HDL Subclasses and the Distribution of Paraoxonase-1 Activity in Patients with ST-Segment Elevation Acute Myocardial

Saska Djekic1, Jelena Vekic2, Aleksandra Zeljkovic2

  • 1Department of Laboratory Diagnostics Public Health Institution "Health Center", 74000 Doboj, Bosnia and Herzegovina.

Insights

Oxidative stress and small, dense LDL increase in heart attack patients, impairing antioxidant function in small HDL particles and altering paraoxonase-1 activity.

Area of Science:

  • Cardiovascular Medicine
  • Lipid Metabolism
  • Biochemistry

Background:

  • Oxidative stress, inflammation, and small, dense low-density lipoproteins (sdLDL) are implicated in cardiovascular disease.
  • High-density lipoprotein (HDL) plays a crucial role in reverse cholesterol transport and possesses antioxidative properties.
  • Paraoxonase-1 (PON1) is an HDL-associated enzyme with protective functions against LDL oxidation.

Purpose of the Study:

  • To investigate the impact of oxidative stress, inflammation, and sdLDL on HDL subclasses and PON1 activity distribution in ST-segment elevation acute myocardial infarction (STEMI) patients.
  • To compare HDL subclasses and PON1 activity distribution between STEMI patients and healthy controls.

Main Methods:

  • Multicentric study involving 69 STEMI patients and 67 healthy controls.
  • Separation of lipoprotein subclasses using polyacrylamide gradient gel electrophoresis.
  • Quantification of HDL subclasses and sdLDL proportions via densitometric scans.
  • Assessment of PON1 activity distribution within HDL subclasses using the zymogram method.

Main Results:

  • STEMI patients exhibited significantly lower proportions of HDL2a and HDL3a, and higher proportions of HDL3b and HDL3c compared to controls.
  • A lower proportion of PON1 activity was found within HDL3b in STEMI patients, while HDL2 showed higher PON1 activity.
  • Positive associations were observed between sdLDL and PON1 activity in HDL3a, and between malondialdehyde (MDA) and PON1 activity in HDL2b in STEMI patients.

Conclusions:

  • Increased oxidative stress and sdLDL are linked to compromised antioxidative function in small HDL3 particles in STEMI.
  • Altered PON1 activity distribution within HDL subclasses contributes to the pathophysiology of STEMI.

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