title: Reducing coronary risk by raising HDL-cholesterol: risk modelling the addition of nicotinic acid to existing therapy.
abstract: OBJECTIVE
  Reduction in total cholesterol (TC) and LDL-cholesterol (LDL-C) forms one of the principal objectives of most cardiovascular secondary prevention strategies. Many patients being treated with statins, however, have significant residual dyslipidaemia, with many having suboptimal HDL-cholesterol (HDL-C) levels. The addition of nicotinic acid to a statin has been shown to improve this profile, although clinical outcome evidence is currently lacking. This study set out to model the impact of nicotinic acid therapy on cardiovascular risk in these patients, based on Framingham risk assessments on a cohort of patients drawn from UK general practitioner records.
  
  
  METHODS
  Cardiovascular risk profiles were extracted from a research database of 602,222 patients from 98 UK general practices. 23 262 statin-treated patients with established cardiovascular disease or diabetes were identified and their 4-year Framingham risk was estimated. Patients who had either TC or HDL-C outside the desirable range then had their lipid profile adjusted in accordance with the likely performance of nicotinic acid, and the Framingham risk was then re-assessed.
  
  
  RESULTS
  Baseline 4-year coronary risk in the group as a whole was 11.5% (95%CI: 11.4-11.6). After adjustment of the lipid profile, this was reduced to 9.7% (95%CI: 9.6-9.8), a reduction in risk of 15.9% (95%CI: 15.1-16.6). When modelling was limited to those with diabetes or an abnormal treated lipid profile, the magnitude of change was increased to 23-29% depending on sex and subgroup.
  
  
  CONCLUSIONS
  Risk factor modelling suggests that raising HDL-C levels using nicotinic acid in statin-treated patients is likely to yield significant incremental clinical benefits. The results of clinical trials currently under way are awaited with interest.
authors.affiliation: Primary Care Informatics, Division of Community Health Sciences, St. George's - University of London, London, UK. jbelsey@jbmedical.com
authors.forename: Jonathan
authors.initials: J
authors.lastname: Belsey
authors.forename: Simon
authors.initials: S
authors.lastname: de Lusignan
authors.forename: Jeremy
authors.initials: J
authors.lastname: van Vlymen
authors.forename: Tom
authors.initials: T
authors.lastname: Chan
authors.forename: Nigel
authors.initials: N
authors.lastname: Hague
mesh_terms: D008076:Cholesterol, HDL / Q000097:blood*; D003327:Coronary Disease / Q000097:blood / Q000517:prevention & control*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage; D009525:Niacin / Q000008:administration & dosage*; D012307:Risk Factors
chemical_list: D008076:Cholesterol, HDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D009525:Niacin