CLINICAL, LABORATORY, AND CORONARY ATHEROSCLEROTIC PREDICTORS OF NON-RESPONSE TO STATIN THERAPY: INSIGHTS FROM THE PROSPECTIVE, MULTICENTER, INTERNATIONAL PARADIGM SERIAL CCTA REGISTRY

Background: While statins reduce the relative risk for MACE by ~30%, significant residual risk remains. We explored the association of clinical, laboratory and coronary atherosclerotic predictors with statin non-response. Methods: The multi-center PARADIGM registry included 2,252 patients who underwent serial CCTA >2 years apart, with 17-segment coronary tree quantification of vessel, lumen and plaque. Patients with statin use at baseline and follow-up CCTA, available outcomes and without interval revacularization were included. Statin non-response was defined as: (1) annualized percent atheroma volume (PAV) progression >1.0%, corrected for calcium progression (ΔPAVcalcium /year below 1st quartile); (2) increase in high risk plaques (HRP) as defined by the presence of ≥2 features (positive remodeling / low attenuation plaque / spotty calcification); and (3) MACE (death, myocardial infarction, or revascularization) after follow-up CCTA. Results: Of 485 patients (61.9 ± 9.2 years, 60% male) on statin therapy followed for 6.8 ± 2.6 years, 158 (32.6%) were non-responders: 36 rapid PAV progression, 70 increase in HRP, and 52 MACE. Of the clinical and laboratory parameters, diabetes and HbA1c were associated with statin non-response. Of the atherosclerotic findings by CCTA, baseline overall PAV and number of HRP features predicted non-response (Figure 1). Conclusion Among patients on statin therapy, diabetes, HbA1c, baseline PAV and HRP features were associated with statin non-response.