Abstract 16913: Greater Coronary Atheroma Regression in Women Compared With Men: A Pooled Analysis of Serial Intravascular Ultrasonography Trials Utilizing High-intensity Statin Therapy
Introduction: High-intensity statin therapy (HIST) reduces cardiovascular events, however sex-related differences in treatment effects are not well characterized, possibly contributing to gender disparities in HIST use. Hypothesis: Sex-related differences in coronary atheroma regression exist following HIST. Methods: We undertook a patient-level post-hoc pooled analysis of 3 randomized trials utilizing serial coronary IVUS to test the anti-atherosclerotic effects of HIST in patients with coronary disease. Sex-related differences in changes (Δ) in coronary percent atheroma volume (PAV) were ascertained following 18-24 months of either atorvastatin 80 mg or rosuvastatin 40 mg. Results: In women (n=451) compared with men (n=1190), levels of on-treatment LDL-C (68±24 vs. 68±22mg/dl, p=0.62) were similar, however HDL-C (53±12 vs. 47±11 mg/dl, p<0.01) and CRP [1.7 (0.9, 3.8) vs. 1.1 (0.6, 2.7) mg/l, p<0.01] were higher. Compared with men, women harbored lower baseline PAV (34.8±8.7 vs. 38.3±8.8%, p<0.001), yet demonstrated greater PAV regression (ΔPAV -1.07±0.26 vs. -0.66±0.23%, p=0.02). When achieved on-treatment LDL-C levels were <70mg/dl, women demonstrated greater PAV regression than men (-1.49±0.21 vs. -0.97±0.13%, p=0.035), however had similar rates of PAV regression with on-treatment LDL-C levels ≥70 mg/dl (-0.63±0.25 vs. -0.42±0.16%, p=0.47). Sex-related differences in atheroma regression did not differ according to achieved levels of HDL-C, non-HDL-C or CRP (Figure). Multivariable analysis revealed female sex to independently associate with PAV regression (coefficient -0.66, p=0.017). Conclusion: Women systematically demonstrate greater degrees of coronary plaque regression compared with men following long-term HIST, especially in the setting of lower achieved LDL-C levels. Further research is required for elucidating mechanisms underpinning sex-related variations in plaque progression-regression.