Carotid Atheromatous Plaque Research Articles

“Role Of Caroto-Vertebral Duplex Ultrasonography In Patients With Cerebro-Vascular Accident - Hemodynamic Characterisation & Etiological Stratification”

Introduction: cerebrovascular accident is defined as a sudden, non convulsive focal neurological deficit resulting due to brain ischemia predominantly caused by the thrombo-embolism or with atheromatous carotid plaque as the embolic source1 . Cerebrovascular accident is the leading cause of morbidity in elderly patients with varying degrees of neurological deficit. Since it is a preventable condition and with timely intervention, the severity of the disease can be minimized. Hence, the aim of the present study was real time visualization of vascular lesions to characterize the morphology of vessels for intimal-media complex & for any plaque or stenosis, to quantify the degree and percentage of stenosis in the caroto-vertebral arteries and to correlate the degree of stenosis with severity of clinical disease. Materials and methods: prospective cross-sectional study was conducted on 100 patients presenting with cva with or without persistent neurological deficit referred to department of radio-diagnosis and imaging from indoor and outdoor departments of jan sewa hospital of dr. S. S. Tantia medical college, sri ganganagar. Results: the majority of patients were in the age group of 60-69 years with 56% being male, 47% presenting with transient ischemic attack, commonest clinical feature being coronary artery disease (29%) followed by haeadache (17%), nausea vomiting (4%), hemiplegia (2%) patients and coma (1%). Hypertension was the most commonest risk factor (59%) followed by diabetes mellitus (18%), hyperlipidemia (14%), atrial fibrillations (5%) and smoking (4%). Majority of plaques were seen in the carotid bulb with variable laterality & echopattern. It was seen that as the degree of stenosis increases the various velocities and their respective ratios (ica psv/ cca psv, ica edv/cca edv, ica psv/cca edv) tend to increase in proportion to the stenosis suggestive of a positive co-relation between them. Conclusion: caroto-vertebral duplex ultrasonography provides a “road map” for carotid endartectomy and/or carotid angioplasty and stenting due to direct visualization of plaque morphology & surface configuration, measurement of the length of stenosed segment, precise determination of grade of stenosis and to get an insight into hemodynamic disorders.

Clinical and subclinical atherosclerosis in patients with systemic sclerosis: an observational, multicentre study of GIRRCS (Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale).

Conflicting results about clinical and subclinical atherosclerosis in systemic sclerosis (SSc) and the associated risk factors have been reported. Hence, we aimed to determine the prevalence of clinical and subclinical atherosclerosis in a large number of Italian SSc patients and the associated risk factors. This study included 613 SSc patients from 11 Italian tertiary Rheumatologic Units. All patients underwent full history taking, clinical examination, and relevant laboratory and radiological investigations. Doppler ultrasonography (US) of the common carotid and upper and lower limbs was performed to measure carotid and femoral intima-media thickness (cIMT and fIMT), and carotid and peripheral atheroma plaques. Doppler US of the brachial artery was performed to measure flow-mediated dilatation (FMD). Patients were mostly women (91.4%) with a median age of 61 years (range, 20-100); a median disease duration of 14 years (range, 0-77) from the onset of the first non-Raynaud's phenomenon (RP); 9.3% had a history of clinical atherosclerosis (9 stable/unstable angina, 21 myocardial infarctions, 24 heart failure, 3 strokes, 8 transient ischaemic attack, 6 intermittent claudication, 10 atrial thrombo-embolism). In 37.1% of patients, subclinical atherosclerosis was detected, after excluding those with a history of clinical atherosclerosis. The prevalence of clinical and subclinical atherosclerosis was higher than that reported by the European Society of Cardiology and observational studies that enrolled Italian healthy individuals as a control group, respectively. A higher prevalence of clinical and subclinical atherosclerosis was detected in SSc Italian patients and correlated with traditional and SSc-related risk factors.

Apnea-Specific Pulse-Rate Response is Associated With Early Subclinical Atherosclerosis in Obstructive Sleep Apnea

IntroductionIn patients with obstructive sleep apnea (OSA), novel metrics such as hypoxic burden (HB) and sleep apnea-specific pulse-rate response (ΔHR) may better correlate with cardiovascular diseases (CVD) than the apnea–hypopnea index (AHI). This manuscript aims to assess the correlation between ΔHR and HB with subclinical atherosclerosis in patients with OSA, testing the hypothesis that elevated ΔHR and HB are associated with subclinical atherosclerosis development. MethodsIn a prospective study, individuals aged 20–65 years with suspected OSA without known comorbidities were consecutively recruited and defined as OSA (AHI≥5events/h) or healthy controls. Using bilateral carotid ultrasonography, common carotid intima-media thickness (CIMT) was assessed and the identification of at least one atheromatous plaque defined the presence of subclinical atherosclerosis. ΔHR, and HB were derived from pulse-oximetry. ResultsWe studied 296 patients of 45±10 years old, of whom 28% were women, and a BMI of 30.3±5.3kg/m2. Overall, 245 had OSA and 51 were healthy controls. After controlling for confounding variables higher ΔHR but not HB, was associated with higher CIMT (p=0.006) and higher time spent with oxygen saturation below 90% (T90) was associated with an increase in carotid atheroma plaques (p=0.032). When stratifying OSA based on HB tertiles, we observed that within tertile 2 of HB, an increase in ΔHR was associated with larger CIMT (p=0.017). ConclusionA higher ΔHR is associated with an increase in CIMT among adult patients with OSA. This study suggests that ΔHR could be a biomarker of risk for CVD in patients with OSA.

Association of carotid atheroma plaque with IL-18 levels and with polymorphisms in the IL-18 receptor gene in a Mediterranean population

BackgroundAtherosclerosis is an inflammatory disease. Interleukin 18 (IL-18) is an inflammatory molecule that has been linked to the development of atherosclerosis and cardiovascular disease. ObjectiveTo evaluate the possible relationship between plasma levels of IL-18 and the presence of atherosclerosis evaluated at the carotid level, as well as to analyze the possible modulation by different polymorphisms in a Mediterranean population. Material and methods746 individuals from the metropolitan area of ​​Valencia were included, recruited over a period of 2 years. Hydrocarbon and lipid metabolism parameters were determined using standard methodology and IL-18 using ELISA. In addition, carotid ultrasound was performed and the genotype of 4 SNPs related to the IL-18 signaling pathway was analyzed. ResultsPatients with higher plasma levels of IL-18 had other associated cardiovascular risk factors. Elevated IL-18 levels were significantly associated with higher carotid IMT and the presence of atheromatous plaques. The genotype with the A allele of the SNP rs2287037 was associated with a higher prevalence of carotid atheromatous plaque. On the contrary, the genotype with the C allele of the SNP rs2293224 was associated with a lower prevalence of atheromatous plaque. ConclusionsHigh levels of IL-18 were significantly associated with a higher carotid IMT and the presence of atheromatous plaques, which appear to be influenced by genetic factors, as evidenced by associations between SNPs in the IL-18 receptor gene and the presence of atheroma plaque.

Association of angiogenesis-associated genes with atherosclerotic plaque progression, intraplaque hemorrhage, and immune infiltration

Mounting evidence suggests that intraplaque angiogenesis is associated with the progression of atherosclerotic plaques and the development of intraplaque hemorrhage. The specificity of intraplaque immune cell infiltration may be associated with abnormalities in the structure and function of the nascent capillaries. Here, we analyzed expression levels of angiogenesis-associated genes in early and advanced carotid atheromatous plaque tissues as well as in stable and intraplaque hemorrhage plaques. Expression profiles of advanced arterial plaques based on angiogenesis-associated genes were classified into subtypes by performing a consensus clustering analysis. The correlation between the immune microenvironment of plaques and expression of angiogenesis-associated genes was also explored using the single sample gene set enrichment analysis method and the CIBERSORT algorithm. We identified hub angiogenesis-associated genes showing similar expression patterns throughout plaque adverse progression, and constructed a prediction model using the random forest algorithm. Receiver operating curves were constructed to evaluate efficacy in identification of intraplaque hemorrhage in a plaque. Our results suggest that heterogeneity of angiogenesis-related genes may promote the malignant development of plaques and cause plaque rupture. In conclusion, we propose a model based on expression of angiogenesis-related genes to predict the risk of plaque rupture.

Transcription Factor Regulation of Gene Expression Network by ZNF385D and HAND2 in Carotid Atherosclerosis.

Carotid intima-media thickness (CIMT) is a surrogate indicator for atherosclerosis and has been shown to predict cardiovascular risk in multiple large studies. Identification of molecular markers for carotid atheroma plaque formation can be critical for early intervention and prevention of atherosclerosis. This study performed transcription factor (TF) network analysis of global gene expression data focusing on two TF genes, ZNF385D and HAND2, whose polymorphisms have been recently reported to show association with CIMT. Genome-wide gene expression data were measured from pieces of carotid endarterectomy collected from 34 hypertensive patients (atheroma plaque of stages IV and above according to the Stary classification) each paired with one sample of distant macroscopically intact tissue (stages I and II). Transcriptional regulation networks or the regulons were reconstructed for ZNF385D (5644 target genes) and HAND2 (781 target genes) using network inference. Their association with the progression of carotid atheroma was examined using gene-set enrichment analysis with extremely high statistical significance for regulons of both ZNF385D and HAND2 (p < 6.95 × 10-7) suggesting the involvement of expression quantitative loci (eQTL). Functional annotation of the regulon genes found heavy involvement in the immune system's response to inflammation and infection in the development of atherosclerosis. Detailed examination of the regulation and correlation patterns suggests that activities of the two TF genes could have high clinical and interventional impacts on impairing carotid atheroma plaque formation and preventing carotid atherosclerosis.

Subclinical Atherosclerosis in a Gout Cohort: Prevalence and Associations.

The current observational, prospective study enrolled 65 patients with gout, diagnosed according to 2015 ACR/EULAR criteria [17], evaluated in Rheumatology Clinic, Emergency County Hospital Craiova, and 40 healthy subjects. This research aimed to determine the presence of subclinical carotid atherosclerosis, revealed by an increased intima media thickness and carotid plaques in gout patients, by US examination. Secondary, we aimed to search for the possible correlations displayed between the presence of subclinical carotid atherosclerosis and several disease variables. CCAIMT over 0.9mm was identified for 19 patients (29.23%), percentage statistically significant different compared to controls (7; 17.5%), p=0,0428. For 23 patients (35.38%) carotid plaques were present at US examination, more prevalent compared to controls (19; 29.23%), p=0.002. Using multivariate logistic regression, we pointed out that SUA (OR 2,103; p=0.0002), age (OR=1,051; p<0.001), disease duration (OR=1.740; p=0.0039) and LDLc (OR=1,003; p=0.0029) were independently associated to an increased IMT in patients with gout, similar results being obtained for carotid plaques. MSKUS was performed for all patients, with important results. The presence of deposits associated with an increased risk of a thick IMT; similar results were obtained for double contour sign, aggregates and tophi. A statistically significant risk was noticed for the presence of deposits (p=0.002). Regarding the presence of carotid atheroma plaques, a higher risk was associated to deposits identification, double contour sign, aggregates, tophi and PD signal. Our results sustain that carotid ultrasound is an easily accessible imagistic method that offers important predictors of atherosclerotic status.

Metabolic Syndrome in Psoriasis Patients-an Observational Study.

Our observational study included on 54 patients with PsO, evaluated into the Dermatology Department of the Emergency County Hospital Craiova, Romania, between August 2023 and January 2024, and 40 controls. Our research proposed determining the prevalence of MetS in a cohort of PsO patients, and its relationship to subclinical atherosclerosis, evaluated by carotid ultrasound. Metabolic syndrome (MetS) was established according to National Cholesterol Education Program (NCP) Adult Treatment Panel (ATP) III criteria for MetS for 35 of the patients (64.81%) vs. 11 of the control group (27.5%), p=0.0003. An overview of each component of MetS depending on the diagnostic criteria for MetS showed that waist and total cholesterol exerted significant differences. Carotid ultrasound evaluation revealed an increased ITM, of over 0.9mm, for 19 (35.18%) or PsO patients, significantly increased compared to controls, as well as the presence of carotid plaques in significantly different percentages (37.03% PsO vs. 17.5% controls, p=0.001). We also noted that for patients with MetS, US examination displayed increased results for IMT compared to those without MetS. The prevalence of carotid atheroma plaque was augmented in patients with MetS and PsO. In our PsO group IMT exerted a positive inter-relation with: age, MetS, blood glucose, disease duration, and PASI. Important to note is that after multiple linear regression analysis, age and MetS were independent indicators of IMT (p=0.02 for age and p=0.001 for MetS). Our findings sustain a firm relationship between MetS and psoriasis and the major consequence of this observation is the inherent risk of cardiovascular events.

Identification of key pyroptosis-related genes and microimmune environment among peripheral arterial beds in atherosclerotic arteries

Atherosclerosis is a chronic inflammatory disease characterized with innate and adaptive immunity but also involves pyroptosis. Few studies have explored the role of pyroptosis in advanced atherosclerotic plaques from different vascular beds. Here we try to identify the different underlying function of pyroptosis in the progression of atherosclerosis between carotid arteries and femoral. arteries. We extracted gene expression levels from 55 advanced carotid or femoral atherosclerotic plaques. The pyroptosis score of each sample was calculated by single-sample-gene-set enrichment analysis (ssGSEA). We then divided the samples into two clusters: high pyroptosis scores cluster (PyroptosisScoreH cluster) and low pyroptosis scores cluster (PyroptosisScoreL cluster), and assessed functional enrichment and immune cell infiltration in the two clusters. Key pyroptosis related genes were identified by the intersection between results of Cytoscape and LASSO (Least Absolute Shrinkage and Selection Operator) regression analysis. Finally, all key pyroptosis related genes were validated in vitro. We found all but one of the 29 carotid plaque samples belonged to the PyroptosisScoreH cluster and the majority (19 out of 26) of femoral plaques were part of the PyroptosisScoreL cluster. Atheromatous plaque samples in the PyroptosisScoreL cluster had higher proportions of gamma delta T cells, M2 macrophages, myeloid dendritic cells (DCs), and cytotoxic lymphocytes (CTLs), but lower proportions of endothelial cells (ECs). Immune full-activation pathways (e.g., NOD-like receptor signaling pathway and NF-kappa B signaling pathway) were highly enriched in the PyroptosisScoreH cluster. The key pyroptosis related genes GSDMD, CASP1, NLRC4, AIM2, and IL18 were upregulated in advanced carotid atherosclerotic plaques. We concluded that compared to advanced femoral atheromatous plaques, advanced carotid atheromatous plaques were of higher grade of pyroptosis. GSDMD, CASP1, NLRC4, AIM2, and IL18 were the key pyroptosis related genes, which might provide a new sight in the prevention of fatal strokes in advanced carotid atherosclerosis.

Asociación de la placa de ateroma carotídea con los niveles plasmáticos de IL-18 y con polimorfismos en el gen del receptor de la IL-18 en la población mediterránea

BackgroundAtherosclerosis is an inflammatory disease. Interleukin 18 (IL-18) is an inflammatory molecule that has been linked to the development of atherosclerosis and cardiovascular disease. ObjectiveTo evaluate the possible relationship between plasma levels of IL-18 and the presence of atherosclerosis evaluated at the carotid level, as well as to analyze the possible modulation by different polymorphisms in a Mediterranean population. Material and methodsSeven hundred and forty-six individuals from the metropolitan area of Valencia were included, recruited over a period of 2 years. Hydrocarbon and lipid metabolism parameters were determined using standard methodology and IL-18 using ELISA. In addition, carotid ultrasound was performed and the genotype of four SNPs related to the IL-18 signaling pathway was analyzed. ResultsPatients with higher plasma levels of IL-18 had other associated cardiovascular risk factors. Elevated IL-18 levels were significantly associated with higher carotid IMT and the presence of atheromatous plaques. The genotype with the A allele of the SNP rs2287037 was associated with a higher prevalence of carotid atheromatous plaque. On the contrary, the genotype with the C allele of the SNP rs2293224 was associated with a lower prevalence of atheromatous plaque. ConclusionsHigh levels of IL-18 were significantly associated with a higher carotid IMT and the presence of atheromatous plaques, which appear to be influenced by genetic factors, as evidenced by associations between SNPs in the IL-18 receptor gene and the presence of atheroma plaque.

Knockdown of ADAMDEC1 ameliorates ox-LDL-induced endothelial cell injury and atherosclerosis progression.

This study was designed to investigate the role of a disintegrin and metalloproteinase domain-like protein decysin 1 (ADAMDEC-1) in atherosclerosis (AS). The Gene Expression Omnibus (GEO) database was utilized to identify differentially expressed genes (DEGs) between carotid atheroma plaque and carotid tissue adjacent atheroma plaque obtained from AS patients. Gene functional enrichment analysis was conducted on DEGs using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). QRT-PCR was employed to quantify mRNAs expression. AS animal model was established using ApoE-/- mice; serum triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels were detected. Aortic sinus atherosclerotic lesions were observed using H&E staining and Oil Red O staining. ADAMDEC-1 was silenced using small interfering RNAs (siRNAs) in human vascular smooth muscle cells (HVSMCs). Cell proliferation, migration, and cell cycle progression were detected by cell count kit-8 (CCK8), 5-ethynyl-2'-deoxyuridine (EDU), wound scratch healing assay, transwell assay, and flow cytometry, respectively. Western blot was used to evaluate various protein expression levels. Our results showed that ADAMDEC-1 was highly expressed in the serum of AS patients, consistent with the in silico results. The elevated TG, LDL-C, and HDL-C levels along with H&E and Oil Red O staining confirmed the successful establishment of the AS mouse model. ADAMDEC-1 expression was also elevated in AS mice. ADAMDEC-1 knockdown in HVSMCs suppressed cell proliferation, inhibited the expression of proliferating cell nuclear antigen (PCNA), and reduced the levels of matrix metalloproteinases (MMP2 and MMP9) proteins. Protein-protein interaction (PPI) analysis indicated that ADAMDEC-1 was associated with CXCL9, CCR5, TNF-α, TNFR1, and NF-κB-p50. The expression levels of CXCL9, CCR5, TNF-α, TNFR1, and NF-κB-p50 increased, while ADAMDEC-1 knockdown attenuated the expression of these proteins. Our study findings substantiate that ADAMDEC-1 may represent a novel target for AS.

Cardiovascular Calcifications Are Correlated with Inflammation in Hemodialysis Patients.

Background and Objectives: The main cause of morbidity and mortality in hemodialysis patients is cardiovascular disease, which is quite common. The main objective of our study was to investigate the relationship between oxidative stress, inflammation, and vascular and valvular calcifications in hemodialysis patients. Materials and Methods: This observational study had 54 hemodialysis patients, with an average age of 60.46 ± 13.18 years. Cardiovascular ultrasound was used to detect and/or measure aortic and mitral valve calcifications, carotid and femoral atheroma plaques, and common carotid intima-media thickness. The aortic calcification score was determined using a lateral abdomen plain radiograph. The inflammatory, oxidative, metabolic, and dietary statuses, as well as demographic characteristics, were identified. Results: There were significant correlations between the levels of IL-6 and carotid plaque number (p = 0.003), fibrinogen level and aortic valve calcifications (p = 0.05), intima-media thickness (p = 0.0007), carotid plaque number (p = 0.035), femoral plaque number (p = 0.00014), and aortic calcifications score (p = 0.0079). Aortic annulus calcifications (p = 0.03) and intima-media thickness (p = 0.038) were adversely linked with TNF-α. Nutrition parameters were negatively correlated with atherosclerosis markers: number of carotid plaques with albumin (p = 0.013), body mass index (p = 0.039), and triglycerides (p = 0.021); number of femoral plaques with phosphorus (0.013), aortic calcifications score with albumin (p = 0.051), intima-media thickness with LDL-cholesterol (p = 0.042). Age and the quantity of carotid plaques, femoral plaques, and aortic calcifications were linked with each other (p = 0.0022, 0.00011, and 0.036, respectively). Aortic annulus calcifications (p = 0.011), aortic valve calcifications (p = 0.023), and mitral valve calcifications (p = 0.018) were all associated with an increased risk of death. Conclusions: Imaging measures of atherosclerosis are adversely connected with dietary status and positively correlated with markers of inflammation and risk of mortality.

MRI and Carotid Duplex assessment of vulnerable carotid atheromatous plaques in acute stroke patients

MRI and Carotid Duplex assessment of vulnerable carotid atheromatous plaques in acute stroke patients

S-38-5: IDENTIFICATION OF FERROPTOSIS-RELATED GENES IN CAROTID ATHEROSCLEROSIS ON BIOINFORMATIC ANALYSIS

Background: Carotid atherosclerosis (CAS) is a common chronic vascular inflammatory disease and one of the main causes of cardiovascular and cerebrovascular diseases (CVDs). Ferroptosis related genes (FRGs) may play a crucial part in pathophysiological processes of CAS. However, the expression profile of FRGs have rarely been adopted to explore the relationship between ferroptosis and CAS. Objects: Therefore, using the expression profile of FRGs to explore the relationship between ferroptosis and CAS may provide new insights for the prevention and treatment of CVD. Methods: The differentially expressed genes (DEGs) of the GSE432192 dataset were obtained from the Gene Expression Omnibus (GEO) database. Ferroptosis related genes (FRGs) were identified by downloading data from the FerrDb database. The GSE432192 dataset contains 32 carotid atheroma plaque samples and 32 macroscopically intact carotid tissue samples adjacent to the atheroma plaque. The differentially expressed FRGs (DE FRGs) of the GSE432192 dataset were screened and analyzed by gene ontology analysis (GO), Kyoto Encyclopedia of Genes and Genomes analysis (KEGG), protein protein interaction network (PPI), and were chosen to explore related miRNAs. Results: The GSE432192 dataset had a total of 41 DE FRGs. The GO analysis results revealed that DE FRGs were mainly enriched in response to oxidative stress, oxidoreductase activity acting on NAD(P)H, and apical part of cell. KEGG analysis results showed that DE FRGs were mainly enriched in ferroptosis and chemical carcinogenesis reactive oxygen species relating pathways. Expressions of top 5 hub genes, as HIF1A, HMOX1, TFRC, CYBB, EGFR, were regarded as focus in the PPI regulatory networks. Conclusions: In this study, Ferroptosis and FRGs may play a vital role in regulating the pathophysiology of CAS.

Clinical application of super sensitive microflow ultrasound on the detection of intraplaque neovascularization in patients with atheromatous carotid artery plaque.

Contrast-enhanced ultrasound (CEUS) is a routine technique for detecting intraplaque neovascularization (IPN). However, the invasiveness and complexity of CEUS severely limit its clinical application. This article aims to investigate the application value of AngioPLUS (AP) technique in assessing IPN formation in patients with atheromatous (AS) carotid artery plaque. Patients diagnosed with carotid artery atherosclerosis combined plaque formation were recruited and their demographic characteristics including serum fasting blood glucose (FBG), triglyceride (TG), and low-density lipoprotein (LDL) were collected. AP was used to scoring intraplaque microvascular flow (IMVF), measuring the thickness and length of the plaque and determining the number of IPN of the plaque. IMVF score evaluated by AP was positively correlated with plaque length, thickness, IPN number, serum TG, LDL and FBG levels in patients with carotid atherosclerosis with plaque. The evaluation results of CEUS score and IMVF classification detected by AP of plaques were consistent in patients with carotid atherosclerosis. IMVF scoring by AP is a promising approach to assess IPN and plaque status in patients with atheromatous carotid artery plaque.

Fluid structure interaction analysis to stratify the behavior of different atheromatous carotid plaques

Fluid structure interaction analysis to stratify the behavior of different atheromatous carotid plaques

Determinants of left ventricular diastolic dysfunction in hemodialysis patients

Introduction: Chronic kidney disease (CKD) induces changes in the myocardium known to influence morbidity and mortality, most severe in patients with end stage renal disease. Objectives: The working hypothesis was that in patients on chronic hemodialysis the prevalence of left ventricular diastolic dysfunction is correlated with the inflammatory, oxidative, metabolic, nutritional, and atherosclerotic status. Patients and Methods: An observational study was performed on 51 patients (age 59.76 ± 13.24 years) on hemodialysis treatment. Transthoracic cardiac ultrasound was conducted to evaluate LVDD. The burden of cardiac and arterial atherosclerosis was evaluated by cardiac ultrasound (aortic and mitral valve calcifications), vascular ultrasound (carotid and femoral atheroma plaques, common carotid intima-media thickness), and by abdominal radiography (aortic calcification score). Demographic and anthropometric parameters were determined. Blood samples were used to determine laboratory parameters reflecting the inflammatory, oxidative, and metabolic/nutrition status. Results: LVDD is positively correlated with the serum level of C-reactive protein (CRP) (P=0.04), the total antioxidant capacity of the serum (P=0.04), the presence (P=0.022) and number (P=0.04) of femoral plaques, the aortic calcification score (P=0.02), aortic valve stenosis (P=0.037), aortic annulus calcifications (P=0.02) and mitral valve calcifications (P=0.041). After the removal of the main confounder, degenerative aortic stenosis, only the associations with serum total antioxidant capacity (P=0.04) and aortic calcification score (P= 0.02) maintain their statistical significance. Conclusion: LVDD is positively correlated with inflammation and oxidative stress markers and with the severity of aortic calcification.

Fluid structure interaction analysis to stratify the behavior of different atheromatous carotid plaques.

In asymptomatic carotid stenosis (ACS), different plaque types, i.e. lipidic (LP), fibrous (FP), and calcific (CP), could have different hemodynamic and structural behaviors. Different carotid plaques, reconstructed from medical imaging of ACS >70%, were analyzed by computing fluid structure interaction (FSI), modeling the spatial distribution of wall shear stresses (WSS), plaque displacements (D), von Mises stresses (VMS), and absorbed elastic energy (AEE) together with their maximum-in-space values at the systole (WSS<inf>syst</inf>, D<inf>syst</inf>, VMS<inf>syst</inf> and AEE<inf>syst</inf>). WSS resulted significantly higher in CP, whereas D and VMS showed the highest values for LP. Regarding AEE<inf>syst</inf> stored by the plaques, LP absorbed in average 2320 J/m3, FP 408 J/m3 (470%) and CP 99 J/m3 (2240%), (P<0.01, P<0.01, and P<0.01, respectively). Depending upon their nature, plaques store different deformations and inner distributions of forces, thus potentially influencing their vulnerability.

Intraplaque calcium and its relation with the progression of carotid atheromatous disease.

Calcification and progression of atheromatous disease (AD) both have been independently related with the risk of stroke. However, the link between the two phenomena is still unclear. The main objective of this study was to analyze the temporal evolution of Ca content of carotid atheromatous plaques and its relation with the progression of carotid AD using quantitative CT Angiography (CTA). Forty-three asymptomatic patients with stenosis of the internal carotid artery (ICA)>50% completed the study. Contrast mold volume and calcium (Ca) content by quantitative CTA and Modified Agatston Score (Ca volume × radiological density) were assessed at baseline and after 12±2 months. Biochemical parameters, including main markers of Ca/Phosphorus (P) metabolism, were determined. CTA measurement showed an increase of volumetric stenosis (volume decrease of the contrast mold), compared to baseline (475.45 [155.6] mm3 × U.H vs. 501.3 [171.9] mm3 × U.H; P=0.04) as well as an increase of intraplaque Ca (64.58 [57.8] mm3 × U.H. vs. 56.8 [52.3] P=0.002). An inverse correlation between baseline Ca content and volumetric stenosis progression (r=-0.481; P<0.001), as well as between the increase of carotid Ca and plasma levels of vitamin D (r=0.4; P=0.025) were also found. Multiple regression analysis found a model with baseline intraplaque Ca, adjusted by Body Mass Index (BMI) as most predictive of carotid AD progression. These results suggest that a higher content of Ca confers greater stability against the progression of carotid AD and, eventually, its ability to generate symptomatology.

Postprandial Hyperlipidemia: Association with Inflammation and Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis.

Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. Results: A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09–12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00–3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01–1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00–1.04); p = 0.049). Conclusion: PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.