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Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors With Statin for ACS Patients

Assiut University · 2026
ClinicalTrials.gov · Datasets · License: Public Domain · 2026
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Cardiovascular diseases (CVDs) remain the leading cause of death globally, with a dominant contribution from atherosclerotic CVD (ASCVD). * Percutaneous coronary intervention (PCI) is a key method for revascularization in ASCVD patients, improving their prognosis. With the continuous advancement of PCI in recent years, its indications have become increasingly diverse. However, patients still face a pronounced residual risk post-PCI. Research indicates that plaque vulnerability and other risk factors contribute to a 15%-20% rate of major adverse cardiovascular events (MACE) within one year following PCI. * The pathological mechanism of atherosclerosis is closely tied to the abnormal deposition of low-density lipoprotein cholesterol (LDL-C) beneath the vascular endothelium. This lipid particle can provoke a chronic inflammatory response in the vessel wall, eventually causing plaque formation. Moreover, the marked elevation of LDL-C levels is highly connected to the occurrence and progression of ASCVD. * Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease worldwide, with a prevalence of approximately 25% (range 14%-32%). * It is regarded as the hepatic manifestation of metabolic syndrome (MetS) and is strongly associated with obesity and diabetes mellitus (DM). * Cardiovascular (CV) disease is one of the leading causes of death in patients with MASLD * Statins are the cornerstone of lipid-lowering therapy, noticeably diminishing LDL-C levels by blockading HMG-CoA reductase. For patients following PCI, several guidelines suggest high-intensity statin therapy to reach a target LDL-C level of ≤1.4 mmol/L and a ≥50% decline from baseline. * However, even with intensive statin therapy, many post-PCI patients still exhibit LDL-C levels above the target limits. * Inhibitors of proprotein convertase subtilisin/kexin type 9(PCSK9) notably decrease plasma LDL-C levels by preventing the binding of PCSK9 protein to LDL-C receptors (LD
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