title: Failure to achieve recommended LDL cholesterol levels by suboptimal statin therapy relates to elevated cardiac event rates.
abstract: OBJECTIVE
  The majority of patients with myocardial infarction (MI) and hypercholesterolaemia does not achieve guideline recommended low-density lipoprotein cholesterol (LDL) levels. Suboptimal dosages of statins explain this dilemma in most patients.
  
  
  METHODS
  We evaluated the relationship between statin treatment quality (optimal: LDL<115 mg/dl, suboptimal: LDL>/=115 mg/dl, no statin therapy despite hypercholesterolaemia) and the subsequent incidence of coronary events (coronary death, nonfatal MI, bypass surgery) over a 30 months follow-up in a large cohort of post MI patients with hypercholesterolaemia (n=2045). Analysis was performed in a nested case-control manner comparing 173 cases with a coronary event and 346 matched controls.
  
  
  RESULTS
  Patients who developed a coronary event were treated optimally in 11.0%, suboptimally in 43.4% (p<0.05 vs. optimal treatment) and were untreated in 45.7% (p<0.001 vs. optimal treatment). Respective numbers in event-free patients were 21.4%, 47.7%, and 30.9%. After adjustment for most potential confounders, including all cardiovascular risk factors and medication, the relative risk of future non-fatal MI and coronary death associated with a suboptimal statin treatment was 2.02 (95% CI 1.04 to 4.18) compared to optimal statin treatment. Moreover, the statin equivalent dose in optimally treated individuals was significantly higher than in suboptimally treated individuals (0.85+/-0.03 vs. 0.78+/-0.02, p<0.05).
  
  
  CONCLUSIONS
  In this community-based study, a lipid lowering therapy with statins into the recommended target range of LDL levels may be associated with decreased cardiovascular risk compared to a statin therapy without titrating the LDL level below 115 mg/dl. Thus, the quality of statin treatment was identified as an independent predictor of coronary events in post MI patients.
authors.affiliation: Klinik und Poliklinik für Innere Medizin II, University of Regensburg, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Baessler
authors.forename: M
authors.initials: M
authors.lastname: Fischer
authors.forename: V
authors.initials: V
authors.lastname: Huf
authors.forename: S
authors.initials: S
authors.lastname: Mell
authors.forename: C
authors.initials: C
authors.lastname: Hengstenberg
authors.forename: B
authors.initials: B
authors.lastname: Mayer
authors.forename: S
authors.initials: S
authors.lastname: Holmer
authors.forename: G
authors.initials: G
authors.lastname: Riegger
authors.forename: H
authors.initials: H
authors.lastname: Schunkert
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D008078:Cholesterol, LDL / Q000097:blood*; D015331:Cohort Studies; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006937:Hypercholesterolemia / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology*; D012307:Risk Factors; D017211:Treatment Failure
chemical_list: D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors