Clínica e Investigación en Arteriosclerosis (English Edition)最新文献

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.

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: 6588 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 (eGFR) 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 eGFR (<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 < 0.001). Very high cardiovascular risk (CVR) 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 eGFR: 8.0%; albuminuria: 6.0%). Most of the patients with CKD had very high CVR. Hypertension, diabetes, prediabetes, increased waist-to-height ratio and ACVD were independently associated with CKD.

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.

Objective

The objective of this paper has focused on assessing the level of health-related lifestyle acquired in Spanish adults in the Spanish cities of Albacete and Murcia, and analyzing the existing differences according to sex and age.

Material and methods

On a sample of 788 subjects aged between 22 and 72, the Health-related Lifestyle Assessment Scale was applied, consisting of 52 items and structured in 7 dimensions that explained a total variance of 66.87% and a Cronbach’s alpha of 0.894.

Results

A percentage of 12 of the adults surveyed have a healthy lifestyle, 53% show a trend to health and 35% poor or unhealthy. Pearson’s χ² tests show a positive and significant association of women with health and a trend of significant improvement in lifestyle with age. The inferential data (t-Student tests and one-factor ANOVA) confirm these differences according to gender and age.

Conclusions

It is necessary to promote preventive programs to improve health in the habits of the population, especially in the 35% that show a poor or unhealthy level of lifestyle.

Despite current standards of care, a considerable risk of atherosclerotic cardiovascular disease remains in both primary and secondary prevention. In this setting, clonal hematopoiesis driven by somatic mutations has recently emerged as a relatively common, potent and independent risk factor for atherosclerotic cardiovascular disease and other cardiovascular conditions. Experimental studies in mice suggest that mutations in TET2 and JAK2, which are among the most common in clonal hematopoiesis, increase inflammation and are causally connected to accelerated atherosclerosis development, which may explain the link between clonal hematopoiesis and increased cardiovascular risk. In this review, we provide an overview of our current understanding of this emerging cardiovascular risk factor.

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.

Background

Lifestyle modifications have been recommended as an essential treatment approach for cardiovascular diseases. Recent studies have shown that eating frequency (EF) correlates with hypertension and related risk of organ damage. This study aimed to examine critical clinical implications to evaluate the association of EF with arterial stiffness parameters as an early marker of atherosclerosis manifestations.

Methods

A cross-sectional descriptive study was performed on 658 participants of the PERSIAN Organizational Cohort study in Mashhad, aged 30–70 years. Arterial stiffness was assessed by measurement markers of arteriosclerosis, including arterial age, augmentation index (AIx), augmentation pressure (AP), carotid-femoral pulse wave velocity (Cf-PWV), and central blood pressure. Differences in anthropometric indices, blood indices, and arterial stiffness parameters were evaluated across EF groups.

Results

Our data demonstrate that EF was positively correlated with total daily energy intake, and favourable profiles of adiposity and blood lipids. Subjects with an increased EF, had significantly lower AIx, AP, Arterial Age and Central blood pressure (P for trend < 0.001) as compared to Lowest EF and not significant with PWV (P for trend, 0.19). Arterial stiffness was also significantly lower in those with increased EF compared with subjects with low EF. By Linear regression analysis, after adjustment for Confounding factors, except PWV, EF showed the associations with all of the non-invasive arterial stiffness parameters.

Conclusion

Increased EF is associated with a lower wave reflection and blood pressure in the central arteries.

Vascular smooth muscle cells (VSMCs) constitute the principal cellular component of the medial layer of arteries and are responsible for vessel contraction and relaxation in response to blood flow. Alterations in VSMCs can hinder vascular system function, leading to vascular stiffness, calcification and atherosclerosis, which in turn may result in life-threatening complications. Pathological changes in VSMCs typically correlate with chronological age; however, there are certain conditions and diseases, such as Hutchinson-Gilford progeria syndrome (HGPS), that can accelerate this process, resulting in premature vascular aging. HGPS is a rare genetic disorder characterized by severe VSMC loss, accelerated atherosclerosis and death from myocardial infarction or stroke during the adolescence. Because experiments with mouse models have demonstrated that alterations in VSMCs are responsible for early atherosclerosis in HGPS, studies on this disease can provide insights into the mechanisms of vascular aging and assess the relative contribution of VSMCs to this process.

Familial chylomicronemia syndrome (FCS) is a genetic entity with autosomal recessive inheritance. Mutations in genes (such as APOC2, APOAV, LMF-1, GPIHBP-1) that code for proteins that regulate the maturation, transport, or polymerization of lipoprotein lipase-1 are the most common causes, but not the only ones. The objective of this study was to report the first documented case in Ecuador.

Clinical case

A 38-year-old man presented with chronic hepatosplenomegaly, thrombocytopenia, pancreatic atrophy, and severe hypertriglyceridemia refractory to treatment. A molecular analysis was performed by next generation sequencing that determined a deficiency of Lipoprotein Lipase OMIM #238600 in homozygosis. Genetic confirmation is necessary in order to establish the etiology of HTGS for an adequate management of this pathology.