Clinica e Investigacion en Arteriosclerosis最新文献

Introduction

SmartLab 2.0 is an innovative concept of multidisciplinary collaboration between the clinical laboratory and the diabetes day unit that was born with the aim of identifying patients at high cardiovascular risk who require priority attention, such as patients with atherogenic dyslipidemia, in order to create a cardiovascular prevention strategy.

Objective

Implementation in the Laboratory Information System (LIS) of an automated biochemical algorithm for the identification of patients with atherogenic dyslipidemia in routine analyses and priority referral to the diabetes day unit.

Material and methods

The algorithm designed in the SIL was: HBA1c > 9.3 + TG > 150 mg/dl + HDLc < 40 mg/dl + LDL/ApoB < 1.3. A comment was inserted alerting the requesting physician of the diagnosis of atherogenic dyslipidemia and priority referral was made from the laboratory to the diabetes day unit in the necessary cases.

Results

In the 1-year period, a total of 899 patients with HBA1c > 7 and atherogenic dyslipidemia criteria were identified. Of these, 203 patients from primary care with HbA1c > 9.3 were referred to the diabetes day hospital.

Conclusions

Reinforcement of cardiovascular prevention is necessary at all levels. The clinical laboratory should play a fundamental role in the diagnosis of dyslipidemias. Early detection of patients at high cardiovascular risk is essential and collaboration between the different clinical units is fundamental to guarantee patient safety.

Introduction and objectives

Cardiovascular diseases continue to lead the ranking of mortality in Spain. The implementation of geostatistical analysis techniques in the clinical laboratory are innovative tools that allow the design of new strategies in primary prevention of cardiovascular disease. The aim of this study was to study the prevalence and geolocation of severe dyslipidemia in the health areas under study in order to implement prevention strategies in primary care. A retrospective cohort study of low-density protein-bound cholesterol, triglyceride and lipoprotein (a) levels in the years 2019 and 2020 were carried out. In addition, a geostatistical analysis was performed including representation in choropleth maps and the detection of clustering clusters, using geographic information in zip code format included in the demographic data of each analytic.

Results

The analytical data included in the study were triglycerides (n = 365,384), low density protein-bound cholesterol (n = 289,594) and lipoprotein to lipoprotein (a) (n = 502). Areas with the highest and lowest percentage of cases were identified for the established cut-off points of LDL-C > 190 mg/dL and TG > 150 mg/dL. Two clustering clusters with statistical significance were detected for cLDL > 190 mg/dL and a total of 6 clusters for TG values > 150 mg/dL.

Conclusions

The detection of clusters, as well as the representation of choropleth maps, can be of great help in detecting geographic areas that require greater attention to intervene and improve cardiovascular risk.

Cardiovascular diseases (CVD) continue to be the main cause of death in our country. Adequate control of lipid metabolism disorders is a key challenge in cardiovascular prevention that is far from being achieved in real clinical practice. There is a great heterogeneity in the reports of lipid metabolism from Spanish clinical laboratories, which may contribute to its poor control. For this reason, a working group of the main scientific societies involved in the care of patients at vascular risk, has prepared this document with a consensus proposal on the determination of the basic lipid profile in cardiovascular prevention, recommendations for its realization and unification of criteria to incorporate the lipid control goals appropriate to the vascular risk of the patients in the laboratory reports.

Anti-PCSK9 monoclonal antibodies have reduced the risk of cardiovascular events in patients with atheroesclerosis cardiovascular disease. However, its use has not been described in hyperlipidemia associated with lorlatinib, a third-generation ALK tyrosin kinasa inhibitor approved as treatment for ALK-positive non-small cell lung cancer.

Background and aims

Triglycerides are the initiators of the metabolic changes that lead to atherogenic dyslipidemia (AD). The APOA5 and APOA1 genes are involved in the response and metabolism of serum lipids and lipoproteins, where single nucleotide polymorphisms (SNP) rs662799 (promoter region) and rs5070 (intronic region) have been associated with the susceptibility to dyslipidemia. Until now, few studies evaluate the association of these polymorphisms with the presentation of hypertriglyceridemia and AD among Mexican children. Therefore, the objective was to determine the association between rs662799 and rs5070 with hypertriglyceridemia and AD in a pediatric population of southeastern Mexico.

Materials and methods

A case–control analysis was performed including 268 infants aged 2–16 years, anthropometric, clinical variables, and serum lipid profiles were analyzed. DNA was extracted from blood samples and genotyping of polymorphisms was executed with the TaqMan SNP genotyping assay. Allele and genotypic frequencies were calculated. For genetic association analysis, logistic regression models were fitted according to models of inheritance.

Results

The SNP rs662799 (C) was significantly associated with hypertriglyceridemia in the overdominant model (OR = 3.89, p = 0.001) and AD in the dominant model (OR = 4.01, p = 0.001). The SNP rs5070 (T) has a protective effect against hypertriglyceridemia in the additive risk model (OR = 0.68, p = 0.03).

Conclusion

Polymorphism rs662799 was significantly associated with cases of hypertriglyceridemia and AD in minors in southeastern Mexico. On the other hand, rs5070 polymorphism was not associated with cases of hypertriglyceridemia or AD.

Introduction

Chronic kidney disease (CKD) is a major health problem that contributes to the development of cardiovascular disorders such as heart failure and arteriosclerotic cardiovascular disease (ACVD). The aims of this study were to determine the prevalence of CKD and to assess its association with ACVD and cardiometabolic risk factors.

Methods

Cross-sectional observational study conducted in primary care setting. Population-based random sample: 6,588 people between 18 and 102 years old (response rate: 66%). Crude and sex- and age-adjusted prevalence rates of CKD according to KDIGO were determined by assessing albuminuria and estimated glomerular filtration rate according to CKD-EPI, and their associations with cardiometabolic factors and ACVD were determined.

Results

The crude prevalence of CKD was 11.48% (95%CI: 10.72–12.27%), without significant difference between men (11.64% [95%CI: 10.49–12.86%]) and women (11.35% [95%CI: 10.34–12.41%]). The age- and sex-adjusted prevalence rate of CKD was 9.16% (men: 8.61%; women: 9.69%). The prevalence of low estimated glomerular filtration rate (< 60 mL/min/1.73 m²) and albuminuria (≥ 30 mg/g) were 7.95% (95%CI: 7.30–8.61) and 5.98% (95%CI: 5.41–6.55), respectively. Hypertension, diabetes, prediabetes, increased waist-to-height ratio, heart failure, atrial fibrillation, and ACVD were independently associated with CKD (P < .001). Very high cardiovascular risk according to SCORE was found in 77.51% (95%CI: 74.54–80.49) of the population with CKD.

Conclusions

The adjusted prevalence of CKD was 9.2% (low estimated glomerular filtration rate: 8.0%; albuminuria: 6.0%). Most of the patients with CKD had very high cardiovascular risk. Hypertension, diabetes, prediabetes, increased waist-to-height ratio and ACVD were independently associated with CKD.

Objective

Vascular smooth muscle cells (VSMCs) undergo a phenotypic-switching process during the generation of unstable atheroma plaques. In this investigation, the potential implication of the tumor necrosis factor superfamily (TNFSF) ligands, in the gene expression signature associated with VSMC plasticity was studied.

Material and methods

Human aortic (ha)VSMCs were obtained commercially and treated with the cytokine TNFSF14, also called LIGHT, the lymphotoxin alpha (LTα), the heterotrimer LTα₁β₂ or with vehicle for 72 h. The effect of the different treatments on gene expression was analyzed by quantitative PCR and included the study of genes associated with myofibroblast-like cell function, osteochondrogenesis, pluripotency, lymphorganogenesis and macrophage-like cell function.

Results

HaVSMCs displayed a change in myofibroblast-like cell genes which consisted in reduced COL1A1 and TGFB1 mRNA levels when treated with LTα or LIGHT and with augmented MMP9 expression levels when treated with LTα. LTα and LIGHT treatments also diminished the expression of genes associated with osteochondrogenesis and pluripotency SOX9, CKIT, and KLF4. By contrary, all the above genes were no affected by the treatment with the trimer LTα₁β₂. In addition, haVSMC treatment with LTα, LTα₁β₂ and LIGHT altered lymphorganogenic cytokine gene expression which consisted of augmented CCL20 and CCL21 mRNA levels by LTα and a reduction in the gene expression of CCL21 and CXCL13 by LIGHT and LTα₁β₂ respectively. Neither, LTα or LIGHT or LTα₁β₂ treatments affected the expression of macrophage-like cell markers in haVSMC.

Conclusions

Altogether, indicates that the TNFSF ligands through their interconnected network of signaling, are important in the preservation of VSMC identity against the acquisition of a genetic expression signature compatible with functional cellular plasticity.