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Published on: May 28, 2019
Association of Circulating PCSK9 With Ischemia-Reperfusion Injury in Acute ST-Elevation Myocardial Infarction
Christina Tiller1, Magdalena Holzknecht1, Ivan Lechner1
1University Clinic of Internal Medicine III, Cardiology and Angiology (C.T., M.H., I.L., F.O., S.E., T.K., A.B., B.M., S.J.R., M.R.), Medical University of Innsbruck, Austria.
Insights
Proprotein convertase subtilisin/kexin 9 (PCSK9) levels rise after ST-elevation myocardial infarction (STEMI) treatment. Elevated PCSK9 48 hours post-PCI correlates with myocardial injury and predicts adverse cardiac events.
Area of Science:
- Cardiology
- Biomarkers
- Medical Imaging
Background:
- Proprotein convertase subtilisin/kexin 9 (PCSK9) is a potential cardiovascular biomarker.
- Its role in acute ST-elevation myocardial infarction (STEMI) requires further elucidation.
- This study investigates PCSK9's association with ischemia-reperfusion injury in STEMI patients.
Purpose of the Study:
- To assess the relationship between PCSK9 levels and myocardial injury markers after primary percutaneous coronary intervention (PCI) in STEMI patients.
- To determine if PCSK9 predicts adverse clinical outcomes following STEMI.
Main Methods:
- Prospective registry substudy of 205 STEMI patients undergoing primary PCI.
- Measurement of serum PCSK9 concentrations at 24 and 48 hours post-PCI.
- Cardiac magnetic resonance imaging (CMR) to assess intramyocardial hemorrhage, microvascular obstruction (MVO), and infarct size.
Main Results:
- PCSK9 levels significantly increased from 24 to 48 hours post-PCI.
- PCSK9 at 24 hours showed no correlation with myocardial injury.
- PCSK9 at 48 hours was significantly associated with intramyocardial hemorrhage, MVO, and larger infarct size.
Conclusions:
- PCSK9 levels dynamically change after STEMI treatment.
- Late PCSK9 elevation (48 hours) is linked to myocardial damage and microvascular dysfunction.
- Higher PCSK9 levels at 48 hours predict major adverse cardiac events in STEMI patients.
Background:
Beyond therapeutic implications, PCSK9 (proprotein convertase subtilisin/kexin 9) has emerged as a promising cardiovascular biomarker. The exact role of PCSK9 in the setting of acute ST-elevation myocardial infarction (STEMI) is incompletely understood. We aimed to investigate the association of PCSK9 with ischemia-reperfusion injury, visualized by cardiac magnetic resonance imaging, in patients with STEMI revascularized by primary percutaneous coronary intervention (PCI).
Methods:
In this prespecified substudy from the prospective MARINA-STEMI (NCT04113356) registry, we included 205 patients with STEMI. PCSK9 concentrations were measured from venous blood samples by an immunoassay 24 and 48 hours after PCI. The primary end point was defined as presence of intramyocardial hemorrhage according to cardiac magnetic resonance T2* mapping. Secondary imaging end points were the presence of microvascular obstruction (MVO) and infarct size. The clinical end point was the occurrence of major adverse cardiac events.
Results:
We observed a significant increase in PCSK9 levels from 24 to 48 hours (268-304 ng/mL; P<0.001) after PCI. PCSK9 24 hours after PCI did not show any relation to intramyocardial hemorrhage, MVO, and infarct size (all P>0.05). PCSK9 concentrations 48 hours post-STEMI were higher in patients with intramyocardial hemorrhage (333 versus 287 ng/mL; P=0.004), MVO (320 versus 292 ng/mL; P=0.020), and large infarct size (323 versus 296 ng/mL; P=0.013). Furthermore, patients with increased PCSK9 levels >361 ng/mL at 48 hours were more likely to experience major adverse cardiac events (15% versus 8%; P=0.002) during a median follow-up of 12 months.
Conclusions:
In patients with STEMI, a significant increase in PCSK9 was observed from 24 to 48 hours after PCI. While PCSK9 levels after 24 hours were not related to myocardial or microvascular injury, PCSK9 after 48 hours was significantly associated with intramyocardial hemorrhage, MVO, and infarct size as well as worse subsequent clinical outcomes.
Registration:
URL: https://www.clinicaltrials.gov; Unique identifier; NCT04113356.
