Abstract 13236: Elevated Serum Proprotein Convertase Subtilisin/Kexin Type 9 Level Independently Predicts Long-Term Cardiovascular Outcomes in Patients With Chronic Coronary Artery Disease
Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) may directly promote atherosclerosis. However, the long-term impact of elevated serum PCSK9 levels on the risk of cardiovascular events has not been fully elucidated. We therefore analyzed the association of serum PCSK9 levels with major adverse cardiovascular events (MACE) in patients with chronic coronary artery disease (CAD).
Methods: Serum PCSK9 levels were measured in 306 patients (171 men; mean age, 68.3 ± 10.5 years) who underwent coronary computed tomography (CT) angiography. Furthermore, 174 patients who were judged to have obstructive CAD were followed-up for a median period of 1584 days (interquartile range [IR] 1334-1790). MACE was defined as death, acute coronary syndrome, and cerebral stroke.
Results: Serum levels of PCSK9 were higher in women (268 ng/mL, IR 211-325) than in men (218 ng/mL, IR 175-284, P<0.001). In age- and gender-adjusted logistic regression analysis, serum PCSK9 levels had a significant association with obstructive CAD (odds ratio 1.63 per 100 ng/mL increase, 95% confidence interval [CI] 1.21-2.19, P=0.001). Among patients with obstructive CAD, 14 patients developed MACE during the follow-up period. Patients in the highest tertile of PCSK9 (≥288 ng/mL) had a significantly higher risk of MACE than those in the lower tertiles (log-rank, P=0.005). In Cox regression analysis using age, gender, estimated glomerular filtration rate (eGFR), hypertension, dyslipidemia, diabetes, smoking, and vulnerable coronary plaque characteristics assessed by CT, including low-density plaque, positive remodeling, and spotty calcification, as covariates, serum PCSK9 level was an independent predictor of MACE (hazard ratio 2.03 per 100 ng/mL increase, 95% CI 1.13-3.62, P=0.017).
Conclusions: Baseline serum PCSK9 level significantly predicted MACE, as well as present coronary stenosis, independent of traditional cardiovascular risk factors and vulnerable plaques.
Author Disclosures: A. Sakamoto: None. N. Ishizaka: None. M. Uehara: None. J. Ando: None. I. Komuro: None.
- © 2016 by American Heart Association, Inc.