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

BACKGROUND: Atherosclerosis is an inflammatory disease. Interleukin 18 (IL-18) is an inflammatory molecule that has been linked to the development of atherosclerosis and cardiovascular disease. OBJECTIVE: To 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 METHODS: Seven 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. RESULTS: Patients 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. CONCLUSIONS: High 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.

Coronary artery properties in atherosclerosis: A deep learning predictive model.

In this work an Artificial Neural Network (ANN) was developed to help in the diagnosis of plaque vulnerability by predicting the Young modulus of the core (E core ) and the plaque (E plaque ) of atherosclerotic coronary arteries. A representative in silico database was constructed to train the ANN using Finite Element simulations covering the ranges of mechanical properties present in the bibliography. A statistical analysis to pre-process the data and determine the most influential variables was performed to select the inputs of the ANN. The ANN was based on Multilayer Perceptron architecture and trained using the developed database, resulting in a Mean Squared Error (MSE) in the loss function under 10-7, enabling accurate predictions on the test dataset for E core and E plaque . Finally, the ANN was applied to estimate the mechanical properties of 10,000 realistic plaques, resulting in relative errors lower than 3%.

Serial analysis of coronary artery disease progression by artificial intelligence assisted coronary computed tomography angiography: early clinical experience.

BACKGROUND: Studies have shown that quantitative evaluation of coronary artery plaque on Coronary Computed Tomography Angiography (CCTA) can identify patients at risk of cardiac events. Recent demonstration of artificial intelligence (AI) assisted CCTA shows that it allows for evaluation of CAD and plaque characteristics. Based on publications to date, we are the first group to perform AI augmented CCTA serial analysis of changes in coronary plaque characteristics over 13 years. We evaluated whether AI assisted CCTA can accurately assess changes in coronary plaque progression, which has potential clinical prognostic value in CAD management. CASE PRESENTATION: 51-year-old male with hypertension, hyperlipidemia and family history of myocardial infarction, underwent CCTA exams for anginal symptom evaluation and CAD assessment. 5 CCTAs were performed between 2008 and 2021. Quantitative atherosclerosis plaque characterization (APC) using an AI platform (Cleerly), was performed to assess CAD burden. Total plaque volume (TPV) change-over-time demonstrated decreasing low-density non-calcified plaque (LD-NCP) with increasing overall NCP and calcified-plaque (CP). Examination of individual segments revealed a proximal-LAD lesion with decreasing NCP over-time and increasing CP. In contrast, although the D2/D1/ramus lesions showed increasing stenosis, CP, and total plaque, there were no significant differences in NCP over-time, with stable NCP and increased CP. Remarkably, we also consistently visualized small plaques, which typically readers may interpret as false positives due to artifacts. But in this case, they reappeared each study in the same locations, generally progressing in size and demonstrating expected plaque transformation over-time. CONCLUSIONS: We performed the first AI augmented CCTA based serial analysis of changes in coronary plaque characteristics over 13 years. We were able to consistently assess progression of plaque volumes, stenosis, and APCs with this novel methodology. We found a significant increase in TPV composed of decreasing LD-NCP, and increasing NCP and CP, with variations in the evolution of APCs between vessels. Although the significance of evolving APCs needs to be investigated, this case demonstrates AI-based CCTA analysis can serve as valuable clinical tool to accurately define unique CAD characteristics over time. Prospective trails are needed to assess whether quantification of APCs provides prognostic capabilities to improve clinical care.

Birefringent crystals deposition and inflammasome expression in human atheroma plaques by levels of uricemia.

OBJECTIVE: To verify the monosodium urate (MSU) crystal deposition in artery walls following a structure assessment and to assess NLRP3 inflammasome expression in human atheroma plaques by levels of uricemia. METHODS: Patients with peripheral arterial disease who were candidates for amputation were recruited and classified as normouricemic or hyperuricemic. During surgery, an artery segment from the amputated limb was sampled, divided and fixed separately by cryo-embedding, 100% ethanol or Glyo-fixx. Samples were assessed by compensated polarized-light microscopy to identify MSU crystals on the artery walls. Afterwards, macrophages, neutrophils and NLRP3 inflammasome components at the plaque were categorized by immunostaining and compared between normouricemics and hyperuricemics. RESULTS: Thirty artery samples from 27 patients were studied; 10 (37.0%) participants were hyperuricemic. Birefringent needle-shaped crystals were found in three samples (10.0%), all processed by frozen sectioning. Other methods showed no crystals. No accompanying inflammatory process was noted, and the presence of crystals was equally distributed across ranges of uricemia, making it unlikely they were MSU crystals. Regarding immunostaining, 28 artery samples were available for analysis, with similar infiltration of macrophages and neutrophils. NLRP3 and gasdermin-D expression were significantly greater in hyperuricemics compared to normouricemics (P=0.044 and P=0.017, respectively). ASC content was numerically larger in hyperuricemics as well, while caspase-1 and IL-1beta expression were similar between groups. CONCLUSIONS: The presence of MSU crystals on artery walls was not confirmed. Hyperuricemia was associated with greater NLRP3 and gasdermin-D expression on human atheroma plaques in patients with peripheral artery disease.

Pathophysiology of Atherosclerosis.

Atherosclerosis is the main risk factor for cardiovascular disease (CVD), which is the leading cause of mortality worldwide. Atherosclerosis is initiated by endothelium activation and, followed by a cascade of events (accumulation of lipids, fibrous elements, and calcification), triggers the vessel narrowing and activation of inflammatory pathways. The resultant atheroma plaque, along with these processes, results in cardiovascular complications. This review focuses on the different stages of atherosclerosis development, ranging from endothelial dysfunction to plaque rupture. In addition, the post-transcriptional regulation and modulation of atheroma plaque by microRNAs and lncRNAs, the role of microbiota, and the importance of sex as a crucial risk factor in atherosclerosis are covered here in order to provide a global view of the disease.

Influence of vessel curvature and plaque composition on drug transport in the arterial wall following drug-eluting stent implantation.

In the last decade, many computational models have been developed to describe the transport of drug eluted from stents and the subsequent uptake into arterial tissue. Each of these models has its own set of limitations: for example, models typically employ simplified stent and arterial geometries, some models assume a homogeneous arterial wall, and others neglect the influence of blood flow and plasma filtration on the drug transport process. In this study, we focus on two common limitations. Specifically, we provide a comprehensive investigation of the influence of arterial curvature and plaque composition on drug transport in the arterial wall following drug-eluting stent implantation. The arterial wall is considered as a three-layered structure including the subendothelial space, the media and the adventitia, with porous membranes separating them (endothelium, internal and external elastic lamina). Blood flow is modelled by the Navier-Stokes equations, while Darcy's law is used to calculate plasma filtration through the porous layers. Our findings demonstrate that arterial curvature and plaque composition have important influences on the spatiotemporal distribution of drug, with potential implications in terms of effectiveness of the treatment. Since the majority of computational models tend to neglect these features, these models are likely to be under- or over-estimating drug uptake and redistribution in arterial tissue.

Factores pronósticos de aterosclerosis subclínica en pacientes dislipidémicos / Prognostic factors subclinical atherosclerosis in dyslipidemic patients

Introducción: La aterosclerosis subclínica es predictora de eventos vasculares futuros y es diagnosticada por imágenes y biomarcadores sin que existan manifestaciones clínicas. Objetivo: Identificar los factores pronósticos asociados con la aterosclerosis subclínica en pacientes dislipidémicos. Método: Se realizó un estudio de cohorte en el Hospital Hermanos Ameijeiras en 1028 pacientes en el periodo de 2016 al 2019. Resultados: La existencia de placa de ateroma fue de 26,9 por ciento. Existieron diferencias significativas relacionadas al tabaquismo (30,0 por ciento vs 23,7 por ciento). En las variables lipídicas, el promedio de los valores de la LDLc fue superior en los pacientes con placa de ateroma y la relación CT/LDL fue mayor en los que no tienen esta alteración. La frecuencia de engrosamiento del complejo íntima-media mayor de 1,0 mm fue de 37,1 por ciento. Existieron diferencias significativas relacionadas al tabaquismo (30,4 por ciento vs 22,4 por ciento) y la presencia de HTA (56,7 por ciento vs 48,8 por ciento ) en las variables lipídicas el promedio de los valores de la HDLc fue superior en los pacientes sin aumento del grosor del complejo íntima-media y la elevación CT/HDL fue mayor en los que presentan dicha alteración. Conclusiones: Los factores que influyen de manera independiente en la probabilidad de formación de las placas de ateroma son la LDLc (elevada), la edad, los triglicéridos y el sexo masculino y los que influyen en la probabilidad para el engrosamiento del complejo íntima-media son la HDLc (baja), el tabaquismo, y la hipertensión arterial(AU)

Introduction: Subclinical atherosclerosis is a predictor of future vascular events and is diagnosed by imaging and biomarkers without any clinical manifestations. Objective: To identify the prognostic factors that are associated with subclinical atherosclerosis in dyslipidemic patients. Method: A cohort study was carried out at the Hermanos Ameijeiras Hospital in 1028 patients in the period from 2016 to 2019. Results: The existence of atheroma plaque was 26.9 percent. There were significant differences related to smoking (30.0 percent vs 23.7 percent). In the lipid variables, the average of the LDLc values ​​is higher in patients with atheroma plaque and the CT/LDL ratio is higher in those without this alteration. Regarding the frequency of thickening of the intima-media complex greater than 1.0 mm, it was 37.1 percent. There were significant differences related to smoking (30.4 percent vs 22.4 percent) and the presence of HTA (56.7 percent vs 48.8 percent in the lipid variables, the average of the HDLc values ​​is higher in the patients without an increase in the thickness of the intima-media complex and the CT/HDL elevation is greater in those with said alteration. Conclusions: The factors that independently influence the probability of atheroma plaque formation are LDLc (elevated), age, triglycerides and male sex, and those that influence the probability of thickening of the intima-media complex. They are HDLc (low), smoking, and high blood pressure(AU)

Antiviral treatment does not improve subclinical atheromatosis in patients with chronic hepatitis caused by hepatitis C virus. / El tratamiento antiviral no mejora la ateromatosis subclínica en pacientes con hepatitis crónica por virus de la hepatitis C.

INTRODUCTION: Chronic infection with hepatitis C virus is a risk factor for developing atheromatous plaques, although the possible effect of virus clearance is unknown. Our aim was to determine whether or not subclinical atheromatosis improved and there was any modification in the composition of the plaques 12 months after eradication of hepatitis C virus by direct-acting antiviral agents. MATERIALS AND METHODS: Prospective study that included 85 patients with chronic hepatitis C virus infection in different stages of fibrosis who were on direct-acting antiviral agents. Patients with a cardiovascular history, diabetes and kidney disease were excluded. An arterial ultrasound (carotid and femoral) was performed to diagnose atheromatous plaques (defined as intima-media thickness ≥1.5mm) and the composition (percentage of lipids, fibrosis and calcium with HEMODYN4 software) was analysed at the beginning of the study and 12 months after stopping the therapy. RESULTS: After follow-up no changes were detected in the intima-media thickness (0.65mm vs. 0.63mm, P=.240) or in the presence of plaques (65.9% vs 71.8%, P=.063). There was also no significant change in their composition or affected vascular territory, with an increase in blood lipid profile (P<.001) after 12 months of treatment. These results were confirmed in subgroups by severity of liver disease. DISCUSSION: The eradication of hepatitis C virus by direct-acting antiviral agents does not improve the atheroma plaques and nor does it vary their composition, regardless of liver fibrosis. More prospective studies are needed to evaluate residual cardiovascular risk after virus eradication.

Anti-Atherosclerotic Effect of a Polyphenol-Rich Ingredient, Oleactiv®, in a Hypercholesterolemia-Induced Golden Syrian Hamster Model.

The development of nutraceutical ingredients has risen as a nutritional solution for health prevention. This study evaluated the effects of Oleactiv®, an ingredient developed for the prevention of atherogenesis, in hypercholesterolemic hamsters. Oleactiv® is a polyphenol-rich ingredient obtained from artichoke, olive and grape extracts as part of fruit and vegetables commonly consumed within the Mediterranean diet. A total of 21 Golden Syrian hamsters were divided into three groups. The standard group (STD) was fed a normolipidemic diet for 12 weeks, while the control group (CTRL) and Oleactiv® goup (OLE) were fed a high-fat diet. After sacrifice, the aortic fatty streak area (AFSA), plasmatic total cholesterol (TC), high-density lipoproteins (HDL-C), non-HDL-C and triglycerides (TG), were assessed. The cholesterol efflux capacity (CEC) of hamster plasma was quantified using a radiolabeled technique in murine macrophages J774. OLE administration induced a significant reduction of AFSA (-69%, p < 0.0001). Hamsters of the OLE group showed a significant decrease of both non-HDL-C (-173 mmol/L, p < 0.05) and TG (-154 mmol/L, p < 0.05). Interestingly, OLE induced a significant increase of total CEC (+17,33%, p < 0,05). Oleactiv® supplementation prevented atheroma development and had positive effects on the lipid profile of hypercholesterolemic hamsters. The increased CEC underlines the anti-atherosclerotic mechanism at the root of the atheroma reduction observed.

Identified key genes related to carotid atheroma plaque from gene expression chip.

As one of the leading reason in morbidity and death in the world, atherosclerosis is usually associated with vessel stenosis, ulceration, and inflammatory cell infiltration. However, the formation mechanism of atheroma plaque is unknown. In this research, we have used bioinformatics tools to identify 118 differential expression genes from a GEO dataset. Besides, we also revealed KYNU as a crucial gene in atheroma plaque development.

Adipo/cytokines in atherosclerotic secretomes: increased visfatin levels in unstable carotid plaque.

BACKGROUND: Novel pro-inflammatory and anti-inflammatory derivatives from adipose tissue, known as adipokines, act as metabolic factors. The aim of this study was to analyse the secreted expression of different adipo/cytokines in secretomes of unstable carotid atherosclerotic plaque versus non-atherosclerotic mammary artery. METHODS: We evaluated the secretion levels of adiponectin, visfatin, lipocalin-2, resistin, IL-6 and TNFR2 by ELISA in human secretomes from cultured unstable carotid atherosclerotic plaque (n = 18) and non-atherosclerotic mammary artery (n = 13). We also measured visfatin serum levels in patients suffering from atherosclerosis and in a serum cohort of healthy subjects (n = 16). RESULTS: We found that visfatin levels were significantly increased in unstable carotid atherosclerotic plaque secretome than in non-atherosclerotic mammary artery secretome. No differences were found with regard the other adipo/cytokines studied. Regarding visfatin circulating levels, there were no differences between unstable carotid atherosclerotic plaque and non-atherosclerotic mammary artery group. However, these visfatin levels were increased in comparison to serum cohort of healthy subjects. CONCLUSIONS: Of all the adipo/cytokines analysed, only visfatin showed increased levels in secretomes of unstable carotid atherosclerotic plaque. Additional human studies are needed to clarify the possible role of visfatin as prognostic factor of unstable carotid atherosclerotic plaque.

Effect of trans-chalcone on atheroma plaque formation, liver fibrosis and adiponectin gene expression in cholesterol-fed NMRI mice.

BACKGROUND: Trans-chalcone is the precursor molecule to flavonoids and possesses antioxidant and anti-inflammatory properties. This study aimed to evaluate the effects of trans-chalcone on atheroma plaque formation and the relevant biochemical parameters in high cholesterol diet (HCD)-fed NMRI mice. METHODS: Fifty male NMRI mice were divided into 5 groups (n=10 per group): control (received a normal diet); HCD (received an additional 2% cholesterol for 18 weeks); sham (received a HCD for 12 weeks and were then shifted to a normal diet and trans-chalcone vehicle (sunflower oil) for 6 weeks), and two experimental groups (received a HCD for 12 weeks and were then shifted to a normal diet and either 12mg/kg or 24mg/kg trans-chalcone for 6 weeks). RESULTS: After 12 weeks, HCD-induced atheroma plaques were observed by hematoxylin and eosin staining of aortic sections. At the end of experiment, the following factors had significantly increased in the HCD group: body weight, insulin resistance, and serum levels of triglycerides, total-cholesterol, glucose, insulin, leptin, liver enzymes (AST and ALT), malondialdehyde and direct bilirubin. The serum levels of high-density lipoprotein cholesterol, adiponectin, superoxide dismutase, and glutathione had considerably decreased. Histologic analysis of liver sections indicated hepatic fibrosis and steatosis. Treatment by both doses of trans-chalcone, particularly the 24mg/kg dose, significantly attenuated these alterations. CONCLUSIONS: Administration of trans-chalcone improved the consequences of atheroma plaque formation and liver fibrosis via increased expression of adiponectin, generation of higher levels of antioxidant enzymes, as well as modulation of serum leptin and lipid profiles.

Proteomic Profile of Unstable Atheroma Plaque: Increased Neutrophil Defensin 1, Clusterin, and Apolipoprotein E Levels in Carotid Secretome.

Because of the clinical significance of carotid atherosclerosis, the search for novel biomarkers has become a priority. The aim of the present study was to compare the protein secretion profile of the carotid atherosclerotic plaque (CAP, n = 12) and nonatherosclerotic mammary artery (MA, n = 10) secretomes. We used a nontargeted proteomic approach that incorporated tandem immunoaffinity depletion, iTRAQ labeling, and nanoflow liquid chromatography coupled to high-resolution mass spectrometry. In total, 162 proteins were quantified, of which 25 showed statistically significant differences in secretome levels between carotid atherosclerotic plaque and nondiseased mammary artery. We found increased levels of neutrophil defensin 1, apolipoprotein E, clusterin, and zinc-alpha-2-glycoprotein in CAP secretomes. Results were validated by ELISA assays. Also, differentially secreted proteins are involved in pathways such as focal adhesion and leukocyte transendothelial migration. In conclusion, this study provides a subset of identified proteins that are differently expressed in secretomes of clinical significance.

Stroke echoscan protocol: a fast and accurate pathway to diagnose embolic strokes.

BACKGROUND AND PURPOSE: Cardiac Echoscan is the simplified transthoracic echocardiogram focused on the main source of emboli detection in the acute stroke diagnosis (Stroke Echoscan). We describe the clinical impact related to the Stroke Echoscan protocol in our Center. METHODS: Acute stroke patients who underwent the Stroke Echoscan by a trained stroke neurologist were included (Echoscan group). All examinations were reviewed by cardiologists. The main embolic stroke etiologies were: ventricular akinesia (VA), severe aortic atheroma (AA) plaque and cardiac shunt (SHUNT). The rate of the embolic stroke etiologies and the median length of stay (LOS) were compared with a cohort of patients studied by cardiologist (Echo group). RESULTS: Eighty acute stroke patients were included. The sensitivity (S) and specificity (E) were: VA (S 98.6%, E 66.7%, k = .7), AA (S 93.3%, E 96.9%, k = .88) and SHUNT (S 100%, E 100%, k = 1), respectively. The rate of AA diagnosis was significantly higher in Echoscan group (18.8% vs. 8.9%; P = .05). Echoscan protocol significantly reduced the LOS: 6 days (IQR 3-10) versus Echo group 9 days (IQR 6-13; P < .001). CONCLUSION: The Echoscan protocol was an accurate quick test, which reduced the length of stay and increased the percentage of severe AA plaque diagnosis.

The human HDL proteome displays high inter-individual variability and is altered dynamically in response to angioplasty-induced atheroma plaque rupture.

Recent findings support potential roles for HDL in cardiovascular pathophysiology not related to lipid metabolism. We address whether HDL proteome is dynamically altered in atheroma plaque rupture. We used immunoaffinity purification of HDL samples from coronary artery disease patients before and after percutaneous transluminal coronary angioplasty (PTCA), a model of atheroma plaque disruption. Samples were analyzed by quantitative proteomics using stable isotope labeling and results were subjected to statistical analysis of protein variance using a novel algorithm. We observed high protein variability in HDL composition between individuals, indicating that HDL protein composition is highly patient-specific. However, intra-individual protein variances remained at low levels, confirming the reproducibility of the method used for HDL isolation and protein quantification. A systems biology analysis of HDL protein alterations induced by PTCA revealed an increase in two protein clusters that included several apolipoproteins, fibrinogen-like protein 1 and other intracellular proteins, and a decrease in antithrombin-III, annexin A1 and several immunoglobulins. Our results support the concept of HDL as dynamic platforms that donate and receive a variety of molecules and provide an improved methodology to use HDL proteome for the systematic analysis of differences among individuals and the search for cardiovascular biomarkers. Biological significance The HDL proteome is an interesting model of clinical relevance and has been previously described to be dynamically altered in response to pathophysiological conditions and cardiovascular diseases. Our study suggests that interindividual variability of HDL proteome is higher than previously thought and provided the detection of a set of proteins that changed their abundance in response to plaque rupture, supporting the concept of HDL as dynamic platforms that donate and receive a variety of molecules.

Mathematical modelling of atheroma plaque formation and development in coronary arteries.

Atherosclerosis is a vascular disease caused by inflammation of the arterial wall, which results in the accumulation of low-density lipoprotein (LDL) cholesterol, monocytes, macrophages and fat-laden foam cells at the place of the inflammation. This process is commonly referred to as plaque formation. The evolution of the atherosclerosis disease, and in particular the influence of wall shear stress on the growth of atherosclerotic plaques, is still a poorly understood phenomenon. This work presents a mathematical model to reproduce atheroma plaque growth in coronary arteries. This model uses the Navier-Stokes equations and Darcy's law for fluid dynamics, convection-diffusion-reaction equations for modelling the mass balance in the lumen and intima, and the Kedem-Katchalsky equations for the interfacial coupling at membranes, i.e. endothelium. The volume flux and the solute flux across the interface between the fluid and the porous domains are governed by a three-pore model. The main species and substances which play a role in early atherosclerosis development have been considered in the model, i.e. LDL, oxidized LDL, monocytes, macrophages, foam cells, smooth muscle cells, cytokines and collagen. Furthermore, experimental data taken from the literature have been used in order to physiologically determine model parameters. The mathematical model has been implemented in a representative axisymmetric geometrical coronary artery model. The results show that the mathematical model is able to qualitatively capture the atheroma plaque development observed in the intima layer.

Detección de Helicobacter Pylori en placas de ateroma / Elicobacter Pilori detected in atheroma plague

Introducción: la infección y la inflamación crónica han sido implicadas como agentes etiológicos para la ateraesclerasis (ATE). Varios estudios han relacionado a la infección por H. Pylori (HP) con la EC, especialmente con los linajes mas virulentos (linaje Cag A). Objetivo: demostrar la presencia del HP en placas de endarterectomías, utilizando una técnica Inmunohistoquimica (lHQ) específica que revela una reacción Ag-Ac mediante un cromógeno. Material y Métodos: se estudiaron 34 placas ATE de distintos territorios vasculares. Se fijaron en formol descalcificándolas en ácido fórmico según necesidad. Fueron incluidos en parafina, cortados y coloreados con H-E y técnicas de IHQ específicas para HP. Luego fueron desparafinados y tratados térmicamente con una solución de recuperación antigénica (lnmuno DNA Retriever with Citrate) utilizando olla a presión. La IHQ se efectuó con un sistema de alta sensibilidad Biotina-Estreptavidina-Peroxidasa-DAB). La observación morfológica evaluó células inflamatorias mononucleares y la identificación de la bacteria en la pared o la luz vascular. Resultados: de los 34 casos estudiados, en 14 se pudo identificar el bacilo en sus diferentes formas (41,17%), asociado a signos de inflamación crónica. Conclusión: el HP estuvo presente en un número sustancial de lesiones ATE y se asoció con inflamación. Estudios recientes sugieren que la presencia de Hp, demostrada por técnicas de IHQ, potenciaría los FR para ATE, induciendo una respuesta celular inflamatoria crónica por irritación persistente de la pared arterial.

Introduction: In general, infection and chronic inflammation have be en implied as etiologic agents for atherosclerosis and in particular coronary illness (CI). Several studies have correlated the infection of Helicobacter pylori with CI, especially with virulent strains (lineage Cag A). Objective: Demonstrate the immunohistochemical presence of H. Pylori in atherosclerotic plaques obtained from endarterectomy of different vascular regions. Material and methods: 34 atherosclerotic plaques of different vascular areas were studied, (25 men and 9 women). The tissues were fixed with 10% neutral buffered-formalin and decalcifying in formic acid 5% was used when necessary. The tissue sections were included in paraffin, cut and colored with H&E and subjected to Immunohistochemistry (lHC) of H.Pylori. Briefly, tissues were deparaffinized and thermally treated with a citrate-based solution of antigenic retrieval (lmmunoDNA Retriever with Citrate, BlO SB, Santa Barbara, CA) using a water bath at 95°C for 1 hour. The IHC was conducted using a high sensitivity BiotinStreptavidin-HRP-DAB IHC system (lmmunoDetector HRPIDAB, BlO SB). The microscopic observation evaluated the' presence of mononuclear inflammatory cells and the identification of the bacteria in the wall or the vascular lumen. Results: Of the 34 cases studied 14 were positive, where one could identify the bacillus in their different forms (41, 17%) associated with chronic inflammation.