Family history of early cardiovascular disease in children with moderate to severe hypercholesterolemia: Relationship to lipoprotein (a) and low-density lipoprotein cholesterol levels

1999 ◽  
Vol 133 (3) ◽  
pp. 237-244 ◽  
Author(s):  
Jay A. Barth ◽  
Richard J. Deckelbaum ◽  
Thomas J. Starc ◽  
Steven Shea ◽  
Lori Mosca ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Family History ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A ◽  
Cholesterol Levels ◽  
History Of

scholarly journals Low‐Density Lipoprotein Cholesterol Corrected for Lipoprotein(a) Cholesterol, Risk Thresholds, and Cardiovascular Events

2020 ◽  
Vol 9 (23) ◽  
Author(s):  
Peter Willeit ◽  
Calvin Yeang ◽  
Patrick M. Moriarty ◽  
Lena Tschiderer ◽  
Stephen A. Varvel ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Clinical Care ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cholesterol Content ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A ◽  
The Impact

Background Conventional "low‐density lipoprotein cholesterol (LDL‐C)" assays measure cholesterol content in both low‐density lipoprotein and lipoprotein(a) particles. To clarify the consequences of this methodological limitation for clinical care, our study aimed to compare associations of “LDL‐C” and corrected LDL‐C with risk of cardiovascular disease and to assess the impact of this correction on the classification of patients into guideline‐recommended LDL‐C categories. Methods and Results Lipoprotein(a) cholesterol content was estimated as 30% of lipoprotein(a) mass and subtracted from “LDL‐C” to obtain corrected LDL‐C values (LDL‐C corr30 ). Hazard ratios for cardiovascular disease (defined as coronary heart disease, stroke, or coronary revascularization) were quantified by individual‐patient‐data meta‐analysis of 5 statin landmark trials from the Lipoprotein(a) Studies Collaboration (18 043 patients; 5390 events; 4.7 years median follow‐up). When comparing top versus bottom quartiles, the multivariable‐adjusted hazard ratio for cardiovascular disease was significant for “LDL‐C” (1.17; 95% CI, 1.05–1.31; P =0.005) but not for LDL‐C corr30 (1.07; 95% CI, 0.93–1.22; P =0.362). In a routine laboratory database involving 531 144 patients, reclassification of patients across guideline‐recommended LDL‐C categories when using LDL‐C corr30 was assessed. In “LDL‐C” categories of 70 to <100, 100 to <130, 130 to <190, and ≥190 mg/dL, significant proportions (95% CI) of participants were reassigned to lower LDL‐C categories when LDL‐C corr30 was used: 30.2% (30.0%–30.4%), 35.1% (34.9%–35.4%), 32.9% (32.6%–33.1%), and 41.1% (40.0%–42.2%), respectively. Conclusions “ LDL‐C” was associated with incident cardiovascular disease only when lipoprotein(a) cholesterol content was included in its measurement. Refinement in techniques to accurately measure LDL‐C, particularly in patients with elevated lipoprotein(a) levels, is warranted to assign risk to the responsible lipoproteins.

scholarly journals Risks of Incident Cardiovascular Disease Associated With Concomitant Elevations in Lipoprotein(a) and Low‐Density Lipoprotein Cholesterol—The Framingham Heart Study

2020 ◽  
Vol 9 (18) ◽  
Author(s):  
Mehdi Afshar ◽  
Jian Rong ◽  
Yang Zhan ◽  
Hao Yu Chen ◽  
James C. Engert ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Absolute Risk ◽  
Clinical Care ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A ◽  
Incident Cardiovascular Disease

Background Elevated lipoprotein(a) is a well‐established risk factor for atherosclerotic vascular disease but is not measured in routine clinical care. Screening of high lipoprotein(a) in individuals with moderate elevations of low‐density lipoprotein cholesterol (LDL‐C) may identify individuals at high risk of cardiovascular disease. Methods and Results We examined 2606 Framingham Offspring participants (median age, 54 years; 45% men) prospectively with a median follow‐up of 15 years (n=392 incident cardiovascular events). Individuals with higher (≥100 nmol/L) versus lower lipoprotein(a) were divided into groups based on LDL‐C <135 mg/dL versus ≥135 mg/dL. In Cox models, after adjustment for known risk factors, high lipoprotein(a) (≥100 nmol/L) and LDL‐C ≥135 mg/dL were each significant predictors of cardiovascular disease (LDL‐C ≥135 mg/dL: hazard ratio [HR], 1.34; 95% CI, 1.09–1.64; P =0.006; high lipoprotein (a): HR, 1.31; 95% CI, 1.03–1.66; P =0.026). Across the groups of high/low lipoprotein (a) and LDL‐C ≥135 mg/dL or <135 mg/dL, the absolute cardiovascular disease risks at 15 years were 22.6% (high lipoprotein(a)/LDL‐C ≥135 mg/dL, n=248), 17.3% (low lipoprotein(a)/LDL‐C ≥135 mg/dL, n=758), 12.7% (high lipoprotein(a)/LDL‐C <135 mg/dL, n=275) and 11.5% (low lipoprotein(a)/LDL‐C <135 mg/dL, n=1328, reference group). Among individuals with LDL‐C ≥135 mg/dL, those with high lipoprotein(a) had a 43% higher risk (HR, 1.43; 95% CI, 1.05–1.97; P =0.02). Presence of high lipoprotein(a) with moderate LDL‐C levels (135–159 mg/dL) yielded absolute risks equivalent to those with LDL‐C ≥160 mg/dL (23.5%, 95% CI, 17.4%–31.3%; and 20.7%, 95% CI, 16.8%–25.3%, respectively). Conclusions Concomitant elevation of LDL‐C ≥135 mg/dL and lipoprotein(a) ≥100 nmol/L is associated with a high absolute risk of incident cardiovascular disease. lipoprotein(a) measurement in individuals with moderate elevations in LDL‐C, who do not otherwise meet criteria for statins, may identify individuals at high cardiovascular risk.

scholarly journals Genetic Predisposition to Low-Density Lipoprotein Cholesterol May Increase Risks of Both Individual and Familial Alzheimer's Disease

2022 ◽  
Vol 8 ◽  
Author(s):  
Jiang-Shan Tan ◽  
Meng-Jin Hu ◽  
Yan-Min Yang ◽  
Yue-Jin Yang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Family History ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
History Of ◽  
Mr Study

Background: Previous observational studies provided conflicting results on the association between low-density lipoprotein cholesterol (LDL-C) level and the risk of Alzheimer's disease (AD).Objective: We used two-sample Mendelian randomization (MR) study to explore the causal associations between LDL-C level and the risks of individual, paternal, maternal, and family history of AD.Methods: Summary-level genetic data for LDL-C were acquired from results of the UK Biobank GWAS. Corresponding data for paternal, maternal, and family history of AD were obtained from the NHGRI-EBI Catalog of human genome-wide association studies. Data for individual AD were obtained from the MR-Base platform. A two-sample MR study was performed to explore the causal association between LDL-C level and the risks of individual, paternal, maternal, and family history of AD.Results: Genetically predicted LDL-C was positively associated with individual [Odds ratio (OR) = 1.509, 95% confidence interval (CI) = 1.140–1.999; P = 4.0 × 10−3], paternal [OR = 1.109, 95% CI = 1.053–1.168; P = 9.5 × 10−5], maternal [OR = 1.132, 95% CI = 1.070–1.199; P = 2.0 × 10−5], and family history of AD [OR = 1.124, 95% CI = 1.070–1.181; P = 3.7 × 10−6] in inverse variance weighted analysis. After performing weighted median and MR-Egger analysis, consistent results were observed. There was no horizontal pleiotropy in the two-sample MR analysis.Conclusions: High level of LDL-C may increase the risks of both individual and familial AD. Decreasing the LDL-C to a reasonable level may help to reduce the related risk.

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