- Email: [email protected]
158: Effects of intensifying lipid-altering therapy on CHD events in a secondary prevention population with high non-HDL cholesterol
Journal of Clinical Lipidology, Vol 2, No 5S, October 2008
S (2000/40 mg) would reduce costs Conclusions: Intensifying lipid-modifying therapy with fixeddose ERN/S combinations would further reduce costs of CHD events more effectively than S monotherapy in a secondary prevention population.
Conclusions: Based on this risk model, intensifying lipid-modifying therapy with selected fixed-dose ERN/S combinations may reduce the number of CHD events relative to simvastatin monotherapy. Funding: Abbott Laboratories
Funding: This activity was funded by Abbott Laboratories 159 158 EFFECTS OF INTENSIFYING LIPID-ALTERING THERAPY ON CHD EVENTS IN A SECONDARY PREVENTION POPULATION WITH HIGH NON-HDL CHOLESTEROL R. Simko1, J. Menzin2, B. Zhang2, S. Charland3, R. Burge1. 1Abbott Labs, Abbott Park, IL, USA, 2 Boston Health Economics, Inc., Waltham, MA, USA, 3University of Colorado, School of Pharmacy, Denver, CO, USA Objective: Patients often fail to reach dyslipidemia treatment goals on the lowest dose of single drug. We assessed the effects of intensified lipidmodifying therapies on rates of coronary events in a cohort of 10,000 people aged 50+ years with CHD and high non-HDL-cholesterol levels. Methods: This modeled analysis used data from the SEACOAST clinical trial and Framingham Heart Study equation for secondary prevention of CHD to calculate expected number of CHD events over 5 years. Results from the SEACOAST trial showed that patients treated with a fixed-dose extended release niacin/simvastatin (ERN/S) combination had significant improvements in non-HDL-C, HDL-C, and triglyceride levels compared to patients treated with simvastatin therapy alone. Age, sex, and coronary risk-factor data for patients with CHD and non-HDL-C cholesterol > 130 mg/dL were obtained from 1999-2002 NHANES. The drugs assessed included simvastatin alone and ERN/ S. Scenarios of interest reflected increasing the dose of simvastatin or adding ERN to simvastatin. Results: We estimated that 1,741 CHD events would occur over 5 years among 10,000 patients treated with 20 mg of simvastatin. CHD events would decrease by 8.9% with 1000/20 mg of ERN/ S. Relative to a dose of 80 mg of simvastatin, intermediate (1000/40 mg) and maximum doses (2000/40 mg) of ERN/S would reduce CHD events by 4.9 and 11.1 percentage points, respectively.
EFFECTS OF PRAVASTATIN AND ATORVASTATIN ON THE HDL CHOLESTEROL AND GLUCOSE METABOLISM IN PATIENTS WITH HYPERCHOLESTEROLEMIA AND GLUCOSE INTOLERANCE J. Sasaki1, M. Aeta2. 1Int Univ Health & Welfare, Fukuoka, Japan, 2Ageta Clinic, Nichinan, Japan Objective: To compare the effects of pravastatin and atorvastatin on HDL cholesterol (HDL-C) and other lipid profiles and glucose metabolism in Japanese patients with elevated LDL cholesterol (LDL-C) levels and glucose intolerance. Method: This study was a multicenter, open-label, parallelgroup trial. Patients with LDL-C levels 140 mg/dl or greater and glucose intolerance were randomly assigned to either pravastatin(10 mg/day) or atorvastatin(10 mg/day) treatment lasting 52 weeks. Laboratory measurements were done for parameters of the lipid profiles and glucose metabolism including insulin. Results: A total of 208 eligible patients were enrolled and efficacy was evaluated in. 183 patients (pravastatin n = 91, atorvastatin n = 92). At 52-week of follow up, there was no difference in the change of HDL-C levels between the two groups (P = 0.36), while a reduction in LDL-C was greater in atorvastatin group than in pravastatin group (P < 0.0001) Fasting plasma glucose levels increased in the atorvastatin group and decreased in the pravastatin group (P = 0.06 for the difference). Changes in fasting insulin level (+2.4 μU/mL for atorvastatin and -8.3 μU/mL for pravastatin) and homeostasis model assessment insulin resistance (+1.6 and 3.4, respectively) showed a statistically significant difference each. Conclusions: In patients with elevated LDL-C levels and glucose intolerance, no difference was observed in HDL-C levels, while treatment with pravastatin was associated with amelioration in insulin sensitivity. Funding: none
S73
S (2000/40 mg) would reduce costs Conclusions: Intensifying lipid-modifying therapy with fixeddose ERN/S combinations would further reduce costs of CHD events more effectively than S monotherapy in a secondary prevention population.
Conclusions: Based on this risk model, intensifying lipid-modifying therapy with selected fixed-dose ERN/S combinations may reduce the number of CHD events relative to simvastatin monotherapy. Funding: Abbott Laboratories
Funding: This activity was funded by Abbott Laboratories 159 158 EFFECTS OF INTENSIFYING LIPID-ALTERING THERAPY ON CHD EVENTS IN A SECONDARY PREVENTION POPULATION WITH HIGH NON-HDL CHOLESTEROL R. Simko1, J. Menzin2, B. Zhang2, S. Charland3, R. Burge1. 1Abbott Labs, Abbott Park, IL, USA, 2 Boston Health Economics, Inc., Waltham, MA, USA, 3University of Colorado, School of Pharmacy, Denver, CO, USA Objective: Patients often fail to reach dyslipidemia treatment goals on the lowest dose of single drug. We assessed the effects of intensified lipidmodifying therapies on rates of coronary events in a cohort of 10,000 people aged 50+ years with CHD and high non-HDL-cholesterol levels. Methods: This modeled analysis used data from the SEACOAST clinical trial and Framingham Heart Study equation for secondary prevention of CHD to calculate expected number of CHD events over 5 years. Results from the SEACOAST trial showed that patients treated with a fixed-dose extended release niacin/simvastatin (ERN/S) combination had significant improvements in non-HDL-C, HDL-C, and triglyceride levels compared to patients treated with simvastatin therapy alone. Age, sex, and coronary risk-factor data for patients with CHD and non-HDL-C cholesterol > 130 mg/dL were obtained from 1999-2002 NHANES. The drugs assessed included simvastatin alone and ERN/ S. Scenarios of interest reflected increasing the dose of simvastatin or adding ERN to simvastatin. Results: We estimated that 1,741 CHD events would occur over 5 years among 10,000 patients treated with 20 mg of simvastatin. CHD events would decrease by 8.9% with 1000/20 mg of ERN/ S. Relative to a dose of 80 mg of simvastatin, intermediate (1000/40 mg) and maximum doses (2000/40 mg) of ERN/S would reduce CHD events by 4.9 and 11.1 percentage points, respectively.
EFFECTS OF PRAVASTATIN AND ATORVASTATIN ON THE HDL CHOLESTEROL AND GLUCOSE METABOLISM IN PATIENTS WITH HYPERCHOLESTEROLEMIA AND GLUCOSE INTOLERANCE J. Sasaki1, M. Aeta2. 1Int Univ Health & Welfare, Fukuoka, Japan, 2Ageta Clinic, Nichinan, Japan Objective: To compare the effects of pravastatin and atorvastatin on HDL cholesterol (HDL-C) and other lipid profiles and glucose metabolism in Japanese patients with elevated LDL cholesterol (LDL-C) levels and glucose intolerance. Method: This study was a multicenter, open-label, parallelgroup trial. Patients with LDL-C levels 140 mg/dl or greater and glucose intolerance were randomly assigned to either pravastatin(10 mg/day) or atorvastatin(10 mg/day) treatment lasting 52 weeks. Laboratory measurements were done for parameters of the lipid profiles and glucose metabolism including insulin. Results: A total of 208 eligible patients were enrolled and efficacy was evaluated in. 183 patients (pravastatin n = 91, atorvastatin n = 92). At 52-week of follow up, there was no difference in the change of HDL-C levels between the two groups (P = 0.36), while a reduction in LDL-C was greater in atorvastatin group than in pravastatin group (P < 0.0001) Fasting plasma glucose levels increased in the atorvastatin group and decreased in the pravastatin group (P = 0.06 for the difference). Changes in fasting insulin level (+2.4 μU/mL for atorvastatin and -8.3 μU/mL for pravastatin) and homeostasis model assessment insulin resistance (+1.6 and 3.4, respectively) showed a statistically significant difference each. Conclusions: In patients with elevated LDL-C levels and glucose intolerance, no difference was observed in HDL-C levels, while treatment with pravastatin was associated with amelioration in insulin sensitivity. Funding: none
S73