Can Niacin Slow the Development of Atherosclerosis in Coronary Artery Disease Patients Already Taking Statins?

B. Greg Brown

Disclosures

Nat Clin Pract Cardiovasc Med. 2005;2(5):234-235. 

In This Article

Synopsis

Low HDL-cholesterol concentrations can be successfully raised by niacin. A low HDL-cholesterol level is recognized as a coronary risk factor and increases the risk of unfavorable events related to coronary atherosclerosis. Unlike for LDL cholesterol, the National Cholesterol Education Program guidelines do not provide target levels for HDL-cholesterol concentration. Few studies have investigated the effect of niacin on coronary events, alone or in combination with statin therapy.

To explore the effect of niacin on carotid intima-media thickness (CIMT), and to find out whether extended-release niacin therapy provides added cardiovascular protection to patients receiving statin monotherapy for coronary artery disease.

The Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2 trial was a US-based, randomized, placebo-controlled, double-blind study carried out from December 2001 to May 2003. Patients aged over 30 years old were eligible for the study if they had coronary vascular disease, were receiving statin therapy and had HDL-cholesterol levels below 1.7 mM/l (45 mg/dl) and LDL-cholesterol levels under 3.4 mM/l (130 mg/dl). Men and women were excluded if their liver-associated enzyme levels were 3 times the upper normal limit, if they had previous liver disease or were intolerant to niacin.

Eligible patients were randomly assigned 500 mg extended-release niacin (Niaspan,® Kos Pharmaceuticals) daily or placebo, both to be taken at night. After 30 days, niacin dose was raised to 1000 mg daily and maintained at this dose for 1 year. Each patient's CIMT was assessed by linear-array 8 MHz probe ultrasonography at baseline and at 1 year. Analysis of CIMT images was masked.

The main endpoint was change in CIMT over 1 year. An increase in liver-associated enzymes, changes in serum lipid levels and admission to hospital for stroke, arterial revascularization, acute coronary syndrome or sudden cardiac death, among others, were some of the secondary endpoints.

Of the 167 patients on baseline statin treatment, 87 patients were assigned additional niacin therapy and 80 were assigned placebo. In total, 149 patients (89.2%) were reassessed at 1 year (study end). Treatment with statin and niacin significantly increased HDL-cholesterol levels by 21%, from 1.0 0.2 mM/l (39 7 mg/dl) to 1.2 ± 0.4 mM/l (47 16 mg/dl), when compared with statin and placebo ( P = 0.002). Although not significant, patients treated with statin and placebo had a higher average increase in CIMT than the statin and niacin-treated patients (0.044 ± 0.100 mm vs 0.014 ± 0.104 mm, P = 0.08). Importantly, the rise in average CIMT was significant for statin and placebo-treated patients but not for patients receiving niacin (0.044 ± 0.100 mm, P < 0.001 and 0.014 ± 0.104 mm, P = 0.23, respectively).

Extended-release niacin slowed the development of atherosclerosis in adults with coronary artery disease, independently from statin therapy.

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