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Articles by Curt D. Furberg
Total Records ( 3 ) for Curt D. Furberg
  Allan Sniderman , Matt McQueen , John Contois , Ken Williams and Curt D. Furberg
  Low-density lipoprotein cholesterol (LDL-C) has been the focus of managing lipoprotein disorders for decades. It is now time to consider a change. Both apolipoprotein B (apoB) and non-high-density lipoprotein cholesterol (HDL-C) have been shown to be more accurate markers of cardiovascular risk than LDL-C. ApoB measures total atherogenic particle number, of which 90% are LDL particles. Therefore, LDL particle number determines plasma apoB in most patients. Non-HDL-C is widely assumed to be superior to LDL-C when triglyceride concentrations are elevated (even modestly) because it includes the cholesterol in very-low-density lipoprotein. However, evidence does not support this concept. Rather, non-HDL-C appears to be an indirect way of estimating apoB. We argue that we should integrate the information from non-HDL-C and apoB for better risk assessment and a better target of therapy.
  Allan D. Sniderman , Ken Williams , Matthew J. McQueen and Curt D. Furberg
  The meta-analysis of the Emerging Risk Factor Collaboration demonstrated that the hazard ratios (HR) of the major cholesterol markers and the major apolipoproteins for vascular disease did not differ significantly in the studies they examined. Their conclusion was that they were functionally interchangeable. We believe there are important limitations in the execution of this study. Nevertheless, even if their findings are correct for groups, their conclusions do not follow for individuals. Conventionally, the HR expresses the increase in risk per standard deviation change for that parameter in a group. However, the predicted risk of vascular disease from an atherogenic parameter depends on its concentration within the individual. Depending on the composition of the apoB lipoproteins, individuals may have either concordant or discordant levels of cholesterol and apoB. For those who are concordant, the two markers predict equal risk. For those who are discordant, the predicted risks for the individual are different. We demonstrate that substantial discordance in the individual HR of non-high-density lipoprotein cholesterol and apoB is common. The result is that even with identical overall HR, apoB points to higher risk in a substantial number of individuals whereas the converse is the case for non- high-density lipoprotein cholesterol. Because we are concerned with risks in individuals, not groups, this discordance is important to appreciate and analyze. Our objective should be to learn how to combine the information from parameters rather than eliminate them and we need to focus on evaluation of risk in individuals and not just groups.
  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.
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