Objective: To evaluate low-density lipoprotein-cholesterol (LDLc) achieved in patients with genetic dyslipidemia treated during one year in Lipid and Vascular Risk Units (LVRU) of the Spanish Society of Arteriosclerosis (SSA).
Design: Observational, longitudinal, retrospective, multicenter national study that included consecutive patients of both sexes over 18 years of age referred due to dyslipidemia to LVRU of the SSA. Information was collected from medical records corresponding to two visits in the lipid unit.
Results: A total of 527 patients (mean age 48 years, 60.0% men) diagnosed with genetic dyslipidemia (241 with heterozygous familial hypercholesterolemia, and 286 with familial combined hyperlipidemia) were included. The mean follow-up was 12.9 months. In the last visit, 94% were taking statins, one third combined with ezetimibe, although only 41% were taking a high-intensity hypolipidemic treatment. Overall, 28.5% of patients attained an LDLc level<100 mg/dL, 35.8% decreased their LDLc by >50%, and 53.8% achieved one of the two. Predictors of target LDLc levels in the multivariate analysis were age, smoking habit and the presence of vascular disease.
Conclusion: Over half of the patients with genetic dyslipidemia followed up by LVRU of SSA achieve LDLc objectives after one year of follow-up. The use of high-intensity hypolipidemic treatment could improve these results.
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http://dx.doi.org/10.1016/j.arteri.2014.04.001 | DOI Listing |
Arch Dermatol Res
January 2025
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Observational studies have shown that the risk of developing herpes zoster (HZ) increases with the use of statins. However, there are many confounding factors in observational studies. Therefore, our Mendelian randomization (MR) study aimed to explore the causal role of lipids in HZ and to assess the causal impact of lipid-lowering drug targets on HZ risk.
View Article and Find Full Text PDFCurr Atheroscler Rep
January 2025
Carbohydrate and Lipid Metabolism Research Unit, Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa.
Purpose Of Review: Homozygous familial hypercholesterolaemia (HoFH) is characterized by marked elevation of low-density lipoprotein cholesterol (LDLC) and premature atherosclerotic cardiovascular disease. This is a review of novel pharmacological therapies to lower LDLC in patients with HoFH.
Recent Findings: Novel therapies can be broadly divided by whether their efficacy is dependent or independent of residual low-density lipoprotein receptor (LDLR) function.
Alzheimers Dement
December 2024
Washington University School of Medicine, Saint Louis, MO, USA.
Background: A recent case report described an individual who was a homozygous carrier of the APOE3 Christchurch (APOE3ch) mutation and resistant to autosomal dominant Alzheimer's Disease (AD) caused by a PSEN1-E280A mutation. Whether APOE3ch contributed to the protective effect remains unclear.
Method: We generated a humanized APOE3ch knock-in mouse and crossed it to an amyloid-β (Aβ) plaque-depositing model.
Alzheimers Dement
December 2024
Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Background: The Brazilian population has been experiencing an increase in the number of older adults, with a simultaneous rise in the incidence of Mild Cognitive Impairment (MCI) and Alzheimer's Disease (AD). Telomeres are structures located at the ends of chromosomes that maintain the structural integrity of the chromosome. There is a shortage of studies correlating telomeres and cognition.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Medical Analysis, Faculty of Applied Science, Tishk International University, KRG, Erbil, Iraq.
Dyslipidemia, an imbalance in blood lipid levels, is a frequent complication of type 2 diabetes mellitus (DM2) and heightens the risk of cardiovascular diseases (CVDs). Statins, which inhibit 3-hydroxy-3-methylglutaryl-CoA reductase, are potent competitive inhibitors that reduce plasma cholesterol levels. However, individual responses to statins can vary markedly, possibly due to genetic variations in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene.
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