Abstract 5146: Statin Therapy Alters the Relationship Between Apolipoprotein B and Both LDL-C and Non-HDL-C in High-Risk Patients: Effect of Race and Ethnic Background
Racial and ethnic subgroups are frequently under-represented in clinical trials of statin therapy. Apolipoprotein (Apo) B provides a measure of atherogenic particles in blood, a predictor for coronary heart disease (CHD) events. Reducing LDL-C to current goals may still leave an excess of atherogenic lipoproteins. A study of predominantly Caucasian high-risk patients suggested that statin therapy may alter the relationship between Apo B and commonly measured lipoproteins. Therapeutic responses in non-Caucasians have not been well studied. This study sought to examine the effect of racial and ethnic backgrounds on these relationships. A pooled analysis of data obtained in the rosuvastatin clinical development program was used to identify 12,269 high CHD risk patients of varying race/ethnic descent (Caucasian, African, Asian, and Hispanic Latino). The relationships between Apo B and both LDL-C and non-HDL-C were compared at baseline and after therapy with rosuvastatin, atorvastatin, or simvastatin. At baseline, an Apo B of 90 mg/dL corresponded to an LDL-C of 114.4 mg/dL for blacks and ~109 mg/dL for Asians and Hispanics (Table⇓). On statin therapy, to reach an Apo B of 90 mg/dL, blacks required an LDL-C of 87.2 mg/dL, while Hispanics required an LDL-C of 78.3 mg/dL. The baseline non-HDL-C that corresponded to an Apo B of 90 mg/dL was highest for Caucasians and lowest for Asians, with almost no differences observed among the ethnic groups on statin therapy. To achieve the Apo B target of 90 mg/dL, statin therapy required 20 –30 mg/dL lower targets for both LDL-C and non-HDL-C. The strong correlation between Apo B and non-HDL-C on statin therapy (R2 =0.88 to 0.92) suggests that non-HDL-C may be a useful surrogate for Apo B in all high-risk patients. For all race/ethnic groups, in order to achieve an Apo B target of 90 mg/dL with statin therapy, LDL-C and non-HDL-C targets need to be closer to those currently recommended for very high CHD risk.