerosis in naïve hepatitis B e antigen (HBeAg) negative subjects.AIMTo assess the rate of carotid plaques and subclinical atherosclerosis in naïve HBeAg negative subjects in comparison with a cohort of healthy controls.METHODSProspective case-control collaborative study conducted in two tertiary hospitals. Four hundred and two subjects prospectively recruited at the outpatient clinic were included from May 2016 to April 2017: 201 naïve HBeAg-negative hepatitis B virus-infected [49 chronic hepatitis B (CHB) and 152 inactive carriers(ICs)] and 201 healthy controls. Anthropomorphic and metabolic measures, liver stiffness and carotid Doppler ultrasound were performed. Subclinical atherosclerosis was established on an intima-media thickness increase of ≥1.2 mm and/or the presence of carotid plaques. Normally distributed quantitative variables were compared with the Student t test and those with a non-normal distribution with the Mann-Whitney U test. Categorical variables were compared between groups using the χ2 or Fisher exact test.RESULTSCarotid plaques were found more often in CHB (32.7%) than ICs (17.1%) or controls (18.4%) (P = 0.048). Subclinical atherosclerosis was also increased in CHB (40.8%) vsICs (19.1%) or controls (19.4%) (P = 0.003). No differences in the risk of atherosclerosis were observed between controls and ICs. The factors independently associated with the presence of carotid plaques were age [odds ratio(OR) 1.43, P < 0.001] and CHB (OR 1.18, P = 0.004) and for subclinical atherosclerosis, age (OR 1.45, P < 0.001), CHB (OR 1.23, P < 0.001) and diabetes (OR 1.13, P = 0.028). In the subset of young subjects (< 50 years), carotid plaques (12.5% vs 1.1%, P = 0.027) and subclinical atherosclerosis (12.5% vs 2.2%, P = 0.058) were more frequent among CHB than ICs.CONCLUSIONUntreated HBeAg-negative CHB is an independent risk factor for carotid plaques and subclinical atherosclerosis, while ICs present a similar risk to controls.

Association between dietary inflammatory index and subclinical carotid atherosclerosis in the general population.

Background and Aims: The association between unhealthy dietary habits and Cardiovascular Diseases (CVDs) has been majorly attributed to the metabolic effects of saturated fats, carbohydrates, and sugars intake. However, macro-and micro-nutrients exert anti-or pro-inflammatory effects beyond their metabolic impact, and whether the balance between their intakes associates with Subclinical Carotid Atherosclerosis (SCA) is an intriguing aspect to be verified.

Changes in gut microbiota and high sensitivity C-reactive protein levels in hypertensive subjects with obesity and subclinical carotid atherosclerosis

Background and Aims: Changes in the composition of the gut microbiota are identified as contributing factors in the development of atherosclerosis and cardiometabolic disease. We aimed to study the content of the main phylotypes of the gut microbiota (GM) and high sensitivity C-reactive protein (hsCRP) levels in patients with arterial hypertension (AH) and abdominal obesity (AO) and previously diagnosed subclinical carotid atherosclerosis (SCA).

Cardiovascular immune-inflammatory markers and cellular aging in the general population

Background and Aims: Leucocyte Telomere Length (LTL) is an index of cellular aging. LTL shortening (TS) physiologically occurs over time but faster TS has been still linked to increased risk of atherosclerosis, even during its subclinical stages. We recently identified a set of proteomic circulating immune-inflammatory markers predicting the progression of Subclinical Carotid Atherosclerosis (SCA), beyond classical risk factors (CVRFs). Is TS over time predicted by markers of systemic low-grade inflammation predisposing to SCA?

Lipoprotein(a) as a biomarker for subclinical coronary and carotid atherosclerosis in asymptomatic patients

Background and Aims: The association between lipoprotein(a) (Lp(a)) and subclinical atherosclerosis measured by CT coronary artery calcium score (CAC) and carotid doppler (CD) in asymptomatic individuals remains unclear. In preliminary studies, our group has previously identified an association between Lp(a) and CAC within Caucasians, but not other ethnicities. Our aim was to evaluate the influence of Lp(a) on CAC and CD in asymptomatic patients in a multi-ethnic tertiary clinic.

The association of air pollutants exposure with subclinical inflammation and carotid atherosclerosis

BackgroundAir pollution is a well-described environmental factor with evidence suggesting a firm association with cardiovascular diseases. The purpose of this study was to determine the association of exposure to gaseous air pollutants on atherosclerosis burden. Methods1955 inhabitants of the Corinthia region, aged 40 years or older, underwent clinical and biochemical assessment as well as carotid ultrasonography to evaluate carotid intima-media thickness (cIMT) and plaque burden. Analyzers recording time series concentration of CO, NO2, and SO2 were located at 4 different open sites (Regions 1, 2, 3 and 4) based on their proximity to industries, highways or shipyards. ResultsA higher concentration of CO, NO2, and SO2 was observed in Region 4 compared to the other regions. Mean cIMT (Region 1: 0.93 ± 0.24 mm; Region 2: 0.96 ± 0.40 mm; Region 3: 0.94 ± 0.39 mm; Region 4: 1.14 ± 0.55 mm, p < 0.001), maximum cIMT (p < 0.001) as well as carotid plaque burden (Region 1: 13.3%; Region 2: 18.8%; Region 3: 22.4%; Region 4: 38.6%, p < 0.001) were significantly higher in individuals of Region 4. Inhabitants of Region 4 had also higher levels of C reactive protein (Region 1: 4.56 ± 4.85 mg/l; Region 2: 3.49 ± 4.46 mg/l; Region 3: 4.03 ± 3.32 mg/l, Region 4: 5.16 ± 8.26 mg/l, p < 0.001). Propensity score analysis revealed higher inter-area differences in mean cIMT of individuals with coronary artery disease (CAD) (high vs low air pollution area: 1.56 ± 0.80 mm; vs. 1.18 ± 0.54 mm, p < 0.001) while there was no difference in cIMT of the matched population without CAD (p = 0.52). ConclusionsAn increased carotid atherosclerotic and inflammatory burden is observed in inhabitants of areas with the highest concentration of air pollutants.

Relationship between Circulating PCSK9 and Markers of Subclinical Atherosclerosis—The IMPROVE Study

(1) Background and purpose: circulating proprotein convertase subtilisin/kexin type 9 (PCSK9) is one of the key regulators of cholesterol metabolism. Despite this, its role as a player in atherosclerosis development is still matter of debate. Here, we investigated the relationships between this protein and several markers of subclinical atherosclerosis. (2) Methods: the IMPROVE study enrolled 3703 European subjects (54–79 years; 48% men; with ≥3 vascular risk factors), asymptomatic for cardiovascular diseases. PCSK9 levels were measured by ELISA. B-mode ultrasound was used to measure markers of carotid subclinical atherosclerosis. (3) Results: in the crude analysis, PCSK9 levels were associated with several baseline measures of carotid intima-media thickness (cIMT) (all p < 0.0001); with cIMT change over time (Fastest-IMTmax-progr) (p = 0.01); with inter-adventitia common carotid artery diameter (ICCAD) (p < 0.0001); and with the echolucency (Grey Scale Median; GSM) of both carotid plaque and plaque-free common carotid IMT (both p < 0.0001). However, after adjustment for age, sex, latitude, and pharmacological treatment, all the afore-mentioned correlations were no longer statistically significant. The lack of correlation was also observed after stratification for sex, latitude, and pharmacological treatments. (4) Conclusions: in subjects who are asymptomatic for cardiovascular diseases, PCSK9 plasma levels do not correlate with vascular damage and/or subclinical atherosclerosis of extracranial carotid arteries.

QRISK3 relation to carotid plaque is higer than that of score in patients with systemic lupus erythematosus

SLE has been described as an independent risk factor for the development of cardiovascular (CV) disease. Recently, the QRESEARCH risk estimator version 3 (QRISK3) calculator has been launched for CV risk assessment in the general population. QRISK3 now includes the presence of SLE as one of its variables for calculating CV risk. Our objective was to compare the predictive capacity between QRISK3 and the Systematic Coronary Risk Evaluation (SCORE) for the presence of subclinical carotid atherosclerosis in patients with SLE. Two hundred and ninety-six patients with SLE were recruited. The presence of subclinical atherosclerosis was evaluated by carotid ultrasound to identify carotid plaque and the thickness of the carotid intima-media (cIMT). QRISK3 and SCORE were calculated. The relationship of QRISK3 and SCORE with each other and with the presence of subclinical carotid atherosclerosis (both carotid plaque and cIMT) was studied. There was no correlation between SCORE and QRISK3 in patients with SLE (Spearman's rho = -0.008, P = 0.90). Although QRISK3 showed a statistically significant correlation with cIMT (Spearman's rho = 0.420, P = 0.000), this relationship was not found between SCORE and cIMT (Spearman's rho = -0.005, P = 0.93). The discrimination capacity of QRISK3 for the presence of carotid plaque was statistically significant and superior to that of SCORE (AUC 0.765 [95% CI: 0.711, 0.820] vs 0.561 [95% CI: 0.494, 0.629], P = 0.000). QRISK3 discrimination for subclinical atherosclerosis is higher than that of SCORE. QRISK3, and not SCORE, should be used for the calculation of CV risk in patients with SLE.

A Nomogram for Identifying Subclinical Atherosclerosis in Chronic Kidney Disease.

PurposeAtherosclerosis contributes substantially to cardiovascular mortality in patients with chronic kidney disease (CKD). But precise risk model for subclinical atherosclerosis in the CKD population is still lacking. The study aimed to develop and validate a nomogram for screening subclinical atherosclerosis among CKD patients without dialysis.Patients and MethodsA total of 1452 CKD stage 1‒5 has been recruited in this cross-sectional study. Subclinical atherosclerosis was diagnosed with carotid ultrasonography. Patients were divided into the training set and validation set. The risk factors of atherosclerosis were identified by the training set and confirmed by the validation set. The receiver operating characteristic (ROC) curves and decision curve analyses (DCA) were executed to evaluate the accuracy of fitted logistic models in training and validation sets. Finally, a nomogram based on constructed logistic regression model in all participants was plotted.ResultsA total of 669 (46.1%) patients were diagnosed with subclinical carotid atherosclerosis. Binary logistic regression analysis showed that males, age, hypertension, diabetes, CKD stages, calcium, platelet, and albumin were risk factors for atherosclerosis. The accuracy of fitted logistic models was evaluated by the area under the ROC curve (AUC), which showed good predictive accuracy in the training set (AUC=0.764 (95% Confidence interval (CI): 0.733–0.794) and validation set (AUC=0.808 (95% CI: 0.765–0.852). A high net benefit was also proven by the DCA. Finally, these predictors were all included to generate the nomogram.ConclusionThis proposed nomogram shows excellent predictive ability and might have a significant clinical implication for detecting subclinical atherosclerosis in patients with CKD.

Brief Report: Subclinical Carotid Artery Atherosclerosis Is Associated With Increased Expression of Peripheral Blood IL-32 Isoforms Among Women Living With HIV.

Persistent inflammation in HIV infection is associated with elevated cardiovascular disease (CVD) risk, even with viral suppression. Identification of novel surrogate biomarkers can enhance CVD risk stratification and suggest novel therapies. We investigated the potential of interleukin 32 (IL-32), a proinflammatory multi-isoform cytokine, as a biomarker for subclinical carotid artery atherosclerosis in virologically suppressed women living with HIV (WLWH). Nested within the Women's Interagency HIV Study, we conducted a cross-sectional comparison of IL-32 between 399 WLWH and 100 women without HIV, followed by a case-control study of 72 WLWH (36 carotid artery plaque cases vs. 36 age-matched controls without plaque). Plasma IL-32 protein was measured by ELISA, and mRNA of IL-32 isoforms (IL-32α, β, γ, D, ε, and θ) was quantified by reverse transcription polymerase chain reaction from peripheral blood mononuclear cells. Plasma IL-32 protein levels were higher in WLWH compared with women without HIV (P = 0.02). Among WLWH, although plasma IL-32 levels did not differ significantly between plaque cases and controls, expression of IL-32 isoforms α, β, and ε mRNA was significantly higher in peripheral blood mononuclear cells from cases (P = 0.01, P = 0.005, and P = 0.018, respectively). Upregulation of IL-32β and IL-32ε among WLWH with carotid artery plaque persisted after adjustment for age, race/ethnicity, smoking, systolic blood pressure, body mass index, and history of hepatitis C virus (P = 0.04 and P = 0.045); the adjusted association for IL-32α was marginally significant (P = 0.07). IL-32 isoforms should be studied further as potential CVD biomarkers. This is of particular interest in WLWH by virtue of altered IL-32 levels in this population.

Toe-brachial index is beyond a peripheral issue in patients with type 2 diabetes.

BackgroundAtherosclerosis is the leading cause of death in patients with diabetes. We aimed to evaluate the association between ankle-brachial index (ABI) and toe-brachial index (TBI) with carotid intima-media thickness (CIMT) in patients with type 2 diabetes (T2DM).MethodsThis cross sectional study included 296 patients with T2DM who met the American Diabetes Association criteria for the assessment of peripheral arterial atherosclerosis. The ABI ≤ 0.9 and TBI ≤ 0.7 were considered as abnormal values. Linear and logistic regression analyses were performed to evaluate the association between TBI/ABI and CIMT.ResultsRight CIMT was significantly greater in the low TBI group (p = 0.03) while, left CIMT did not show a significant difference. Each 0.1-unit decrease in TBI value was independently associated with 0.017 mm increase in the right CIMT (β ± SE; -0.017 ± 0.005, p = 0.002) and with odds of the presence of increased CIMT [odds ratio and 95% confidence interval: 1.21 (1.02, 1.44)] after adjustment with all traditional risk factors. There was not any significant association between ABI and increased CIMT.ConclusionsBeyond a suitable tool for the diagnosis of peripheral artery disease in patients with T2DM, TBI can be applied for prediction of subclinical carotid atherosclerosis.

Assessment of Carotid Artery Distensibility and Elasticity in Patients with Asthma.

As asthma and atherosclerosis have similar pathophysiological mechanisms and risk factors, asthmatic patients may have an increased risk of atherosclerosis. This study aimed to determine the possibility of a higher risk of atherosclerosis in asthma patients compared with healthy controls by measuring carotid elasticity and distensibility. This was a cross-sectional study on 326 participants including 221 patients (129 [58.37%] females) with persistent asthma, aged 46.47±11.58 years, body mass index (BMI) of 29.74±3.99, and 105 healthy control subjects (60 [57.14%] females) aged 46.08±11.35 years, and BMI of 29.42±3.76. Of the 221 patients with asthma, 75 (33.93%) had mild, 74 (33.48%) had moderate and 72 (32.57%) had severe asthma. The carotid distensibility and elasticity were recorded and compared in both patients and control groups. There was no statistically significant difference between the patients and healthy control groups in terms of age, BMI and gender (p=0.775, p=0.482, and p=0.834, respectively). A statistically significant difference was determined between the patient and control groups in respect of both distensibility and elasticity (10.93±1.64 vs. 11.5±1.31, p=0.002 and 0.21±0.03 vs. 0.22±0.04, p=0.001, respectively). Statistically significant differences were determined between the control group and the asthma subgroups in respect of distensibility and elasticity (p<0.001, for both comparisons). The results showed that the difference was mainly due to the patients with severe asthma. Carotid distensibility and elasticity were decreased in asthmatic patients, and the main reason for this decrease was the patients in the severe asthma group. These results may suggest that the risk of subclinical carotid atherosclerosis is increased in patients with asthma, especially those with severe asthma.

Dapagliflozin increases the lean-to total mass ratio in type 2 diabetes mellitus

We compared the effect of dapagliflozin versus glibenclamide on the ratio of lean-to total mass in patients with type 2 diabetes mellitus, carotid subclinical atherosclerosis, HbA1c 7.0–9.0% and 40–70 years-old. Ninety-eight patients (61% male; mean age 57 ± 7 years) were randomized into dapagliflozin 10 mg/day or glibenclamide 5 mg/day on top of metformin. Body composition was measured by Dual Energy X-Ray at randomization and after 12 weeks of treatment. Glycemic control was equivalent in both groups. Dapagliflozin decreased total body mass (−2741 g [95% CI: −3360 to 1945]; p < 0.001) and lean mass (−347 g [95% CI: −761 to −106]; p < 0.001), while glibenclamide increased total body mass (1060 g [95% CI: 140 to 1836]; p < 0.001) and lean mass (929 g [95% CI: 575 to 1283]; p < 0.001) for the differences between arms. The lean-to-total mass ratio increased by 1.2% in the dapagliflozin group and 0,018% in the glibenclamide group (p < 0.001). Dapagliflozin reduced the risk of a negative balance in the lean-to total mass ratio [OR: 0.16 (95% CI: 0.05 to 0.45); p < 0.001] even after adjustment for baseline lean-to total mass ratio, waist circumference, HOMAIR, HbA1c, mean of the two hands handgrip strength and gait speed [OR: 0.13 (95% CI: 0.03–0.57); p < 0.007]. In conclusion, under equivalent glycemic control, dapagliflozin reduced total body mass but increased the ratio of lean-to-total mass when compared with glibenclamide.

Dietary nitrate prevents progression of carotid subclinical atherosclerosis through blood pressure-independent mechanisms in patients with or at risk of type 2 diabetes mellitus.

To test if 6months' intervention with dietary nitrate and spironolactone could affect carotid subclinical atherosclerosis and stiffness, respectively, vs. placebo/doxazosin, to control for blood pressure (BP). A subgroup of participants in our double-blind, randomized-controlled, factorial VaSera trial had carotid imaging. Patients with hypertension and with/at risk of type 2 diabetes were randomized to active nitrate-containing beetroot juice or placebo nitrate-depleted juice, and spironolactone or doxazosin. Vascular ultrasound for carotid diameter (CD, mm) and intima-media thickness (CIMT, mm) was performed at baseline, 3- and 6-months. Carotid local stiffness (CS, m/s) was estimated from aortic pulse pressure (Arteriograph) and carotid lumen area. Data were analysed by modified intention to treat and using mixed-model effect, adjusted for confounders. In total, 93 subjects had a baseline evaluation and 86% had follow-up data. No statistical interactions occurred between the juice and drug arms and BP was similar between the juices and between the drugs. Nitrate-containing vs. placebo juice significantly lowered CIMT (-0.06 [95% confidence interval -0.12, -0.01],P = .034), an overall difference of ~8% relative to baseline; but had no effect on CD or CS. Doxazosin appeared to reduce CS from baseline (-0.34 [-0.62, -0.06]) however, no difference was detected vs. spironolactone (-0.15 [-0.46, 0.16]). No differences were detected between spironolactone or doxazosin on CIMT and CD. Our results show that 6months' intervention with dietary nitrate influences vascular remodelling, but not carotid stiffness or diameter. Neither spironolactone nor doxazosin had a BP-independent effect on carotid structure and function.

The beneficial effect over 3 years by pictorial information to patients and their physician about subclinical atherosclerosis and cardiovascular risk: Results from the VIPVIZA randomized clinical trial

ObjectiveNon-adherence to guidelines and preventive measures is a major challenge, particularly so to obtain long-term adherence to lifestyle changes and recommended medication. The objective was to investigate if pictorial information regarding subclinical carotid atherosclerosis provided to individuals and physicians gave sustained effects on cardiovascular risk beyond the previously reported effect after 1 year and up to 3 years. MethodsA Prospective Randomized Open Blinded End-point (PROBE) trial. Within a CVD prevention program in Västerbotten County, Sweden, 3532 healthy individuals aged 40, 50 or 60 years were enrolled and 1:1 randomized to intervention (n = 1749; pictorial information with additional prevention materials to participants and physicians) or control group (n = 1783; no pictorial information to participants and physicians). Preventive measures were managed within primary care. Participants were investigated at baseline during 2013–2016 and at follow-up after 1 and 3 years. ResultsA beneficial effect on cardiovascular risk was observed at 3-year follow-up; Framingham Risk Score (FRS) was 13.38 for the intervention group and 14.08 for the control group (p = 0.047) and SCORE was 1.69 vs. 1.82 (p = 0.022). The effect observed at 1-year was sustained over 3 years after adjustment for sex and education and more pronounced among participants with a severe atherosclerotic picture at baseline. ConclusionsThis study provides evidence of sustained beneficial effects on the adherence to prevention guidelines over 3 years of pictorial information about subclinical carotid atherosclerosis, resulting in lower cardiovascular risk regardless of sex and educational level. Direct visualization of the underlying still subclinical atherosclerotic disease, rather than just indirect information about risk factors and statistical risk of future myocardial infarction, stroke and death, is one way to tackle the problem of non-adherence to prevention of cardiovascular diseases.

POS0728 QRISK3 RELATION TO CAROTID PLAQUE IS HIGHER THAN THAT OF SCORE IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

Background:Systemic lupus erythematosus (SLE) has been described as an independent risk factor for the development of cardiovascular (CV) disease. Recently, QRESEARCH risk estimator version 3 (QRISK3) calculator has been released for the assessment of CV risk in general population. QRISK3 now includes the presence of SLE as one of its variables for the calculation of CV risk.Objectives:We aim to compare, in patients with SLE, the predictive capacity between QRISK3 and Systematic COronary Risk Evaluation (SCORE) for the presence of carotid subclinical atherosclerosis.Methods:296 patients with SLE were recruited. The presence of carotid plaque and carotid intima media thickness (cIMT) were assessed through ultrasound. QRISK3 and SCORE were calculated. The relation of QRISK3 and SCORE between themselves and to the presence of carotid subclinical atherosclerosis (both carotid plaque and cIMT) was studied.Results:Most of the patients were female (95%) and average age was 51 ± 12 years. Traditional cardiovascular risk factors were prevalent, as shown in table 1. Most SLE patients were in the no activity (41%) or mild activity (29%) categories as shown by the SLEDAI scores. SLICC and Katz indexes were, respectively, 1 (IQR 0-2) and 2 (IQR 1-4). Seventy-one percent of the patients had a SLICC/ACR DI score equal to or higher than 1, and 39% had a Katz index equal to or higher than 3. Almost half of the patients (47%) were taking prednisone (the median dose of those 139 patients on prednisone was 5 [IQR 2.5-5] mg/day at the time of the study). DMARDs use was reported in 77% of the patients and 69% were taking hydroxychloroquine at the time the study was performed. SCORE and QRISK3 did not correlate between them in patients with SLE. In this sense, QRISK3, both calculated including the SLE item (Rho Spearman r=-0.008, p=0.90) or not (Rho Spearman r=-0.009, p=0.96), did not correlate with SCORE. This lack of correlation was also found when the corresponding categorizations of both scores were used. For example, patients with a QRISK&gt; = 10 did not show a higher SCORE when compared to patients with a QRISK3 &lt;10 (1.26 vs. 1.30, p=0.90). Similarly, QRISK3 was not different between the low, moderate, high and very-high SCORE CV risk categories.Relation of QRISK3 and SCORE to cIMT and to the presence of carotid plaque is shown in Figure 1. QRISK3 was statistically significantly correlated with cIMT (Rho Spearman r=-0.420, p=0.000). However, this relation was not found between SCORE and cIMT (Rho Spearman r=-0.005, p=0.93). Moreover, QRISK3 showed a statistically significant discrimination for the presence of carotid plaque (AUC 0.765 (95%CI 0.711-0.820). This relation was found to be significant both when QRISK3 was calculated with the SLE variable item or not. However, in patients with SLE, SCORE did not show a significant discrimination for the presence of carotid plaque (0.561 (95%CI 0.494-0.629). Additionally, a statistical significant difference was observed between the AUC of QRISK3 and SCORE (p=0.000).Table 1.Characteristics of SLE patientsSLE patients(n=296) Age, years51 ± 12 Female, n (%)280 (95) Body mass index, kg/m227 ± 6 Systolic blood pressure, mmHg127 ± 19Cardiovascular co-morbidity Smoking, n (%)74 (25) Diabetes, n (%)14 (5) Hypertension, n (%)119 (40) Dyslipidemia, n (%)115 (39)Analytical and lipid profile CRP, mg/dl1.9 (0.9-4.9) Cholesterol, mg/dl198 ± 38 LDL cholesterol, mg/dl110 ± 29SLE related dataDisease duration, years17 (10-25)SLICC1 (0-2)SLEDAI2 (0-4)Current prednisone, n (%)139 (47)Hydroxychloroquine, n (%)205 (69)Subclinical atherosclerosisCarotid IMT, microns630 ± 122Carotid plaques, n (%)108 (36)Figure 1.Relation of QRISK3 and SCORE to cIMT and carotid plaque.Conclusion:QRISK3 discrimination for carotid plaque is higher than that of the SCORE. QRISK3, and not SCORE, should be use for the calculation of CV risk in patients with SLE.Disclosure of Interests:None declared

Pictorial information about subclinical atherosclerosis reduces the CVD risk: Results from the VIPVIZA RCT

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): Region Västerbotten and the Swedish Research Council Background The VIPVIZA trial has previously shown beneficial effects on cardiovascular disease (CVD) risk scores 1 year after sending pictorial information of carotid ultrasound imaging (Picture 1) to individuals and their physicians Purpose To investigate whether the beneficial effects on CVD-risk observed at 1-year were sustained over three years Methods VIPVIZA is a pragmatic prospective open-label randomized controlled trial with blinded evaluators performed within a CVD prevention programme integrated in the regular primary health care in Västerbotten County, Sweden. Individuals aged 40, 50 or 60 years old with one CVD risk factor were enrolled and randomised 1:1 to intervention (n = 1749, pictorial information about subclinical atherosclerosis provided to participants and physicians, Picture 1) or control group(n = 1783, no information to participants or physicians). Intervention participants also recieved a follow-up phone call and the corresponding physicians written guideline-based information about the clinical significance of carotid ultrasound results. Participants were examined at baseline (2013-2016), after one and at three years Results A significant beneficial effect on cardiovascular risk was observed at the 3-year follow-up; Framingham Risk Score (FRS) was 13.38 for the intervention group and 14.08 for the control group(p = 0.047) and SCORE was 1.69 vs. 1.82(p = 0.022) respectively. The 3-year results adjusted for sex and educational level showed significant differences between the intervention and control group in FRS, SCORE, P-Total-Cholesterol, P-LDL-Cholesterol and waist circumference in favour of the intervention group. Analysis by sex showed difference in differences(DID) in FRS for men -1.19(95% CI -2.01 to -0.37) and -0.50(95% CI -0.93 to -0.07) for women and in SCORE for men -0.20(95% CI -0.33 to -0.06) and -0.08 (95% CI -0.13 to -0.04) for women, between the two groups over 3 years. Similarly, there were significant differences in DID in all educational groups. Further stratification by baseline FRS and SCORE risk category, showed a beneficial pattern of the intervention in all risk groups, however the DID at the 3-year follow-up was statistically significant only in the intermediate risk group for both FRS -1.34(95% CI -2.13 to -0.56) and SCORE -0.19(95% CI -0.32 to -0.05) Conclusions This study provides evidence of sustained effects over three years of pictorial information of subclinical carotid atherosclerosis on the reduction of cardiovascular risk regardless of sex and educational level. Importantly, a statistically significant intervention effect was seen in the intermediate risk group, where the majority of CVD events occur. Visualization of subclinical atherosclerosis may be one way to approach individuals at intermediate risk of CVD, a group where sufficient prevention is often overlooked. However, further studies are needed to investigate the intervention effect on hard end points as CVD-events and death. Abstract Figure. Picture 1

Assessment of Subclinical Carotid Atherosclerosis in Patients with Chronic Obstructive Pulmonary Disease

Background: Elevated coronary morbidity and mortality of patients with chronic obstructive pulmonary diseases (COPD). Common intimate-media thickening (CCA-IMT) and carotid plaques are replacement markers of atherosclerosis and predictors of CV cases. Purpose and objectives: The present research aimed at assessing and evaluating the incidence of subclinical carotid atherosclerotic vascular diseases in patients with COPD Sujets and methods: a cross-sectional sample of 75 topics has been conducted; 25 stable COPD patients and 50 controls (25 patients with other chest diseases and 25 apparently healthy persons). They were divided into three groups: Group I: 25 healthy COPD patients (Global initiative for Chronic Obstructive Lung Disease Recommendations 2020 diagnosis and gravity of COPD) (GOLD 2020). Group II: 25 people and other underlying pulmonary conditions. Group III: 25 people seemingly well. The thesis lasted between 6 and 12 months Results: The prevalence of carotid disease in COPD patients was slightly higher than controls. Multinomial analyses of logistic regression have shown COPD to be an independent carotid plague indicator. Conclusion: Subclinical atherosclerosis is greatly correlated with COPD. These results will help to prepare appropriate strategies for CV prevention.

Sex Modifies the Association of Fibroblast Growth Factor 21 With Subclinical Carotid Atherosclerosis.

Background and Aims: Fibroblast growth factor 21 (FGF21), an emerging metabolic hepatokine, is associated with atherosclerosis. An interaction with sex has been described in various populations. We aimed to study whether sex modulates the relationship between FGF21 and subclinical carotid atherosclerosis in a diabetes-enriched multiethnic population of Singapore. We explore differences in intermediary mechanisms, in terms of hypertension, lipids, and inflammation, between FGF21 and atherosclerosis.Methods: We recruited 425 individuals from a single diabetes center in Singapore, and demographics, anthropometry, metabolic profile, FGF21, and carotid ultrasonography were performed. Multivariable logistic regression models were used to study the association between subclinical atherosclerosis and FGF21 adjusting for age, ethnicity, body mass index (BMI), hemoglobin A1c (HbA1c), systolic and diastolic blood pressures, and low-density lipoprotein (LDL)-cholesterol separately for males and females as two groups after an interaction test.Results: An interaction test assessing interaction by sex on the relationship between subclinical atherosclerosis and FGF21 showed a significant interaction with sex (Pinteraction = 0.033). In the female subgroup, significant independent associations of standardized lnFGF21 with subclinical atherosclerosis were seen, with 1 SD increment in lnFGF21 being associated with 1.48-fold (95% CI: 1.03, 2.12; p = 0.036) increase in risk. In the male subgroup, the association of subclinical atherosclerosis with standardized lnFGF21 was not significant [odds ratio (OR) (95% CI): 0.90 (0.63, 1.28); p = 0.553]. We found sex interactions with pulse pressure being significantly associated in females only and triglycerides and C-reactive protein being associated with males only.Conclusion: FGF21 is positively associated with subclinical carotid atherosclerosis in women, but not in men. The sex–racial patterns in the mechanisms by which FGF21 causes subclinical atherosclerosis needs to be explored in larger population-based studies and mechanistically studied in greater detail.