Elsevier

The American Journal of Cardiology

Volume 133, 15 October 2020, Pages 54-60
The American Journal of Cardiology

Relation of Proprotein Convertase Subtilisin/Kexin Type 9 to Cardiovascular Outcomes in Patients Undergoing Percutaneous Coronary Intervention

https://doi.org/10.1016/j.amjcard.2020.07.032Get rights and content

The pharmacological inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has been shown to drastically affect low-density lipoprotein cholesterol levels and associated cardiovascular diseases. However, the potential effectiveness of PCSK9 serum levels as a biomarker for cardiovascular risk remains unclear. Serum PCSK9 levels in patients who underwent percutaneous coronary intervention (PCI) may predict long-term outcomes. PCSK9 levels were measured in 749 consecutive patients with coronary artery disease undergoing PCI. These patients were classified into 2 groups according to their serum levels of PCSK9. The primary end point was a composite of the major adverse cardiac events (MACE), including cardiac death, myocardial infarction, stroke, and any revascularization. The median PCSK9 level was 302.82 ng/ml. During a median follow-up of 28.4 months, a total of 38 (5.1%) MACE was recorded, and 50 (6.7%) patients died from any cause. Multivariate Cox regression analysis showed that compared with a lower serum PCSK9 level, a higher serum PCSK9 level was independently associated with a higher rate of MACE (adjusted hazard ratio 2.290, 95% confidence interval 1.040 to 5.045, p = 0.040) and all-cause death (adjusted hazard ratio 2.511, 95% confidence interval 1.220 to 5.167, p = 0.026). Results were consistent after propensity-score matching (MACE, adjusted HR 2.236, 95% CI 1.011-5.350, p = 0.047; all-cause death, adjusted HR 2.826, 95% CI 1.258-6.349, p = 0.012). Baseline serum PCSK9 levels were associated with long-term cardiovascular clinical outcomes and mortality during the long-term follow-up after PCI in patients with coronary artery disease.

Section snippets

Methods

We screened 796 consecutive patients with coronary artery disease (CAD) scheduled for PCI at Incheon St. Mary's Hospital between September 2015 and November 2017. Patients with cardiogenic shock, end-stage renal disease who were on dialysis, without sufficient blood samples, or who did not undergo PCI were excluded. Of the 796 eligible patients, 749 had samples available to measure the serum level of PCSK9. All participants provided written informed consent to participate before PCI and blood

Results

The mean age of all available 749 patients was 65.9 ± 11.8 years old, and 66.5% of the patients were men. Among them, 35.4% had a history of dyslipidemia, and 31.4% received statins before the index admission. Table 1 presents the baseline characteristics according to the groups divided by the median PCSK9 level. The median serum PCSK9 level was 302.82 mg/ml (interquartile range 234.30 to 366.91). The frequencies of women, hypertension, diabetes mellitus, dyslipidemia, chronic kidney disease,

Discussion

The present investigation demonstrates that higher serum PCSK9 levels are associated with not only MACE but also all-cause mortality in patients with CAD under PCI. The serum PCSK9 level predicts future adverse events independently of potential confounding factors, such as previous statin use or lipid profiles.

Previous studies concerning the prognostic value of serum PCSK9 have demonstrated inconsistent results. In the cohort studies including populations without CAD, contradictory results had

Author Contributions

Ik Jun Choi: Conceptualization, Methodology, Formal analysis, Writing - original draft, Writing - review & editing; Sungmin Lim: Conceptualization, Writing - original draft, Writing - review & editing; Dongjae Lee: Formal analysis; Won Jik Lee: Formal analysis; Kwan Yong Lee: Formal analysis, Writing - review & editing; Mi-Jeong Kim: Methodology, Supervision; Doo Soo Jeon: Methodology, Supervision, Writing - review & editing

Disclosures

All authors declare they have no conflicts of interest regarding the contents of this article.

Acknowledgments

The authors acknowledge Eunsun Kang and Miyoung Youm for their excellent support. The authors are grateful for the cooperation of clinical research coordinators and members of Institute for Bio-Medical convergence, Incheon St. Mary's Hospital, The Catholic University of Korea.

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