Role of perilipin 2 in microvascular obstruction in patients with ST-elevation myocardial infarction

Michele Russo1, Rocco A Montone2, Domenico D'Amario2

  • 1Department of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, L.go F. Vito, 1, 00168, Rome, Italy.

Abstract

Insights

Perilipin 2 (PLIN2) levels in ST-elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention (PCI) are linked to microvascular obstruction (MVO) and predict major adverse cardiovascular events (MACEs). Further research into PLIN2 as a cardioprotective target is suggested.

Area of Science:

  • Cardiology
  • Biochemistry
  • Vascular Biology

Background:

  • Coronary microvascular obstruction (MVO) is a frequent complication after percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI) patients.
  • The precise mechanisms underlying MVO remain incompletely understood.
  • Perilipin 2 (PLIN2) plays a role in macrophage lipid metabolism and plaque inflammation, suggesting a potential involvement in MVO pathogenesis.

Purpose of the Study:

  • To investigate the association between PLIN2 levels and MVO in STEMI patients undergoing primary PCI.
  • To evaluate the predictive role of PLIN2 for major adverse cardiovascular events (MACEs) in these patients.

Main Methods:

  • A cohort of STEMI patients undergoing primary PCI was studied.
  • PLIN2 levels were measured in peripheral blood monocytes.
  • MVO was assessed via coronary angiography.
  • MACEs (cardiac death, non-fatal MI, heart failure readmission, target vessel revascularization) were tracked during follow-up.

Main Results:

  • 33% of the 100 STEMI patients experienced MVO.
  • Patients with MVO exhibited significantly higher PLIN2 levels compared to those without MVO (P=0.019).
  • Multivariate analysis confirmed PLIN2 as an independent predictor of MVO (OR=12.325, P=0.022) and MACEs (HR=26.904, P=0.007).

Conclusions:

  • PLIN2 is independently associated with MVO in STEMI patients post-PCI.
  • PLIN2 serves as an independent predictor of MACEs following STEMI.
  • These findings highlight PLIN2 as a potential therapeutic target for cardioprotection in STEMI.

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