3,308 publications found
Sort by
Impact of the Spanish consensus for improving lipid control on patients admitted for an acute coronary syndrome.

In 2020, the Spanish Society of Cardiology published a consensus to improve lipid control in secondary prevention patients. This study was aimed to assess the impact of the implementation of this consensus in clinical practice. Non-interventional, national and multicenter study, with a prospective and retrospective design in two cohorts. Implementation of the consensus was performed on the prospective cohort. Prospective cohort included patients with acute coronary syndrome (ACS) from December 2020 to March 2022 and were followed-up for 3 months. Retrospective cohort included patients with ACS in the same hospital, matched for main baseline clinical characteristics, between August 2019 to February 2020, with a follow-up of 3 months. Additionally, patients were included if they had previously received lipid-lowering therapy and LDL cholesterol (LDL-C) was >55mg/dL. A total of 516 patients were included (245 in the prospective cohort and 271 in the retrospective cohort). Overall, mean age was 67.9±11.4 years, 73.8% were men, and 35.8% had diabetes. At discharge, 98.4% and 98.9%, respectively (P=0.71) were taking statins (90.6% vs 88.9%; P=0.564 high intensity statins), 58.4% vs 33.2%; P<0.001 ezetimibe, 1.2% vs 0.4%; P=0.35 PCSK9 inhibitors. During the follow-up, the dose of statins was increased in 11.4% vs 3.3% (P<0.001), and ezetimibe was added in 25.7% vs 25.8% (P=0.976). At study end, significantly more patients achieved LDL-C <55mg/dL in the prospective cohort (45.6% vs 33.5%; p=0.013). The implementation of the Spanish lipid consensus was associated with a significant improvement of LDL-C control after only 3 months.

Open Access
Missense mutation Q384K in the APOB gene affecting the large lipid transfer module of apoB reduces the secretion of apoB-100 in the liver without reducing the secretion of apoB-48 in the intestine.

Molecular genetic testing of patients with hypobetalipoproteinemia may identify a genetic cause that can form the basis for starting proper therapy. Identifying a genetic cause may also provide novel data on the structure-function relationship of the mutant protein. To identify a genetic cause of hypobetalipoproteinemia in a patient with levels of low density lipoprotein cholesterol at the detection limit of 0.1 mmol/l. DNA sequencing of the translated exons with flanking intron sequences of the genes adenosine triphosphate-binding cassette transporter 1, angiopoietin-like protein 3, apolipoprotein B, apolipoprotein A1, lecithin-cholesterol acyltransferase, microsomal triglyceride transfer protein and proprotein convertase subtilisin/kexin type 9. The patient was homozygous for mutation Q384K (c.1150C>A) in the apolipoprotein B gene, and this mutation segregated with hypobetalipoproteinemia in the family. Residue Gln384 is located in the large lipid transfer module of apoB that has been suggested to be important for lipidation of apolipoprotein B through interaction with microsomal triglyceride transfer protein. Based on measurements of serum levels of triglycerides and apolipoprotein B-48 after an oral fat load, we conclude that the patient was able to synthesize apolipoprotein B-48 in the intestine in a seemingly normal fashion. Our data indicate that mutation Q384K severely reduces the secretion of apolipoprotein B-100 in the liver without reducing the secretion of apolipoprotein B-48 in the intestine. Possible mechanisms for the different effects of this and other missense mutations affecting the large lipid transfer module on the two forms of apoB, are discussed.

Severe hypertriglyceridemia prevalence at a primary care setting in Catalonia, Spain.

Hypertriglyceridemia (HTG) increases the risk of cardiovascular disease and pancreatitis, and its prevalence varies across populations. To determine the prevalence of moderate-to-severe hypertriglyceridemia (msHTG, 500-879mg/dl) and severe hypertriglyceridemia (sHTG, ≥ 880mg/dl) in a primary care population in Catalonia, Spain, and to categorize them according to presence/absence of factors potentially causing HTG. Retrospective analysis of clinical and laboratory data in SIDIAP (Information System for the Development of Primary Care Research) from 2010, 2013, 2016, and 2019. We considered medications with hypolipidemic effects and those potentially increasing TG levels. We developed logistic regression models adjusted by age and sex to calculate the probability of having ms/sHTG according to covariates of interest. In the study years, 36.2‒42.0% of the >3.5 million active primary care users had ≥1 TG determination. Prevalence for msHTG was 0.7% and for sHTG 0.2% among those with recorded TG. In 2019, 54.7% were female; median (IQR) age was 62.5 (49.4‒73.7) years. Prevalence was higher in 36‒50-year-old persons (1.3% msHTG, 0.4% sHTG) and men (1.1% msHTG, 0.3% sHTG). Most cases were associated with secondary and <20% with non-secondary causes, the latter being most prevalent in young patients. The secondary causes more strongly associated with msHTG/sHTG were obesity, uncontrolled diabetes mellitus (DM) and gamma-glutamyl transferase >100U/L. The prevalence of msHTG was 0.7% and that of sHTG was 0.2% between 2010 and 2019 among individuals with recorded TG. msHTG/sHTG most often affected men around their fifties and people with obesity and uncontrolled DM. Most msHTG and sHTG cases were associated with the presence of secondary causes.