Background: The addition of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, evolocumab, to statin therapy produced incremental regression of atherosclerotic plaques and a collaborative prevention of cardiovascular events in patients with coronary artery disease. The effect on fibrous-cup thickness, or extension of the atherosclerotic plaque with PCSK9-inhibitor, for several weeks after onset of acute coronary syndrome (ACS) has never been reported. Methods: This study aimed to examine the effect of evolocumab on fibrous-cap thickness, as well as the extent of the atherosclerotic plaque, by serial optical coherence tomography (OCT) analysis in patients with ACS. All patients received rosuvastatin 5 mg/day from at least 24 h after onset of ACS. Patients received evolocumab (140 mg every 2 weeks) 1 week after the onset of ACS in the statin plus evolocumab group. Patients took only rosuvastatin in the statin monotherapy group. OCT was performed to assess intermediate, non-culprit lesions just 4 and 12 weeks after emergent percutaneous coronary intervention. Results: OCT analysis revealed that the increase in fibrous-cap thickness and decrease in macrophage grade were greater with a narrower lipid arc and shorter lipid length, which were associated with lower low-density lipoprotein cholesterol (LDL-C) in the statin plus evolocumab group than in the statin alone treatments, even for a short term after ACS onset. Conclusions: Addition of the PCSK9-inhibitor evolocumab to statin therapy might produce incremental growth in fibrous-cap thickness and regression of the lipid-rich plaque, which were associated with greater reduction of LDL-C even for a short term in the early phase of ACS.

Because systemic inflammation after coronary intervention places patients at increased risk of subsequent cardiac events, we aimed to compare clinical outcomes and chronic serum inflammation markers of paclitaxel-eluting stents (PES) and sirolimus-eluting stents (SES) in hemodialysis patients. Paclitaxel-eluting stents and SES were implanted in 36 patients with 46 lesions, and 32 patients with 40 lesions, respectively. In addition to 1-year major adverse cardiac event (MACE) rates, high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), neopterin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) were also compared before and 9 months after percutaneous coronary intervention (PCI). The incidence of MACE was significantly lower in the PES group than in the SES group (11.1 vs. 25.0 %, respectively, P = 0.042), mainly due to the reduction of target lesion revascularization in the PES group (6.5 vs. 17.5 %, P = 0.003). The logarithm of hs-CRP as well as IL-6 decreased significantly 9 months post-PCI compared with pre-PCI in the PES group (hs-CRP: 3.65 ± 0.35 vs. 2.91 ± 0.48, P = 0.007; IL-6: 6.73 ± 3.66 vs. 2.61 ± 2.29, P = 0.017) but not in the SES group (hs-CRP: 3.33 ± 0.29 vs. 3.42 ± 0.27, P not significant; IL-6: 6.08 ± 4.97 vs. 5.66 ± 4.29, P not significant). However, neopterin, ICAM-1, and VCAM-1 remained unchanged both pre-PCI and 9 months post-PCI in both groups. Moreover, MACE were less frequent in patients with decreased hs-CRP levels 9 months post-PCI compared with patients without decreased hs-CRP levels (P = 0.002) in all patients. Paclitaxel-eluting stents appear to be more effective than SES in reducing MACE rates, especially target lesion revascularization, and may be able to stabilize local inflammatory changes of target lesions specifically in patients on hemodialysis. Thus PES, which inhibit in-stent restenosis and cardiac events in hemodialysis patients, may play an important role in suppression of chronic inflammatory response in target lesions as compared with SES. Chronic continuous inflammation plays an important role after implantation of both types of stent with regard to in-stent restenosis in patients on hemodialysis.

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Long stenting using the XIENCE stent which was guided by IVUS for diffuse, long lesions was associated with favorable clinical outcomes at two years in daily clinical practice.