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Articles by Allan D. Sniderman
Total Records ( 8 ) for Allan D. Sniderman
  Allan D. Sniderman
 

Background

Low-density lipoprotein (LDL)-lowering with pharmacologic therapy has been repeatedly shown to substantially reduce risk of vascular disease. LDL cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (HDL-C) are the cholesterol indices used to measure the adequacy of LDL-lowering therapy, whereas apolipoprotein B (ApoB) is the most widely used index of atherogenic particle number.

Objective

This study examines whether LDL-lowering therapy reduces cholesterol indices and ApoB to the same extent. If they are not equally affected, they may not be equally informative about change in risk.

Methods

Data from 11 studies, which include 17,035 subjects, were analyzed. All the statins in common use were included, as well as all the doses at which they are commonly used. More limited data are presented on combination therapy with statins and ezetimibe.

Results

Reductions in LDL-C, non-HDL-C, and ApoB differed significantly, averaging 42.1%, 39.6%, and 33.1%, respectively (P < 0.001 ApoB versus LDL-C or non-HDL-C). Mean value for the measure in question was expressed as the percentile level from a distribution analysis of two reference populations (Framingham Offspring Study and National Health and Nutrition Examination Survey III). The lower the population percentile, the more effective the apparent response. For LDL-C, non-HDL-C, and ApoB, these were the 21st, the 29th, and the 55th percentile of the population, respectively. This value for ApoB was significantly different from both LDL-C and non-HDL-C (P < 0.001). Very similar results were obtained in eight studies of LDL-lowering in 889 subjects in which the responses of LDL-C and LDL particle number (LDL-P) assessed by nuclear magnetic resonance spectroscopy were compared. LDL-C was reduced to the 27th percentile of the population, whereas LDL-P was only reduced to the 51st percentile of the population (P < 0.001).

Conclusions

Many patients who achieve LDL-C and non-HDL-C target levels will not have achieved correspondingly low population-equivalent ApoB or LDL-P targets. Reliance on LDL-C and non-HDL-C can create a treatment gap in which the opportunity to give maximal LDL-lowering therapy is lost.

  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 D. Sniderman
  Not available
  John H. Contois , G. Russell Warnick and Allan D. Sniderman
  There is little understanding of the reliability of laboratory measurements among clinicians. Low-density lipoprotein cholesterol (LDL-C) measurement is the cornerstone of cardiovascular risk assessment and prevention, but it is fraught with error. Therefore, we have reviewed issues related to accuracy and precision for the measurement of LDL-C and the related markers non-high-density lipoprotein cholesterol (non-HDL-C) and apolipoprotein B. Despite the widespread belief that LDL-C is standardized and reproducible, available data suggest that results can vary significantly as the result of methods from different manufacturers. Similar problems with direct HDL-C assays raise concerns about the reliability of non-HDL-C measurement. The root cause of method-specific bias relates to the ambiguity in the definition of both LDL and HDL, and the heterogeneity of LDL and HDL particle size and composition. Apolipoprotein B appears to provide a more reliable alternative, but assays for it have not been as rigorously tested as direct LDL-C and HDL-C assays.
  Michael H. Davidson , Christie M. Ballantyne , Terry A. Jacobson , Vera A. Bittner , Lynne T. Braun , Alan S. Brown , W. Virgil Brown , William C. Cromwell , Ronald B. Goldberg , James M. McKenney , Alan T. Remaley , Allan D. Sniderman , Peter P. Toth , Sotirios Tsimikas , Paul E. Ziajka , Kevin C. Maki and Mary R. Dicklin
  The National Cholesterol Education Program Adult Treatment Panel guidelines have established low-density lipoprotein cholesterol (LDL-C) treatment goals, and secondary non-high-density lipoprotein (HDL)-C treatment goals for persons with hypertriglyceridemia. The use of lipid-lowering therapies, particularly statins, to achieve these goals has reduced cardiovascular disease (CVD) morbidity and mortality; however, significant residual risk for events remains. This, combined with the rising prevalence of obesity, which has shifted the risk profile of the population toward patients in whom LDL-C is less predictive of CVD events (metabolic syndrome, low HDL-C, elevated triglycerides), has increased interest in the clinical use of inflammatory and lipid biomarker assessments. Furthermore, the cost effectiveness of pharmacological intervention for both the initiation of therapy and the intensification of therapy has been enhanced by the availability of a variety of generic statins. This report describes the consensus view of an expert panel convened by the National Lipid Association to evaluate the use of selected biomarkers [C-reactive protein, lipoprotein-associated phospholipase A2, apolipoprotein B, LDL particle concentration, lipoprotein(a), and LDL and HDL subfractions] to improve risk assessment, or to adjust therapy. These panel recommendations are intended to provide practical advice to clinicians who wrestle with the challenges of identifying the patients who are most likely to benefit from therapy, or intensification of therapy, to provide the optimum protection from CV risk.
  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.

  Allan D. Sniderman , Shofiqui Islam , Salim Yusuf and Matthew J. McQueen
 

Background

Patients with increased numbers of cholesterol-depleted apolipoprotein B (apoB) particles frequently have multiple other abnormalities, which might confound the comparison of apoB and non-high-density-lipoprotein-cholesterol (non-HDL-C) as markers of cardiovascular risk.

Objective

We wanted to determine whether the superiority of apoB over non-HDL-C as a marker of cardiovascular risk in the INTERHEART study is due to such variables that act as confounders of the primary comparison.

Methods

To test for confounding, cases and controls were first separated into 3 groups on the basis of the percentile levels within the study of non-HDL-C and apoB with discordance defined as a difference of 5 percentile points. Logistic regression was used to compute odds ratio of myocardial infarction (as an outcome) for different categories, assuming concordance as reference adjusted for other confounders.

Results

Plasma triglyceride and non-HDL-C levels were highest in the discordant group with lowest risk and lowest in the discordant group with highest risk, whereas apoB was highest in the discordant group with the highest risk and lowest in the discordant group with the lowest group. Moreover, no significant change was found in the odds ratio for either discordant group when adjusted for the effect of any of the variables examined, evidence that none confounded the primary comparison.

Conclusion

Factors such as hypertriglyceridemia do not confound the comparison of apoB and non-HDL-C, further evidence that apoB is superior to non-HDL-C as a marker of the importance of the apoB atherogenic lipoproteins in cardiovascular risk.

  Allan D. Sniderman , James A. Sloand , Philip K.T. Li , Ken Story and Joanne M. Bargman
 

Background

Glucose, the conventional osmotic agent in peritoneal dialysis (PD) solutions, may contribute to atherogenic dyslipoproteinemia and increased cardiovascular risk.

Objective

To determine whether a low-glucose PD regimen may improve the serum lipid and lipoprotein profile in patients with diabetes.

Methods

A prospective, open-label, parallel group, multinational, randomized, controlled trial with a 6-month follow-up, comprising 251 patients with diabetes receiving PD. Patients were randomized to a low-glucose PD regimen (dextrose-based PD solution plus icodextrin, a starch polymer, and amino acids) or a conventional PD regimen (dextrose PD solutions). Serum lipid and apolipoprotein profiles were determined at baseline and 3 and 6 months.

Results

Serum triglycerides, very low-density-lipoprotein cholesterol, and apolipoprotein B (apoB) decreased significantly in the intervention group at both 3 and 6 months compared with baseline (serum triglycerides: median change at 3 months −0.5 mmol/L, P < .001, at 6 months −0.3 mmol/L, P < .001; very low-density-lipoprotein cholesterol: −0.3 mg/dL, P < .001; −0.3 mg/dL, P < .001; and apoB: −8.5 mg/dL, P < .001; −3.6 mg/dL, P = .043, respectively) and also compared with the control group. In contrast, apoB levels increased significantly in the control group at 3 and 6 months compared with baseline (5.3 mg/dL, P = .041; 5.2 mg/dL, P = .007, respectively). Percentage of patients on lipid-lowering medications at baseline and intensity of therapy was equivalent in each group. The apoB decrease was not affected by lipid-lowering medications in the intervention group.

Conclusion

A low glucose-PD regimen significantly improved the atherogenic lipoprotein phenotype compared with PD patients treated with a conventional glucose regimen.

 
 
 
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