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. Design and setting: 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). Conclusion: 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. 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. Design and setting: 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 suboptimally treated individuals (0.85 ± 0.03 vs. 0.78 ± 0.02, p <0.05). Conclusion: 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.