PCSK9 inhibition
PCSK9 inhibitors cut post-PCI coronary slow flow and cardiovascular events in STEMI patients with CKD and elevated Lp(a), 323-patient study finds (Catheter Cardiovasc Interv 2025)
Original title: PCSK-9 Inhibitors Can Significantly Improve the Coronary Slow Flow Caused by Elevated Lipoprotein (a) in ST-Elevation Myocardial Infarction Patients With Chronic Kidney Disease
This study included 323 STEMI patients undergoing PCI between October 2017 and June 2023, split into chronic kidney disease (CKD, n = 132) and non-CKD (n = 191) groups, to test whether elevated Lp(a) and PCSK9 inhibitor therapy affect coronary slow flow or no-reflow after intervention. CKD patients had markedly higher Lp(a) than non-CKD patients (median 36.75 vs. 15.90 mg/dL, P = 0.0001), and among CKD patients, those with elevated Lp(a) had far more post-PCI slow flow/no-reflow than those with normal Lp(a) (38.3% vs. 13.7%, P = 0.002); elevated Lp(a) was an independent risk factor for slow flow/no-reflow in STEMI patients with CKD (OR 2.985, P = 0.027). Among CKD patients with elevated Lp(a), those treated with PCSK9 inhibitors had significantly better post-PCI coronary flow and fewer composite cardiovascular events at 1-year follow-up than those without (22.2% vs. 51.1%, P = 0.008). The authors conclude PCSK9 inhibitors improve coronary flow and reduce cardiovascular events specifically in this high-risk CKD-plus-elevated-Lp(a) STEMI subgroup.
Original abstract
Background: 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.
Aims: 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.
Methods: 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.
Results: 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).
Conclusions: 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.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.