Letter by Saleh Regarding Article, “Carotid Atherosclerosis Evolution When Targeting a Low-Density Lipoprotein Cholesterol Concentration <70 mg/dL After an Ischemic Stroke of Atherosclerotic Origin”

OBJECTIVE: The aim of this study was to evaluate lipoprotein(a) (Lp(a)), total cholesterol, high density lipoprotein cholesterol (HDL), low density lipoprotein cholesterol (LDL), very low density lipoprotein cholesterol (VLDL ), triglycerides , apolipoprotein A (apo A) and B100 (apo B100), uric acid, glycaemic and insulin plasmatic concentrations in patients affected by acute stroke. In this group of patients, we have compared the variables between type 2 diabetic patients and non-diabetic patients. METHOD: We evaluate a total of 34 non-diabetic patients (22 males and 12 females; mean age 66.71 ± 10.83 years) and a group of 26 type 2 diabetic patients (15 males and 11 females; mean age 66.35 ± 9.92 years) in a cross-sectional study. RESULTS: Mean Lp(a) concentration did not significantly differ between type 2 diabetic patients and non-diabetic subjects (29.49 ± 23.09 vs 44.81 ± 44.34 mg/dl). The distribution of Lp(a)levels was highly skewed towards the higher levels in both groups, being over 30 mg/dl in 50%. Lp(a) concentration was positively correlated with abdominal adiposity, using waist-hip ratio(WHR)(p< 0.05). No association was found between Lp(a) and others risk factors like sex, age, other lipidic parameters and the presence of stroke. CONCLUSIONS: Our results showed that there were no significant differences between diabetic and non-diabetic patients' serum Lp(a) levels, which indicates that elevated Lp(a) levels were associated with ischemic stroke, irrespective of the presence of type 2 diabetes mellitus (type 2 DM).

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Positive association between small dense low-density lipoprotein cholesterol concentration and biomarkers of inflammation, thrombosis, and prediabetes in non-diabetic adults

Atherosclerosis ◽

10.1016/j.atherosclerosis.2018.06.806 ◽

2018 ◽

Vol 275 ◽

pp. e253

Author(s):

T. Su

Keyword(s):

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Positive Association ◽

Lipoprotein Cholesterol ◽

Cholesterol Concentration ◽

Low Density ◽

Low Density Lipoprotein Cholesterol

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Lipoprotein cholesterol concentrations in the plasma of human subjects as measured in the fed and fasted states.

Clinical Chemistry ◽

10.1093/clinchem/34.12.2456 ◽

1988 ◽

Vol 34 (12) ◽

pp. 2456-2459 ◽

Cited By ~ 68

Author(s):

J S Cohn ◽

J R McNamara ◽

E J Schaefer

Keyword(s):

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Plasma Triglyceride ◽

Lipoprotein Cholesterol ◽

Cholesterol Concentration ◽

Low Density ◽

Low Density Lipoprotein Cholesterol ◽

Plasma Triglyceride Concentration ◽

Triglyceride Concentration ◽

Friedewald Formula

Abstract Lipoprotein cholesterol concentrations in plasma are routinely estimated by using the Friedewald formula, whereby very-low-density lipoprotein cholesterol (VLDL-C) is estimated to be one-fifth the plasma triglyceride concentration. Ordinarily, this formula is applied only to plasma sampled from patients in the fasted state. To determine whether lipoprotein cholesterol measurements are altered substantially in plasma sampled from nonfasting subjects, we obtained postprandial blood samples from 22 healthy subjects (nine men, 13 women, ages 22-79 years) fed a fat-rich meal (1 g fat per kilogram body wt.). The plasma triglyceride concentration increased postprandially in all subjects (233 +/- 16% of baseline at 3 h). The mean cholesterol concentration in plasma was essentially unchanged. High-density lipoprotein cholesterol (HDL-C) was significantly decreased (94 +/- 2% at 3 h, P less than 0.001). VLDL-C and low-density lipoprotein cholesterol (LDL-C), estimated by the Friedewald formula, were compared with measurements obtained by modified Lipid Research Clinics (LRC) methodology. As measured by either method, VLDL-C increased and LDL-C decreased significantly after the fat-rich meal. These postprandial changes were significantly greater (P less than 0.01) when estimated by the Friedewald formula than by LRC methodology. We conclude that (a) lipoprotein cholesterol concentrations measured in the fed subject differ significantly from those measured in the fasted subject, and (b) plasma must be obtained after at least a 12-h fast if an individual's risk of coronary heart disease is to be accurately assessed.

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Statin-based therapy for primary and secondary prevention of ischemic stroke: A meta-analysis and critical overview

International Journal of Stroke ◽

10.1177/1747493019873594 ◽

2019 ◽

Vol 15 (4) ◽

pp. 377-384 ◽

Cited By ~ 1

Author(s):

Haralampos Milionis ◽

George Ntaios ◽

Eleni Korompoki ◽

Konstantinos Vemmos ◽

Patrik Michel

Keyword(s):

Ischemic Stroke ◽

Secondary Prevention ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Lipoprotein Cholesterol ◽

Lipid Lowering ◽

Low Density ◽

Low Density Lipoprotein Cholesterol ◽

Primary And Secondary Prevention ◽

Prevention Trials

Background and aims To reassess the effect of statin-based lipid-lowering therapy on ischemic stroke in primary and secondary prevention trials with regard to achieved levels of low-density lipoprotein-cholesterol in view of the availability of novel potent hypolipidemic agents. Methods English literature was searched (up to November 2018) for publications restricted to trials with a minimum enrolment of 1000 and 500 subjects for primary and secondary prevention, respectively, meeting the following criteria: adult population, randomized controlled design, and recorded outcome data on ischemic stroke events. Data were meta-analyzed and curve-estimation procedure was applied to estimate regression statistics and produce related plots. Results Four primary prevention trials and four secondary prevention trials fulfilled the eligibility criteria. Lipid-lowering therapy was associated with a lower risk of ischemic stroke in primary (risk ratio, RR 0.70, 95% confidence interval, CI, 0.60–0.82; p < 0.001) and in the secondary prevention setting (RR 0.80, 95% CI 0.70–0.90; p < 0.001). Curve-estimation procedure revealed a linear relationship between the absolute risk reduction of ischemic stroke and active treatment-achieved low-density lipoprotein-cholesterol levels in secondary prevention (adjusted R-square 0.90) in support of “the lower the better” hypothesis for stroke survivors. On the other hand, the cubic model followed the observed data well in primary prevention (adjusted R-square 0.98), indicating greater absolute risk reduction in high-risk cardiovascular disease-free individuals. Conclusions Statin-based lipid-lowering is effective both for primary and secondary prevention of ischemic stroke. Most benefit derives from targeting disease-free individuals at high cardiovascular risk, and by achieving low treatment targets for low-density lipoprotein-cholesterol in stroke survivors.

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Elevation of Low-Density Lipoprotein Cholesterol Concentration with Over-the-Counter Fish Oil Supplementation

Annals of Pharmacotherapy ◽

10.1345/aph.1h695 ◽

2007 ◽

Vol 41 (7-8) ◽

pp. 1296-1300 ◽

Cited By ~ 5

Author(s):

Jennifer M Malinowski ◽

Kimberly Metka

Keyword(s):

Fish Oil ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Lipoprotein Cholesterol ◽

Cholesterol Concentration ◽

Low Density ◽

Low Density Lipoprotein Cholesterol ◽

Over The Counter ◽

Epa And Dha ◽

Fish Oil Supplementation

Objective: To report a case of elevated low-density lipoprotein cholesterol (LDL-C) concentration in a patient taking fish oil supplements for hypertriglyceridemia. Case Summary: A 63-year-old white woman had been taking 2.7 g of eico-sapentaenotc acid (EPA) and docosahexaenoic acid (DHA) daily in 9 g of over-the-counter (OTC) fish oil capsules for triglyceride lowering. Prior to the adverse event, she had baseline fasting triglyceride (TG) and LDL-C concentrations of 278 mg/dL and 106 mg/dL, respectively. After 6 weeks of treatment with fish oil, fasting TG levels decreased by 47.5% (-132 mg/dL) and the LDL-C increased by 75% (+80 mg/dL). Discontinuation of therapy for 6 weeks resulted in TG returning to high concentrations (334 mg/dL; +56 mg/dL change from baseline) and LDL-C decreasing toward baseline (143 mg/dL; +37 mg/dL change from baseline). Discussion: Fish oil, an omega-3 polyunsaturated fatty acid, consists of EPA and DHA. EPA and DHA are thought to inhibit the synthesis of triglycerides in the liver. Type IV dyslipidemic patients may develop increased LDL-C levels while taking fish oil to lower triglycerides due to possible down-regulation of the LDL-C receptor in hepatic cells and formation of larger LDL particles. Use of the Naranjo probability scale indicates a probable relationship between elevations in LDL-C from baseline and initiation of fish oil treatment for hypertriglyceridemia. It is unknown whether any component within this particular product could have contributed to such an unusual elevation in LDL-C. Conclusions: This case documents a much higher LDL-C elevation associated with OTC fish oil supplementation than has been previously identified in the literature. Healthcare providers should be advised that LDL-C levels may increase with use of OTC fish oil and should monitor patients periodically for such elevations. The significance of this Increase on clinical outcomes is not known.

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