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Articles by Patrick Couture
Total Records ( 3 ) for Patrick Couture
  Anne Gangloff , Jean Bergeron , Patrick Couture , Rebecca Martins , Robert A. Hegele and Claude Gagne
  Not available
  Allan Sniderman , George Thanassoulis , Patrick Couture , Ken Williams , Ahsan Alam and Curt D. Furberg
  Researchers from the Cholesterol Treatment Trialists' (CTT) Collaboration have argued for maximal lowering of low-density lipoprotein cholesterol (LDL-C) by the use of pharmacologic agents, with the strongest evidence coming from the five comparison statin studies in their second meta-analysis. The CTT meta-analysis has many strengths but also a number of limitations, which have not been discussed and which, given the clinical implications, require consideration. Among these are: (1) the impact and validity of including revascularizations within a composite primary end point; (2) the inclusion of the A-Z study, whose design does not allow for valid comparisons of two statin regimens; (3) the fact that baseline LDL-C levels in the comparison studies were not low enough to test whether statin therapy reduces risk significantly in groups with an initial low LDL-C; and, most important, (4) authors of the five studies compared doses at the extremes of statin regimens. However, the clinical choice is not between the lowest and the greatest dose of a statin statin regimens, for example, between 10 and 80 mg atorvastatin, but, more realistically, between intermediate and high dose, that is, between 40 and 80 mg atorvastatin. On the basis of the CTT meta-analysis, we calculate that any potential gain from increasing the dose from 40 to 80 mg atorvastatin would be very small, at best a further 2% further reduction in clinical events. The increase in dose, unfortunately, would likely be associated with increased side effects and decreased compliance. Accordingly, whether net benefit would be demonstrable cannot be assumed. It follows that definitive evidence supporting maximal lowering of LDL-C or maximal dose of statins is still lacking and guidelines, if they are to be evidence-based, should acknowledge this uncertainty.
  Allan D. Sniderman , Andre Tremblay , Jacqueline De Graaf and Patrick Couture
 

Objective

To characterize the composition of very-low-density lipoprotein (VLDL) particles and the proportion of VLDL to total apolipoprotein B (apoB) particles in patients with hypertriglyceridemia caused by excess VLDL.

Methods

Subjects were selected from 2023 consecutive patients attending the Lipid Clinic at the Laval University Centre. Plasma lipids, apoB, and apoA-I were measured and chylomicron lipids and VLDL and LDL lipids and apoB determined after ultracentrifugation. Patients with hypertriglyceridemia caused by excess VLDL were divided into four groups on the basis of triglyceride and apoB.

Results

A total of 440 controls, 387 subjects with normotriglyceridemic hyperapoB, 38 with type III dysbetalipoproteinemia, 270 with mild hypertriglyceridemic normoapoB, 163 with moderate hypertriglyceridemic normoapoB, 458 with mild hypertriglyceridemic hyperapoB, and 295 subjects with moderate hypertriglyceridemic hyperapoB were compared. In patients with hypertriglyceridemia caused by excess VLDL, the VLDL particles were triglyceride and cholesterol-enriched. HyperapoB is associated with greater low-density lipoprotein (LDL) apoB than normoapoB, whereas greater triglycerides are associated with greater VLDL apoB. Thus, the ratio of VLDL apoB/total apoB was significantly less in those with mild hypertriglyceridemia compared with those with moderate hypertriglyceridemia, irrespective of the plasma apoB.

Conclusions

The apoB phenotypes in hypertriglyceridemia caused by excess VLDL appear to be determined by the extent to which VLDL secretion increases, the extent to which VLDL particles can be converted to LDL particles, and the effects of core lipid exchange. More accurate characterization of hypertriglyceridemia caused by excess VLDL should lead to a better understanding of the determinants of VLDL clearance and conversion to LDL as well as of the atherogenic potential of VLDL.

 
 
 
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