title: Correction of low HDL cholesterol to reduce cardiovascular risk: practical considerations relating to the therapeutic use of prolonged-release nicotinic acid (Niaspan).
abstract: BACKGROUND
  Substantial residual cardiovascular risk persists despite effective LDL lowering treatment in populations at elevated risk for adverse cardiovascular outcomes. Low HDL cholesterol is an independent cardiovascular risk factor and occurs in about one-third of patients treated for dyslipidaemia in Europe. Moreover, randomised intervention studies have shown that increasing HDL cholesterol improves cardiovascular outcomes. Correcting low HDL cholesterol therefore presents a rational and proven strategy for intervention to produce further reductions in cardiovascular risk beyond those possible with a statin alone. Nicotinic acid (niacin in the USA) is the most effective agent currently available for increasing levels of HDL cholesterol.
  A once-daily, prolonged-release formulation of nicotinic acid (Niaspan) is as effective on HDL cholesterol as the immediate-release formulation, and is equally effective at increasing HDL cholesterol whether or not patients are already taking a statin. Niaspan also shares the antiatherogenic benefit of nicotinic acid, and induced regression of atherosclerosis in patients with cardiovascular disease during a period of treatment of up to 2 years. The incidence of flushing, the principal side effect of nicotinic acid, is lower with Niaspan than with immediate-release nicotinic acid. Simple practical measures are available to minimise the incidence and impact of flushing, including careful dose titration and avoiding hot or spicy foods near the time of ingestion of Niaspan. The potential for hepatotoxicity, muscle toxicity or marked exacerbation of hyperglycaemia in diabetes with Niaspan is very low, with or without concomitant statin treatment.
  
  
  CONCLUSIONS
  Niaspan provides a practical means of delivering the cardioprotective benefits associated with correction of low HDL cholesterol.
authors.affiliation: Charité-Universitaetsmedizin, Berlin, Germany. anja.vogt@charite.de
authors.forename: A
authors.initials: A
authors.lastname: Vogt
authors.forename: U
authors.initials: U
authors.lastname: Kassner
authors.forename: U
authors.initials: U
authors.lastname: Hostalek
authors.forename: E
authors.initials: E
authors.lastname: Steinhagen-Thiessen
mesh_terms: D002318:Cardiovascular Diseases / Q000517:prevention & control*; D008076:Cholesterol, HDL / Q000187:drug effects / Q000378:metabolism*; D003692:Delayed-Action Preparations; D050171:Dyslipidemias / Q000150:complications / Q000188:drug therapy*; D005483:Flushing / Q000139:chemically induced; D006801:Humans; D000960:Hypolipidemic Agents / Q000009:adverse effects; D009525:Niacin / Q000009:adverse effects / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D008076:Cholesterol, HDL; D003692:Delayed-Action Preparations; D000960:Hypolipidemic Agents; D009525:Niacin