Effects of Nicotinic Acid Plus Simvastatin Versus Simvastatin Alone on Carotid and Femoral Intima-Media Thickness in Patients With Peripheral Artery Disease (NASCIT) (NASCIT)
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|ClinicalTrials.gov Identifier: NCT00712049|
Recruitment Status : Unknown
Verified July 2011 by Medical University of Vienna.
Recruitment status was: Recruiting
First Posted : July 9, 2008
Last Update Posted : July 22, 2011
Dyslipidaemia is characterized by low plasma levels of high-density lipoprotein cholesterol (HDL-c), elevated triglycerides and an increase in low density lipoprotein (LDL-c) particles, and has been unequivocally established as a most important cardiovascular risk factor. While statins are effective in reducing plasma levels of LDL-c, these drugs have only modest effects on raising HDL-c (typically by less than 10%), even with aggressive statin therapy. However, increasing evidence suggests that low HDL-c might be at least as relevant as high LDL-c in promoting the development and progression of atherosclerosis. The beneficial effect of raising HDL-c on clinical outcome has already been demonstrated by several studies.
Nicotinic acid is the most potent agent available for raising plasma levels of HDL-c by up to 29% at clinically recommended doses, and substantially lowers triglycerides and LDL-c. Furthermore, nicotinic acid is also the most potent lipid lowering agent available that reduces Lp(a), an independent marker of cardiovascular risk. In a recent study patients with coronary artery disease had a 21% increase in HDL-c and a 13% decrease in triglycerides, and these beneficial effects on lipid status may have contributed to a stabilization or regression of carotid intima-media-thickness (IMT).The impact in patients with advanced atherosclerosis like peripheral artery disease (PAD) in unknown.
The investigators hypothesized that nicotinic acid in addition to statin therapy may inhibit progression of peripheral arterial atherosclerosis. Therefore, the aim of the present randomized controlled trial is to investigate the effects of nicotinic acid (daily dose starting with 500 mg, up to 2000mg) in addition to simvastatin (40 mg daily) versus simvastatin (40mg daily) monotherapy in patients with low serum HDL-C levels and PAD with respect to changes of carotid and femoral IMT, changes of patients´ lipid status and occurrence of major adverse cardiovascular events (MACE).
|Condition or disease||Intervention/treatment||Phase|
|Dyslipidemia Atherosclerosis||Drug: simvastatin Drug: Nicotinic Acid||Phase 4|
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||200 participants|
|Intervention Model:||Parallel Assignment|
|Masking:||None (Open Label)|
|Official Title:||Effects of Nicotinic Acid Plus Simvastatin Versus Simvastatin Alone on Carotid and Femoral Intima-Media Thickness in Patients With Peripheral Artery Disease (NASCIT)-A Randomized Controlled Trial|
|Study Start Date :||June 2008|
Active Comparator: 1
Nicotinic acid + Simvastatin
simvastatin 40 mgDrug: Nicotinic Acid
daily dose starting with 500 mg, up to 2000mg
Active Comparator: 2
simvastatin 40 mg
- change of carotid and femoral IMT from baseline to 6 and 12 months follow up and occurrence of major adverse cardiovascular events (MACE) [ Time Frame: 6 and 12 months ]
- changes of grey scale median (GSM) score from baseline to follow-up, and changes of serum levels of total cholesterol, low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), triglycerides and lipoprotein (a). [ Time Frame: 6 and 12 months ]
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00712049
|Medical University Vienna||Recruiting|
|Vienna, Austria, 1090|
|Contact: Renate Koppensteiner, Prof. Dr. 00431404004671 firstname.lastname@example.org|
|Sub-Investigator: Martin Schillinger, Prof. Dr.|
|Sub-Investigator: Jasmin Amighi, Dr.|
|Sub-Investigator: Schila Sabeti, Dr.|
|Principal Investigator:||Renate Koppensteiner, Prof. Dr.||Division of Angiology, Department of Internal Medicine II, Medical University Vienna|