Abstract 18737: Effect of Non-Statin Lipid-Lowering Drug Therapy on Coronary Plaque Composition as Assessed by Coronary Computed Tomography Angiography

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Abstract

Introduction: Statin therapy effectively prevents cardiovascular events. Non-statin lipid-lowering drug therapy (NS-LLDT) is typically used as second-line therapy in patients intolerant to statins. While statin therapy has been shown to increase calcified plaque volume, the effect of NS-LLDT on plaque composition is unknown.

Objective: To determine whether NS-LLDT, alone or in combination with statin therapy, affects plaque composition in patients undergoing coronary computed tomography angiography (cCTA).

Methods: We analyzed patients enrolled in a prospective, multicenter registry (CONFIRM) of patients undergoing cCTA. Patients with known lipid-lowering therapy status and without previously established coronary artery disease were included in the analysis. Multivariate ordinal regression, adjusted for cardiac risk factors, was performed to determine the effect of lipid-lowering therapy (NS-LLDT, statin, or both) on the number of coronary artery segments (none, 1-2, or >2 segments) with each plaque type (non-calcified (NCP), partly calcified (PCP), or calcified (CP)).

Results: Of the 27,125 patients in CONFIRM, 4945 patients met the inclusion criteria. 146 (3.0%) patients were on NS-LLDT, 1725 (34.9%) were on statin therapy, and 225 (4.6%) were on both NS-LLDT and statin therapy. At baseline, patients on lipid-lowering therapy had more prevalent risk factors compared to patients not on lipid-lowering therapy. NS-LLDT, as compared to no NS-LLDT, was not associated with a higher number of segments possessing NCP (OR 1.29, 95% CI 0.81-2.00, p = 0.26), PCP (OR 1.27, 95% CI 0.82-1.92, p = 0.27), or CP (OR 1.30, 95% CI 0.90-1.86, p = 0.16). Patients on NS-LLDT plus statin therapy, in comparison to patients on statin therapy alone, did not have a different prevalence of NCP (OR 0.90, 95% CI 0.62-1.29, p = 0.58), PCP (OR 1.02, 95% CI 0.72-1.43, p = 0.91), or CP (OR 1.21, 95% CI 0.87-1.67, p = 0.26), suggesting no interaction between NS-LLDT and statin therapy.

Conclusions: NS-LLDT was not associated with differences in plaque composition by cCTA, and did not modify the impact of statin therapy on plaque composition. The absence of an effect of NS-LLDT on plaque composition could explain the superiority of statin therapy in prevention of cardiovascular events.

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