Abstract
Coronary slow flow and no reflow significantly predict poor prognosis in acute myocardial infarction (AMI) patients, especially those with chronic kidney disease (CKD). Early identification of factors contributing to these conditions can mitigate ischemic events and improve outcomes. This study aimed to investigate the association between elevated lipoprotein (a) [Lp(a)] levels and proprotein convertase subtilisin/kexin Type 9 (PCSK-9) inhibitor therapy with coronary slow flow or no reflow after percutaneous coronary intervention (PCI) in AMI patients with CKD. A total of 323 ST-elevation myocardial infarction (STEMI) patients who underwent PCI between October 2017 and June 2023 were included. Patients were divided into CKD (n = 132) and non-CKD (n = 191) groups. Lp(a) levels and the prevalence of coronary slow flow or no reflow after PCI were evaluated. STEMI patients with CKD were further categorized into elevated Lp(a) (n = 81) and normal Lp(a) (n = 51) subgroups. Logistic analysis identified risk factors for coronary slow flow/no reflow after PCI. The impact of PCSK-9 inhibitors on outcomes was also assessed in the elevated Lp(a) subgroup. STEMI patients with CKD had significantly higher Lp(a) levels compared to those without CKD (median 36.75 vs. 15.90 mg/dL, p = 0.0001). CKD patients with elevated Lp(a) had a higher prevalence of coronary slow flow/no reflow after PCI than those with normal Lp(a) (38.3% vs. 13.7%, p = 0.002). Logistic regression analysis identified elevated Lp(a) as an independent risk factor for slow flow/no reflow after PCI in STEMI patients with CKD (OR = 2.985, p = 0.027). In CKD patients with elevated Lp(a), PCSK-9 inhibitors significantly improved post-PCI coronary flow and reduced composite cardiovascular events during 1-year follow-up (22.2% vs. 51.1%, p = 0.008). Elevated Lp(a) is an independent risk factor for coronary slow flow or no reflow after PCI in STEMI patients with CKD. PCSK-9 inhibitors improve coronary blood flow and reduce cardiovascular events in these patients.
Published Version
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