160 Association of HDL Cholesterol with Cancer Incidence in Type 2 Diabetes: A Case of Reverse Causality? J. Morton 1,2,∗ , S. Zoungas 3,4 , Q. Li 3 , D. Celermajer 1,2,5 , J. Chalmers 3 , M. Woodward 3 , M. Ng 1,2,5 1 The
Heart Research Institute, Australia Medical School, University of Sydney, Australia 3 The George Institute for Global Health, University of Sydney, Australia 4 School of Public Health, Monash University, Australia 5 Department of Cardiology, Royal Prince Alfred Hospital, Australia 2 Sydney
Low levels of high density lipoprotein cholesterol (HDLC) have been associated with an increased risk of cancer. Whether this is a true causal association or due to reverse causality remains unclear. We examined the association between HDL-C and cancer incidence using prospective data from ADVANCE, a large clinical trial of patients with type 2 diabetes. Methods: 11,140 patients with type 2 diabetes, with ≥1 vascular risk factor were followed for a median of 5.0 years. Cox proportional hazard models, adjusting for a range of covariates (age, gender, smoking status, BMI, total cholesterol, alcohol use, statin use and randomised treatment groups) assessed baseline HDL-C levels and cancer incidence reported as serious adverse events. Results: 699 cancers were recorded, 48% occurring within the first 2.5 years of follow up. For each 0.4 mmol (1 SD) lower baseline HDL-C there was a 14% higher risk of cancer (HR 0.86, 95%CI 0.78–0.94, p = 0.0008), which remained significant after adjustment for a range of confounders and randomized treatment allocation (adjusted HR 0.90, 95%CI 0.81–0.99, p = 0.028). However, when cancers occurring within the first 2.5 years of follow up were excluded, no significant association was found (adjusted HR 0.98, 95%CI 0.86–1.11, p = 0.70). Conclusions: Low baseline HDL-C levels were associated with a higher risk of developing cancer in the first 2.5 years of follow up but not in the second 2.5 years of follow up. This suggests the association is due to reverse causality: that cancer results in lower HDL-C levels rather than the lower HDL-C causing the cancer. http://dx.doi.org/10.1016/j.hlc.2012.05.170 161 Bergamot Polyphenolic Fraction Potentiates Rosuvastatin-Induced Effect on LDL-Cholesterol, Triglycerides and HDL Cholesterol R. Walker 1,∗ , V. Mollace 2 , F. Romeo 2 1 Sydney
Adventist Hospital, Australia of Rome, Italy
2 University
Background: Statins have a strong evidence-base as part of the management of cardiovascular disease. Bergamot polyphenolic fraction (BPF), a juice extract from citrus bergamia, has been found to reduce significantly blood cholesterol, triglycerides and oxyLDL in
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animal models and patients with hyperlipidaemia. We report on the effect of BPF in patients suffering from combined dyslipidaemia either untreated or treated with rosuvastatin. Methods: A prospective, open-label, parallel group, controlled study of 77 patients with low-density lipoprotein cholesterol (LDL-C) levels of >4.1 mmol/L and triglycerides levels >2.54 mmol/L was performed. Patients were randomly assigned to five groups, all receiving low fat diet: a control group, two groups receiving rosuvastatin (10 and 20 mg/day for 30 days), a group receiving BPF alone (1000 mg/day for 30 days) and, finally, a group receiving BPF (1000 mg/day) plus rosuvastatin (10 mg/day) for 30 days. Results: Rosuvastatin doses reduced LDL-C by 42 + 4% and 56 + 5%, respectively. Similar effect was seen in total cholesterol and non-high-density lipoprotein cholesterol (non-HDL-C) levels. In BPF-treated group, a 31 + 3% reduction of LDL-C and a significant improvement on the lipid profile was seen, including a significant reduction by 37 + 3% of triglycerides. Addition of BPF (1000 mg/daily) to rosuvastatin (10 mg/day) significantly enhanced rosuvastatin effect on serum cholesterol compared to rosuvastatin 20 mg alone (LDL-C reduction was 52 + 4%), with further reduction in triglycerides and increases in HDL cholesterol. Conclusion: Our data has clearly demonstrated that bergamot derived antioxidant polyphenols synergise with rosuvastatin, suggesting a role in statin-intolerant patients. http://dx.doi.org/10.1016/j.hlc.2012.05.171 162 Expression of Fat Mobilising Genes in Human Epicardial Adipose Tissue L. Eng 1,∗ , I. Jaffer 2 , M. Riederer 3 , P. Shah 2 , P. Peters 2 , F. Quehenberger 4 , A. Woods 2 , G. Kostner 3 , K. Kostner 1 1 Department of Cardiology, Mater Adult Hospital, Brisbane, Australia 2 Department of Cardiothoracic Surgery, Princess Alexandra Hospital, Brisbane, Australia 3 Institute of Molecular Biology and Biochemistry, Medical University of Graz, Austria 4 Institute for Medical Informatics, Statistics and Documentation, Medical University of Graz, Austria
Background: Epicardial adipose tissue (EAT) mass correlates with Metabolic Syndrome and coronary artery disease (CAD). However, little is known about the expression of genes involved in triglyceride (TG) storage and mobilisation in EAT. We therefore analysed the expression of genes involved in fat mobilisation in EAT in comparison to subcutaneous abdominal adipose tissue (AAT) in CAD patients and in controls. Methods: EAT and AAT were obtained during coronary artery bypass graft (CABG) surgery from 16 CAD patients and from 14 non-CAD patients presenting for valve surgery. The state of atherosclerosis was assessed by
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Heart, Lung and Circulation 2012;21:S1–S142