Genest, J. et al. 2009 Canadian Cardiovascular Society/Canadian guidelines for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease in the adult-2009 recommendations. Can. J. Cardiol. 25, 567-579

McGill University Health Centre, Montreal, Canada.
The Canadian journal of cardiology (Impact Factor: 3.94). 10/2009; 25(10):567-79. DOI: 10.1016/S0828-282X(09)70715-9
Source: PubMed

ABSTRACT The present article represents the 2009 update of the Canadian Cardiovascular Society guidelines for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease in the adult.

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Available from: Robert A Hegele, Feb 13, 2015
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    • "Hyperlipidaemia has an important effect on development and progression of various cardiovascular diseases and atherosclerosis. Both moderate hyperlipidaemia and severe hyperlipidaemia are associated with cardiovascular disease [6]. Recent study indicates that a fundamental defect is an overproduction of large VLDL-C, which triggers a sequence of lipoprotein changes, leading to increased remnant particles, smaller LDL-C, and decreased HDL-C [7]. "
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    ABSTRACT: Ultraperformance liquid chromatography coupled with quadrupole time-of-flight synapt high-definition mass spectrometry metabolomics was used to characterize the urinary metabolic profiling of diet-induced hyperlipidaemia in a rat model. Analysis was done by orthogonal partial least squares discriminant analysis, correlation analysis, heat map analysis, and KEGG pathways analysis. Potential biomarkers were chosen by S-plot and were identified by accurate mass, isotopic pattern, and MS/MS fragments information. Significant differences in fatty acid, amino acid, nucleoside, and bile acid were observed, indicating the perturbations of fatty acid, amino acid, nucleoside, and bile acid metabolisms in diet-induced hyperlipidaemia rats. This study provides further insight into the metabolic profiling across a wide range of biochemical pathways in response to diet-induced hyperlipidaemia.
    Journal of Analytical Methods in Chemistry 03/2014; 2014(11):184162. DOI:10.1155/2014/184162 · 0.79 Impact Factor
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    • "However, despite current therapeutic use of statins as monotherapy even in optimal doses and achieving target LDL-C reduction, a significant number of patients with mixed atherogenic dyslipidemia are at high risk for coronary events (Grundy et al. 2004). The Friedewald equation which is frequently used to estimate LDL-C in routine patient care; is a central focus of clinical practice guidelines throughout the world, including in the United States (Smith et al. 2011), Europe (Reiner et al. 2011), and Canada (Genest et al. 2009). The Friedewald equation indirectly estimates LDL-C as total cholesterol minus high-density lipoprotein cholesterol minus triglycerides/5 in milligrams per deciliter. "
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    ABSTRACT: Objective: The Friedewald equation is frequently used to estimate low-density lipoprotein cholesterol (LDL-C) in routine patient care; however, recently many limitations have emerged regarding its use. Aim: Analyse the use of Friedewald equation for dyslipidemia in metabolic syndrome. Methods: Subjects were selected with metabolic syndrome that fulfilled consensus statement for Asians Indians and excluded those with triglyceride (TG) ≥400mg/dl, and chronic liver and/or kidney disease. Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), TGs, and LDL-C were measured with direct assays. LDL-C was further estimated using the equation and compared with LDL-C by direct assay. Results: The mean and standard deviation of TC, TGs, HDL-C, and LDL-C were 194.77±24.38mg/dl, 174.84±60.27mg/dl (p<0.0001), 40.68±5.40mg/dl (p<0.05), and 122.30±19.30mg/dl among subjects with metabolic syndrome. On the other hand, Friedewald estimated LDL-C and VLDL-C were 121.29±18.84mg/dl and 35.08±12.65mg/dl (p<0.0001). Furthermore, a statistically significant higher TGs/HDL-C (p<0.0001) and LDL-C/HDL-C ratios was observed in subjects with metabolic syndrome. However, no significant differ-ence was recorded between the two methods of estimating LDL-C. Conclusion: TGs/HDL-C was found significantly higher among subjects with metabolic syndrome; however, no significant difference between both Friedewald equation and direct measurement method for LDL-C estimation was observed. Hence, the accuracy of LDL-C estimation formulas and direct methods for measurement in patients with the metabolic syndrome requires further exploration. Keywords: Dyslipidemia, Friedewald Equation, Metabolic Syndrome.
    02/2014; 2(1). DOI:10.14419/ijm.v2i1.2370
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    • "Guidelines for target levels of plasma lipids are based on results from randomized controlled trials and from meta-analyses. The absolute target levels still are under debate, but most guidelines have similar approaches in identifying and defining targets [4, 22–26] and most identify LDL-C levels as the primary target for treatment. In European guidelines [3•, 4], the target of LDL-C is adapted to total CV risk level (Table 1) with a lower level for subjects with very high cardiovascular risk (Table 2). "
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    ABSTRACT: A number of plasma lipid parameters have been used to estimate cardiovascular risk and to be targets for treatment to reduce risk. Most risk algorithms are based on total cholesterol (T-C) or low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C), and most intervention trials have targeted the LDL-C levels. Emerging measures, which in some cases may be better for risk calculation and as alternative treatment targets, are apolipoprotein B and non-HDL-C. Other lipid measures that may contribute in risk analysis are triglycerides (TG), lipoprotein(a), and lipoprotein-associated phospholipase A2. The primary treatment target in cardiovascular prevention is LDL-C, and potential alternative targets are apoB and non-HDL-C. In selected individuals at high cardiovascular (CV) risk, TG should be targeted, but HDL-C, Lp(a), and ratios such as LDL-C/HDL-C or apoB/apoAI are not recommended as treatment targets. Lipids should be monitored during titration to targets. Thereafter, lipids should be checked at least once a year or more frequently to improve treatment adherence if indicated. Monitoring of muscle and liver enzymes should be done before the start of treatment. In stable conditions during treatment, the focus should be on clinical symptoms that may alert muscle or liver complications. Routine measurement of CK or ALT is not necessary during treatment with statins.
    Current Cardiology Reports 09/2013; 15(9):397. DOI:10.1007/s11886-013-0397-8 · 1.93 Impact Factor
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