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PCSK9 is a predictive biomarker of major adverse events after acute myocardial infarction
Ahmad Hayek1, Simon Leboube2, Camille Brun3
1Univ Lyon, CarMeN Laboratory, INSERM, INRA, INSA Lyon, Université Claude Bernard Lyon 1, Groupement Hospitalier Est, Bâtiment B13, 59 boulevard Pinel, F-69500 Bron, France; Unité de Soins Intensifs Cardiologiques, Hôpital Louis Pradel, Hospices Civils de Lyon, 59 boulevard Pinel, F-69500 Bron, France.
Insights
Proprotein convertase subtilisin/kexin type 9 (PCSK9) levels rise after ST-elevation myocardial infarction (STEMI). Elevated PCSK9 is linked to major adverse cardiovascular events, suggesting it as a potential therapeutic target.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Clinical Research
Background:
- Proprotein convertase subtilisin/kexin type 9 (PCSK9) influences LDL cholesterol metabolism, vascular inflammation, and plaque stability.
- The specific role of PCSK9 in the context of ST-elevation myocardial infarction (STEMI) requires further elucidation.
Purpose of the Study:
- To investigate dynamic changes in plasma PCSK9 levels during hospitalization for STEMI.
- To determine the association between PCSK9 levels and the occurrence of major adverse cardiovascular events (MACE).
Main Methods:
- A prospective study involving 346 STEMI patients treated with percutaneous coronary intervention (PCI) who had not previously used PCSK9 inhibitors.
- Plasma PCSK9 levels were quantified using ELISA at admission and discharge.
- Cardiac magnetic resonance imaging assessed infarct size and left ventricular ejection fraction (LVEF) at one month, with clinical events tracked for 12 months.
Main Results:
- PCSK9 plasma levels demonstrated a significant increase from admission to 48 hours post-STEMI.
- Higher PCSK9 levels at 48 hours were correlated with a substantially increased risk of MACE, including ischemic events.
- Multivariable analysis confirmed that elevated PCSK9 independently predicted MACE, highlighting its prognostic significance.
Conclusions:
- PCSK9 levels significantly increase following STEMI.
- Elevated PCSK9 post-STEMI is an independent predictor of adverse cardiovascular outcomes.
- PCSK9 emerges as a potential prognostic biomarker and a viable therapeutic target for mitigating cardiovascular risk in post-MI patients.
Background:
Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates low-density lipoprotein cholesterol (LDLc) metabolism and is implicated in vascular inflammation and plaque vulnerability. Its role following ST-elevation myocardial infarction (STEMI) remains under investigation.
Objective:
To assess changes in PCSK9 plasma levels during hospitalization for STEMI and evaluate their association with major adverse cardiovascular events (MACE).
Methods:
In this prospective, single-center study (2016-2021), 346 STEMI patients undergoing percutaneous coronary intervention (PCI) without prior PCSK9 inhibitor use were enrolled. PCSK9 levels were measured at admission and discharge using ELISA. Infarct size and left ventricular ejection fraction (LVEF) were evaluated by cardiac magnetic resonance imaging at one month. Clinical events were recorded over a 12-month follow-up.
Results:
PCSK9 plasma levels increased significantly from admission to 48 h (median 321.4 pg/mL, IQR [266.1-377.3]). Higher 48 h PCSK9 levels (≥ Q2-Q4) were associated with increased MACE (HR 9.2, 95% CI 3.9-21.7, p = 0.008), including ischemic events (HR 3.8, CI 1.05-14.0). In multivariable analysis, elevated PCSK9 remained independently associated with MACE (adjusted HR 7.5, CI 1.02-54.8, p = 0.049).
Conclusion:
PCSK9 levels rise post-STEMI and are independently associated with worse clinical outcomes. PCSK9 may serve as a prognostic biomarker and therapeutic target to reduce cardiovascular risk post-MI.
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