scholarly journals Assessing the Accuracy of Estimated Lipoprotein(a) Cholesterol and Lipoprotein(a)‐Free Low‐Density Lipoprotein Cholesterol

2022 ◽  
Author(s):  
Weili Zheng ◽  
Michael Chilazi ◽  
Jihwan Park ◽  
Vasanth Sathiyakumar ◽  
Leslie J. Donato ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Particle Number ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Interquartile Range ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Lipoprotein A ◽  
C 50

Background Accurate measurement of the cholesterol within lipoprotein(a) (Lp[a]‐C) and its contribution to low‐density lipoprotein cholesterol (LDL‐C) has important implications for risk assessment, diagnosis, and treatment of atherosclerotic cardiovascular disease, as well as in familial hypercholesterolemia. A method for estimating Lp(a)‐C from particle number using fixed conversion factors has been proposed (Lp[a]‐C from particle number divided by 2.4 for Lp(a) mass, multiplied by 30% for Lp[a]‐C). The accuracy of this method, which theoretically can isolate “Lp(a)‐free LDL‐C,” has not been validated. Methods and Results In 177 875 patients from the VLDbL (Very Large Database of Lipids), we compared estimated Lp(a)‐C and Lp(a)‐free LDL‐C with measured values and quantified absolute and percent error. We compared findings with an analogous data set from the Mayo Clinic Laboratory. Error in estimated Lp(a)‐C and Lp(a)‐free LDL‐C increased with higher Lp(a)‐C values. Median error for estimated Lp(a)‐C <10 mg/dL was −1.9 mg/dL (interquartile range, −4.0 to 0.2); this error increased linearly, overestimating by +30.8 mg/dL (interquartile range, 26.1–36.5) for estimated Lp(a)‐C ≥50 mg/dL. This error relationship persisted after stratification by overall high‐density lipoprotein cholesterol and high‐density lipoprotein cholesterol subtypes. Similar findings were observed in the Mayo cohort. Absolute error for Lp(a)‐free LDL‐C was +2.4 (interquartile range, −0.6 to 5.3) for Lp(a)‐C<10 mg/dL and −31.8 (interquartile range, −37.8 to −26.5) mg/dL for Lp(a)‐C≥50 mg/dL. Conclusions Lp(a)‐C estimations using fixed conversion factors overestimated Lp(a)‐C and subsequently underestimated Lp(a)‐free LDL‐C, especially at clinically relevant Lp(a) values. Application of inaccurate Lp(a)‐C estimations to correct LDL‐C may lead to undertreatment of high‐risk patients.

scholarly journals Relationship between C-reactive protein and features of the metabolic syndrome in military pilots in the Serbia and Montenegro

2005 ◽  
Vol 62 (11) ◽  
pp. 811-819
Author(s):  
Aleksandra Jovelic ◽  
Goran Radjen ◽  
Stojan Jovelic ◽  
Marica Markovic
Keyword(s):  
Metabolic Syndrome ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
C Reactive Protein ◽  
Low Density Lipoprotein Cholesterol ◽  
Reactive Protein

Background/Aim. C-reactive protein is an independent predictor of the risk of cardiovascular events and diabetes mellitus in apparently healthy men. The relationship between C-reactive protein and the features of metabolic syndrome has not been fully elucidated. To assess the cross-sectional relationship between C-reactive protein and the features of metabolic syndrome in healthy people. Methods. We studied 161 military pilots (agee, 40?6 years) free of cardiovascular disease, diabetes mellitus and active inflammation on their regular annual medical control. Age, total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglycerides, fasting glucose, glycosylated hemoglobin, blood pressure, smoking habit, waist circumference and body mass index were evaluated. Plasma C-reactive protein was measured by the immunonephelometry (Dade Behring) method. Metabolic syndrome was defined according to the National Cholesterol Education Program Expert Panel. Results. The mean C-reactive protein concentrations in the subjects grouped according to the presence of 0, 1, 2 and 3 or more features of the metabolic syndrome were 1.11, 1.89, 1.72 and 2.22 mg/L, respectively (p = 0.023) with a statistically, significant difference between those with 3, and without metabolic syndrome (p = 0.01). In the simple regression analyses C-reactive protein did not correlate with the total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, body mass index and blood pressure (p > 0.05). In the multiple regression analysis, waist circumference (? = 0.411, p = 0.000), triglycerides to high density lipoprotein cholesterol ratio (? = 0.774, p = 0.000), smoking habit (? = 0.236, p = 0.003) and triglycerides (? = 0.471, p = 0.027) were independent predictors of C-reactive protein. Conclusions. Our results suggested a cross-sectional independent correlation between the examined cardiovascular risk factors as the predominant features of metabolic syndrome and C-reactive protein in the group of apparently healthy subjects. The lack of correlation of C-reactive protein with the total cholesterol and low density lipoprotein cholesterol in our study may suggest their different role in the process of atherosclerosis and the possibility to determine C-reactive protein in order to identify high-risk subjects not identified with cholesterol screening.

The Effects of Low-Density Lipoprotein and High-Density Lipoprotein on Blood Viscosity Correlate with their Association with Risk of Atherosclerosis in Humans

1997 ◽  
Vol 92 (5) ◽  
pp. 473-479 ◽  
Author(s):  
Gregory D. Sloop ◽  
David W. Garber
Keyword(s):  
High Density Lipoprotein ◽  
Total Cholesterol ◽  
High Density Lipoprotein Cholesterol ◽  
Blood Viscosity ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol

1. Increased blood or plasma viscosity has been observed in almost all conditions associated with accelerated atherosclerosis. Cognizant of the enlarging body of evidence implicating increased viscosity in atherogenesis, we hypothesize that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis. 2. Blood viscometry was performed on samples from 28 healthy, non-fasting adult volunteers using a capillary viscometer. Data were correlated with haematocrit, fibrinogen, serum viscosity, total cholesterol, high-density lipoprotein-cholesterol, triglycerides and calculated low-density lipoprotein-cholesterol. 3. Low-density lipoprotein-cholesterol was more strongly correlated with blood viscosity than was total cholesterol (r = 0.4149, P = 0.0281, compared with r = 0.2790, P = 0.1505). High-density lipoprotein-cholesterol levels were inversely associated with blood viscosity (r = −0.4018, P = 0.0341). 4. To confirm these effects, viscometry was performed on erythrocytes, suspended in saline, which had been incubated in plasma of various low-density lipoprotein/high-density lipoprotein ratios. Viscosity correlated directly with low-density lipoprotein/high-density lipoprotein ratio (n = 23, r = 0.8561, P < 0.01). 5. Low-density lipoprotein receptor occupancy data suggests that these effects on viscosity are mediated by erythrocyte aggregation. 6. These results demonstrate that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity in healthy subjects correlate with their association with risk of atherosclerosis. These effects on viscosity may play a role in atherogenesis by modulating the dwell or residence time of atherogenic particles in the vicinity of the endothelium.

Sign in / Sign up

Export Citation Format

Share Document