Hideki Yano1, Shigeo Horinaka2, Toshihiko Ishimitsu2. 1. Department of Cardiology and Nephrology, Dokkyo Medical University, Mibu, Tochigi, Japan. Electronic address: hideki-y@cvc.pref.gunma.jp. 2. Department of Cardiology and Nephrology, Dokkyo Medical University, Mibu, Tochigi, Japan.
Abstract
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.
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.
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