Atherogenic dyslipidemia as evidenced by the lipid triad: prevalence and associated risk in statin-treated patients in ambulatory care.
OBJECTIVE
The prevalence of atherogenic dyslipidaemia (AD) can be assessed using the lipid triad (low high-density lipoprotein cholesterol [HDL-C] < 35 mg/dl, high triglyceride (TG) levels (≥ 200 mg/dl) and a high total cholesterol HDL-C ratio (TC/HDL-C>5). The aim of the present analysis was (1) to describe the prevalence of the lipid triad, (2) to quantify the associated cardiovascular risk on the basis of the PROCAM score, and (3) to calculate the additional risk reduction that can be obtained by adding nicotinic acid (NA) to a pre-existing statin therapy (model based on the outcomes of a previous randomized controlled study).


METHODS
Descriptive post-hoc analysis of the German 4E registry in 24,500 patients receiving statins for primary cardiovascular prevention in ambulatory care.


RESULTS
The sample comprised 24,500 patients in primary prevention, who had an overall 10-year risk of 16.2%. The prevalence of patients with lipid triad was 24.0%. The mean estimated risk reduction in the total sample (calculated on the basis of a mean LDL-C decrease by 24.3% and other lipid parameter changes) achieved after 6-week statin treatment was 46.6%, the estimated additional relative risk reduction by NA 45.1% (total effect compared to baseline about 70%). In the lipid triad group, the additional relative risk reduction by NA treatment was 42.9%. Relative treatment effects were consistent, irrespective of age and gender. Limitations of this analysis include the use of the TC/HDL-C ratio instead of the direct small dense LDL-C measurements, and the unknown variations of effect size of NA induced lipid reduction when used in combination with statins.


CONCLUSIONS
Our model calculations indicate that the residual risk which persists after statin treatment could be substantially lowered if besides LDL-C also HDL-C and TG would be addressed, e.g. by adding NA to statin therapy. Definitive prospective studies are needed to confirm this hypothesis.
Institute for Clinical Pharmacology, Public Health Association Saxony, Technical University Dresden, Germany. kurt_bestehorn@msd.de
Kurt
K
Bestehorn
Wenefrieda
W
Smolka
David
D
Pittrow
Helmut
H
Schulte
Gerd
G
Assmann
D000328:Adult; D000368:Aged; D000553:Ambulatory Care / Q000379:methods / Q000706:statistics & numerical data; D050197:Atherosclerosis / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology; D008076:Cholesterol, HDL / Q000032:analysis / Q000097:blood; D008078:Cholesterol, LDL / Q000032:analysis / Q000097:blood; D050171:Dyslipidemias / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy* / Q000453:epidemiology*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008055:Lipids / Q000032:analysis / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D012042:Registries; D012307:Risk Factors; D014280:Triglycerides / Q000032:analysis / Q000097:blood
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D014280:Triglycerides