The low-density lipoprotein cholesterol lowering is an ineffective surrogate marker of statin responsiveness to predict cardiovascular outcomes: The 10-year experience of matched population (a STROBE-compliant article).

Statins therapy decrease both low-density lipoprotein cholesterol (LDL-C) levels and the risk of atherosclerotic cardiovascular disease (ASCVD) with considerable individual variability. Whether the amount of LDL-C lowering is a surrogate maker of statin responsiveness to ASCVD prevention has not been fully investigated. Among 2352 eligible patients with statin prescriptions in a cardiovascular center between January 2005 and February 2014, one-third of patients (33%) on statin therapy failed to achieve effective reductions in LDL-C (LDL-C level reduction of less than 15%). By using, propensity-score matched population (480 pairs, n = 960), the 5-year cumulative incidences of total major adverse cardiac events (MACE) were evaluated. The 5-year total MACE did not differ between normal cholesterol responders and non-responders (15.4% vs 16.1%, respectively; P = .860). In the subgroup analysis, male sex, older age, percutaneous coronary intervention, and heart failure were positive predictors, and dyslipidemia at the beginning of statin therapy was the only negative predictor of MACE in the 5-year follow-up (all P value < .05). However, cholesterol responsiveness after statin therapy did not influence the incidence of MACE (P = .860). The amount of LDL-C lowering did not predict beneficial effect on clinical outcomes of ASCVD after statin therapy. This result supports that given statin therapy, total ASCVD risk reduction should be tailored, which may not dependent to adherence to degree of LDL-C lowering or LDL-C goal based treatment.