ORCID Profile
0000-0002-8414-3847
Current Organisation
Université Laval
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Publisher: Elsevier BV
Date: 04-2017
Publisher: Elsevier BV
Date: 09-2018
DOI: 10.1016/J.CJCA.2018.05.015
Abstract: Familial hypercholesterolemia (FH) is an autosomal codominant lipoprotein disorder characterized by elevated low-density lipoprotein cholesterol (LDL-C) and high risk of premature atherosclerotic cardiovascular disease. Definitions for FH rely on complex algorithms that are on the basis of levels of total or LDL-C, clinical features, family history, and DNA analysis that are often difficult to obtain. We propose a novel simplified definition for FH. Definite FH includes: (1) elevated LDL-C (≥ 8.50 mmol/L) or (2) LDL-C ≥ 5.0 mmol/L (for age 40 years or older ≥ 4.0 mmol/L if age younger than 18 years and ≥ 4.5 mmol/L if age is between 18 and 39 years) when associated with at least 1 of: (1) tendon xanthomas or (2) causal DNA mutation in the LDLR, APOB, or PCSK9 genes in the proband or first-degree relative. Probable FH is defined as subjects with an elevated LDL-C (≥ 5.0 mmol/L) and the presence of premature atherosclerotic cardiovascular disease in the patient or a first-degree relative or an elevated LDL-C in a first-degree relative. LDL-C cut points were determined from a large database comprising > 3.3 million subjects. To compare the proposed definition with currently used algorithms (ie, the Simon Broome Register and Dutch Lipid Clinic Network), we performed concordance analyses in 5987 in iduals from Canada. The new FH definition showed very good agreement compared with the Simon Broome Register and Dutch Lipid Clinic Network criteria (κ = 0.969 and 0.966, respectively). In conclusion, the proposed FH definition has diagnostic performance comparable to existing criteria, but adapted to the Canadian population, and will facilitate the diagnosis of FH patients.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 02-2014
DOI: 10.1161/ATVBAHA.113.302185
Abstract: To assess the effect of a Mediterranean diet (MedDiet) with and without weight loss (WL) on apolipoprotein B 100 (apoB 100 ) metabolism in men with metabolic syndrome. The diet of 19 men with metabolic syndrome (age, 24–62 years) was first standardized to a North American isoenergetic control diet for 5 weeks, followed by an isoenergetic MedDiet for an additional 5 weeks under full-feeding conditions (MedDiet−WL). Participants next underwent a 20-week supervised WL program under free-living conditions (−10.2±2.9% body weight P .01) and finally consumed the MedDiet (5 weeks) under weight-stabilizing feeding conditions (MedDiet+WL). In vivo kinetic of apoB 100 was assessed in the fasted state at the end of the 3 controlled diets using a bolus of D 3 -leucine. Compared with the control diet, MedDiet−WL reduced low-density lipoprotein (LDL)-apoB 100 pool size (−14.2%, P .01) primarily through an increase in LDL-apoB 100 fractional catabolic rate (+30.4%, P =0.02) and increased LDL particle size ( P .01) but had no effect on very-LDL (VLDL)-apoB 100 pool size or triglyceride concentrations, despite a significant increase in VLDL-apoB 100 fractional catabolic rate (+25.6% P =0.03). MedDiet+WL had no further effect on LDL-apoB 100 pool size and fractional catabolic rate but further increased LDL particle size and reduced VLDL-apoB 100 pool size versus the control diet primarily through an increase in VLDL-apoB 100 fractional catabolic rate (+30.7% P .01). Consumption of MedDiet increases LDL size and reduces LDL-apoB 100 concentrations primarily by increasing the catabolism of LDL even in the absence of WL in men with metabolic syndrome. MedDiet seems to have a trivial effect on VLDL concentrations and kinetics unless accompanied by significant WL. —URL: www.clinicaltrials.gov . Unique identifier: NCT00988650.
Publisher: Portland Press Ltd.
Date: 23-11-2009
DOI: 10.1042/CS20090402
Abstract: The objectives of this analysis are to re-examine the foundational studies of the in vivo metabolism of plasma LDL (low-density lipoprotein) particles in humans and, based on them, to reconstruct our understanding of the governance of the concentration of plasma LDL and the maintenance of cholesterol homoeostasis in the hepatocyte. We believe that regulation of cholesterol homoeostasis within the hepatocyte is demonstrably more complex than envisioned by the LDL receptor paradigm, the conventional model to explain the regulation of plasma LDL and the fluxes of cholesterol into the liver, a model which was generated in the fibroblast but has never been fully validated in the hepatocyte. We suggest that the LDL receptor paradigm should be reconfigured as the apoB (apolipoprotein B) paradigm, which states that the rate at which LDL particles are produced is at least an important determinant of their concentration in plasma as the rate at which they are cleared from plasma and that secretion of cholesterol within VLDL (very-low-density lipoprotein) particles is an important mechanism of maintaining cholesterol homoeostasis within the hepatocyte. These two paradigms are not mutually exclusive. The LDL receptor paradigm, however, includes only one critical aspect of the regulation of plasma LDL, namely the rate at which LDL particles are cleared through the LDL receptor pathway, but ignores another – the rate at which LDL particles are added to the plasma compartment. The apoB paradigm includes both and points to a different model of how the hepatocyte achieves cholesterol homoeostasis in a complex metabolic environment.
No related grants have been discovered for Patrick Couture.