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Objective: To determine whether sagittal abdominal diameter (SAD) is associated with the metabolic syndrome independently of visceral fat area (VFA) and waist circumference (WC)., Methods: Forty-three high-risk vascular patients were evaluated for metabolic syndrome criteria and underwent magnetic resonance imaging (MRI) to quantify SAD and VFA at the L4-L5 disc. COMPARISONS: 1. Baseline differences in patients with and without the metabolic syndrome 2. Forward binary logistic regression analysis of predictors of the metabolic syndrome with SAD, VFA and WC as independents 3. Correlates of SAD., Results: Patients with metabolic syndrome had greater SAD, VFA and WC than patients without the metabolic syndrome (P < 0.01). Of SAD, VFA and WC, only SAD was associated with metabolic syndrome on forward binary logistic regression; beta 0.68, Wald's statistic 10.8 (P = 0.001) and c-statistic 0.89 (P < 0.001). A > 22.7 cm SAD threshold identified metabolic syndrome with a 91% sensitivity and 80% specificity. SAD correlated with waist circumference (r = 0.918), high-density lipoprotein-cholesterol (r = -0.363), triglyceride (r = 0.401), fasting glucose (r = 0.428) and the QUICK index of insulin sensitivity (r = -0.667) (all P < 0.05)., Conclusions: MRI-measured SAD is associated with the metabolic syndrome and renders the current gold standard of VFA redundant. This measure of obesity-related cardiovascular risk requires validation and evaluation in a prospective cohort.

Obesity, metabolic syndrome and diabetes are conditions with increasing prevalence around the world. Cardiovascular risk in diabetics is often so high as to overlap with event rates observed in those with established coronary disease and this has lead to diabetes being classified as a coronary risk equivalent. However, despite the elevated risk of cardiovascular events associated with diabetes and the metabolic syndrome, these patients often have normal low density lipoprotein (LDL) cholesterol despite frequent increases in apolipoprotein B, triglycerides and nonhigh density lipoprotein (HDL) cholesterol. In contrast to LDL cholesterol, non-HDL cholesterol represents cardiovascular risk across all patient populations but is currently only recommended as a secondary target of therapy by the ATP III report for patients with hypertriglyceridemia. This article provides an overview of the studies that shown non-HDL cholesterol to be superior to LDL cholesterol in predicting cardiovascular events and presents the case for non-HDL cholesterol being the more appropriate primary target of therapy in the context of the obesity pandemic. Adopting non-HDL cholesterol as the primary therapeutic target for all patients will conceivably lead to an appropriate intensification of therapy for high risk patients with low LDL cholesterol.

Abstract: Objective: Increasing insulin resistance is associated with a shift in cholesterol metabolism to increased synthesis and decreased absorption. Since statins inhibit cholesterol synthesis, we hypothesized that insulin-resistant patients will have greater LDL cholesterol (LDL-C) response to statins than insulin-sensitive patients. Methods: High-risk vascular patients not on lipid-lowering therapy were recruited and treated with Atorvastatin 80mg for 6 weeks. Percent LDL-C response to Atorvastatin was related to insulin sensitivity using the quantitative insulin sensitivity check index (QUICKI). Comparisons: (1) correlation between %LDL-C response and QUICKI. (2) Differences in cholesterol metabolism markers in insulin-resistant (lowest tertile QUICKI) vs insulin-sensitive patients (highest tertile of QUICKI). (3) Correlation of QUICKI with percent LDL-C response after correction for cholesterol metabolism markers. Results: 154 patients were enrolled of which 66 were suitable for this sub-study. Average LDL-C reduction was 57±12% (mean±SD). QUICKI correlated negatively with percent LDL-C reduction (Pearson''s r =−0.258, p =0.037) and on regression analysis explained ∼7% (R 2 =0.067) of the variation in percent LDL-C response which approximates that reported by pharmacogenomics. Insulin-resistant patients had higher levels of cholesterol synthesis markers (desmosterol, lathosterol) and lower levels of absorption markers (cholestanol, sitosterol) and the correlation between QUICKI and percent LDL-C response ceased to be significant when these factors were controlled for. Conclusions: Insulin-resistant patients have superior LDL-C responses to statin therapy and that this may be related to increased cholesterol synthesis. Background: Patients with features of the metabolic syndrome, e.g. high triglycerides (TG) and low high density lipoprotein cholesterol (HDL-C) may have an enhanced benefit from statin therapy. A retrospective analysis from the 4S investigators where the study population was stratified by HDL-C and TG quartiles revealed variations in statin efficacy. Patients who fell into both the lowest quartile of HDL-C (<39mg/dl) and highest quartile of TG (>159mg/dl) had a greater frequency of features of the metabolic syndrome (high BMI, hypertension, diabetes) than the patients in the highest quartile of HDL-C (>52mg/dl) and lowest quartile of TG (<98mg/dl). The 4S investigators suggested that patients with low HDL-C and high TG achieved an enhanced clinical benefit from statins compared to patients with high HDL-C and low TG with hazard ratios of 0.48 and 0.86 respectively and a treatment-by-subgroup interaction p value of 0.03 . Since the clinical benefit of statin therapy is directly proportional to achieved percent reduction in low density lipoprotein cholesterol (LDL-C) , we hypothesized that insulin-resistant patients would have greater percent decreases in LDL-C with statin therapy. [Copyright &y& Elsevier]

Objective: To determine whether liver fat percent (LFP) is associated with the metabolic syndrome independently of visceral fat area (VFA). Methods: 43 High-risk vascular patients not on lipid-lowering therapy were evaluated for the Adult Treatment Panel III (ATPIII) metabolic syndrome criteria and underwent magnetic resonance imaging (MRI) to quantify VFA and subcutaneous fat area (SFA) at the L4-L5 disc and liver magnetic resonance spectroscopy (MRS) to quantify LFP. Comparisons: 1. Baseline differences in patients with and without the metabolic syndrome 2. Forward binary logistic regression analysis of predictors of the metabolic syndrome with VFA, SFA and LFP as independents 3. Correlates of LFP. Results: 43 patients were included in analysis. Patients with metabolic syndrome had greater VFA, SFA and LFP than patients without the metabolic syndrome (all p < 0.01). Of VFA, SFA and LFP, only LFP was associated with the diagnosis of the metabolic syndrome on forward binary logistic regression with an OR of 1.17 per 1% increase in LFP (p = 0.015). A 4% LFP threshold identified the metabolic syndrome with 84% sensitivity and 82% specificity. LFP correlated with waist circumference (r = 0.768), HDL-cholesterol (r = -0.342), triglyceride (r = 0.369), fasting glucose (r = 0.584) and the QUICK Index of insulin sensitivity (r = -0.679) (all p < 0.05) Conclusions: LFP is associated with the metabolic syndrome and renders the current gold standard of VFA redundant in this analysis. This measure of obesity-related cardiovascular risk requires further validation and evaluation in a prospective cohort. [ABSTRACT FROM AUTHOR]