LAUSR

We investigated the effect of low-density lipoprotein cholesterol (LDL-C) on the geometry of coronary bifurcation lesions. A total of 300 non-left main bifurcation lesions in 298 patients from J-REVERSE registry were classified according to statin treatment status at admission (NT, non-treated; ST, statin-treated) and were further subdivided based on LDL-C levels with a cutoff of 100 mg/dL (NT–high, n = 76 lesions; NT–low, n = 46; ST–high, n = 99 and ST–low, n = 79). In addition, a group with strict control of LDL-C (< 70 mg/dL) was defined (ST–SC; n = 19). The NT–high group had higher angled bifurcations compared to that in the NT–low group (59.1° ± 21.5° vs. 50.3° ± 18.6°, p = 0.02). In the multivariate analysis, NT–high group was an independent factor contributing on generation of higher angled (> 80°) lesion (odds ratio 3.77, 95% CI 1.05–13.5, p = 0.04). The NT–low group had more men (95.6 vs. 81.6%, p = 0.03), and greater plaque volume in the distal main vessel (7.1 ± 3.2 mm3/mm vs. 5.7 ± 2.7 mm3/mm, p = 0.02), compared to those in the NT–high group. LDL-C was more likely to remain high after statin treatment in younger patients (65.3 ± 3.6 years vs. 68.6 ± 8.4 years, p = 0.02) and current smokers (36.7 vs. 16.9%, p = 0.004). The ST–SC group had limited luminal volume expansion compared to that in the ST–high group (proximal: 6.7 ± 1.4 mm3/mm vs. 7.7 ± 2.3 mm3/mm, p = 0.04; distal: 5.3 ± 1.5 mm3/mm vs. 6.5 ± 1.9 mm3/mm, p = 0.04), regardless of similar plaque volumes. Elevated LDL-C is likely to promote the generation of higher angled bifurcation lesions and multiple risk factors lead to a more progressed bifurcation lesion even in patients with lower LDL-C levels.