Key result
Combined elevation of PCSK9 and PTX3 above the median was independently associated with an increased risk of MACE in STEMI patients undergoing primary PCI (HR 2.90; p=0.010).
Why the study?
The study was designed to determine the prognostic value of combined plasma PCSK9 and pentraxin 3 measurements according to culprit-plaque morphology in STEMI patients undergoing primary PCI.
Does the combined elevation of PCSK9 and PTX3 predict MACE in STEMI patients undergoing primary PCI?
Cohort (n=235)
Does the combined elevation of PCSK9 and PTX3 predict MACE in STEMI patients undergoing primary PCI?
Hazard Ratio: 2.9
Absolute Event Rate: 31.9% vs 15.3%
p-value: p=0.010
Combined measurement of PCSK9 and PTX3 enhances risk stratification for MACE in STEMI patients undergoing primary PCI, particularly those with plaque erosion.
Combined PCSK9/PTX3 elevation may refine MACE risk prediction by plaque morphology in STEMI; leaves open prospective validation before clinical adoption.
BACKGROUND AND AIM: The aim of prospective study was to determine the prognostic value of combined measures of plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) and pentraxin 3 (PTX3) according to the culprit-plaque morphology (plaque rupture versus plaque erosion) in relation to the in patients with acute ST-elevated myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention. METHODS: A total of 434 patients with STEMI aged ≥18 years who underwent pre-intervention OCT imaging of culprit lesions between March 2017 and March 2019 were enrolled. Finally, 235 patients who meet the inclusion criteria were enrolled and the cohort was divided into 3 groups according to PCSK9 and PTX3 levels: group A: PCSK9 < median and Pentraxin 3 (N = 72/30.6%); group B: PCSK9 ≥ median or Pentraxin 3≥ median (N = 91/38.7%); group C: PCSK9 ≥ median and Pentraxin 3≥ median (N = 72/30.6%). MACEs were defined as a composite of all-cause death, myocardial infarction (MI) recurrence, and ischemic stroke, revascularization and heart failure. OUTCOMES: During a median follow-up of 2.01 years, 50 patients has occurred MACE. Two-year MACE was higher in group C (23/31.9%) than in group B (16/17.6%) and group A (11/15.3%) (p = 0.028). There was a correlation between PCSK9 and PTX3 (r = 0.302, p < 0.003). In multivariable analysis adjusted for age, gender, risk factors, and serum indexes, being in group C remained independently associated with an increased risk of MACE (hazard ratio [HR]: 2.90; p = 0.010), and group B tended to have higher MACE (HR: 1.76; p = 0.172) compared with group A. Among patients with plaque erosion by OCT, group C was independently associated with an increased risk of MACE (HR: 9.04; p = 0.048) after fully adjustment. However, the significant association was absence among patients with plaque rupture. CONCLUSION AND RELEVANCE: This study demonstrated the usefulness of combined measures of PCSK9 and PTX3 to enhance risk stratification in patients with STEMI especially among patients with plaque erosion. Patients with elevation of both PCSK9 and PTX3 had a markedly increased risk of MACE.
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Zhao et al. (2021) conducted a cohort in ST-elevated myocardial infarction (STEMI) (n=235). Combined elevation of PCSK9 and PTX3 (≥ median) vs. PCSK9 and PTX3 < median was evaluated on MACE (composite of all-cause death, myocardial infarction recurrence, ischemic stroke, revascularization and heart failure) (HR 2.90, p=0.010). Combined elevation of PCSK9 and PTX3 above the median was independently associated with an increased risk of MACE in STEMI patients undergoing primary PCI (HR 2.90; p=0.010).
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