Comparison of the Safety and Efficacy of a Combination Tablet of Niacin Extended Release and Simvastatin vs Simvastatin Monotherapy in Patients With Increased Non–HDL Cholesterol (from the SEACOAST I Study)

Ballantyne, Christie M.; Davidson, Michael; McKenney, James M.; Keller, L; Bajorunas, Daiva R.; Karas, Richard H.

doi:10.1016/j.amjcard.2008.02.092

Cited by 87 publications

(78 citation statements)

References 11 publications

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“…The primary end point in SEACOAST was the median percent change in non-HDL-C during the period from baseline to week 24, beginning from the end of the simvastatin run-in. 25,26 In SEACOAST I, the niacin ER/simvastatin (1,000 mg/ 20 mg and 2,000 mg/20 mg) FDC therapies produced significant, dose-related improvements in non-HDL-C, HDL-C, TG, and lipoprotein A (Lp[a]), compared with simvastatin (20 mg) monotherapy. 26 Figure 15 shows a 22.5% reduction in non-HDL-C levels with high-dose niacin ER/simvastatin versus a 7.4% reduction with simvastatin monotherapy.…”

Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

“…25,26 In SEACOAST I, the niacin ER/simvastatin (1,000 mg/ 20 mg and 2,000 mg/20 mg) FDC therapies produced significant, dose-related improvements in non-HDL-C, HDL-C, TG, and lipoprotein A (Lp[a]), compared with simvastatin (20 mg) monotherapy. 26 Figure 15 shows a 22.5% reduction in non-HDL-C levels with high-dose niacin ER/simvastatin versus a 7.4% reduction with simvastatin monotherapy. Although there was a dose-related response in LDL-C level reduction, there were no significant differences between groups in this lipid parameter; simvastatin alone resulted in a 7.1% decrease in LDL-C levels, whereas high-dose niacin ER/simvastatin FDC therapy produced a 14.2% reduction.…”

Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

“…86 The Safety and Efficacy of Fixed Dose Niacin ER and Simvastatin Combination Therapy (SEACOAST) trial, which investigated niacin ER/simvastatin FDC therapy, has been recently published. 25,26 This 24-week randomized clinical trial compared simvastatin monotherapy with a novel combination of niacin ER/simvastatin in patients with mixed dyslipidemia, as identified by elevated levels of non-HDL-C. 25,26 After a simvastatin run-in phase during which patients received either 20 mg or 40 mg of simvastatin for at least 2 weeks, patients were assigned to either simvastatin low-dose groups (SEACOAST I) or simvastatin high-dose groups (SEACOAST II), which were determined by the final run-in simvastatin dose. Patients were then randomized to 1 of 3 treatment groups in each half of the study.…”

Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

“…In SEACOAST I, the treatment groups were simvastatin (20 mg), niacin ER/simvastatin (1,000 mg/20 mg), and niacin ER/ simvastatin (2,000 mg/20 mg). 26 In SEACOAST II, which included more intensive lipid-modifying therapy during both the run-in phase and the 24-week trial phase, the treatment groups were simvastatin (80 mg), niacin ER/simvastatin (1,000 mg/ 40 mg), and niacin ER/simvastatin (2,000 mg/40 mg). The primary end point in SEACOAST was the median percent change in non-HDL-C during the period from baseline to week 24, beginning from the end of the simvastatin run-in.…”

Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

“…Recent reports from Ballantyne et al have demonstrated the significant benefits of niacin ER/simvastatin FDC therapy for simultaneously modifying several abnormal lipid parameters. 25,26 This supplement seeks to outline the significant progress that has been made in the treatment of cardiovascular disease and dyslipidemia, particularly through the use of lipid-lowering statin therapy. However, much can still be done to decrease the burden of cardiovascular disease as manifested through morbidity and mortality, as well as through the associated increasing health care costs.…”

Section: Introductionmentioning

confidence: 99%

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Targeting Low HDL-Cholesterol to Decrease Residual Cardiovascular Risk in the Managed Care Setting

Cziraky

Watson

Talbert³

2008

JMCP

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Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

Section: ■■ Model-based Analyses Of Pharmacotherapymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Targeting Low HDL-Cholesterol to Decrease Residual Cardiovascular Risk in the Managed Care Setting

Cziraky

Watson

Talbert³

2008

JMCP

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Major Lipids, Apolipoproteins, and Risk of Vascular Disease

Angelantonio¹,

Sarwar²,

Perry³

et al. 2009

JAMA

2,268

745

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Context Associations of major lipids and apolipoproteins with the risk of vascular disease have not been reliably quantified. Objective To assess major lipids and apolipoproteins in vascular risk. Design, Setting, and Participants Individual records were supplied on 302 430 people without initial vascular disease from 68 long-term prospective studies, mostly in Europe and North America. During 2.79 million person-years of follow-up, there were 8857 nonfatal myocardial infarctions, 3928 coronary heart disease [CHD] deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes. Main Outcome Measures Hazard ratios (HRs), adjusted for several conventional factors, were calculated for 1-SD higher values: 0.52 loge triglyceride, 15 mg/dL high-density lipoprotein cholesterol (HDL-C), 43 mg/dL non-HDL-C, 29 mg/dL apolipoprotein AI, 29 mg/dL apolipoprotein B, and 33 mg/dL directly measured low-density lipoprotein cholesterol (LDL-C). Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. Results The rates of CHD per 1000 person-years in the bottom and top thirds of baseline lipid distributions, respectively, were 2.6 and 6.2 with triglyceride, 6.4 and 2.4 with HDL-C, and 2.3 and 6.7 with non-HDL-C. Adjusted HRs for CHD were 0.99 (95% CI, 0.94-1.05) with triglyceride, 0.78 (95% CI, 0.74-0.82) with HDL-C, and 1.50 (95% CI, 1.39-1.61) with non-HDL-C. Hazard ratios were at least as strong in participants who did not fast as in those who did. The HR for CHD was 0.35 (95% CI, 0.30-0.42) with a combination of 80 mg/dL lower non-HDL-C and 15 mg/dL higher HDL-C. For the subset with apolipoproteins or directly measured LDL-C, HRs were 1.50 (95% CI, 1.38-1.62) with the ratio non-HDL-C/HDL-C, 1.49 (95% CI, 1.39-1.60) with the ratio apo B/apo AI, 1.42 (95% CI, 1.06-1.91) with non-HDL-C, and 1.38 (95% CI, 1.09-1.73) with directly measured LDL-C. Hazard ratios for ischemic stroke were 1.02 (95% CI, 0.94-1.11) with triglyceride, 0.93 (95% CI, 0.84-1.02) with HDL-C, and 1.12 (95% CI, 1.04-1.20) with non-HDL-C. Conclusion Lipid assessment in vascular disease can be simplified by measurement of either total and HDL cholesterol levels or apolipoproteins without the need to fast and without regard to triglyceride.

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