Abstract T P92: Paraoxonase Gene Polymorphism and Carotid Atherosclerosis in Acute Ischemic Stroke

Abstract

Background: Atherosclerosis in the carotid artery is one of the main causes of acute ischemic stroke. Lipid oxidation has been known to play an important role in the pathogenesis of atherosclerosis. Paraoxonase (PON) is involved in lipid oxidation and has anti-atherogenic activity. PON single-nucleotide polymorphism (SNP) is associated with serum concentration, the activity of paraoxonase, and an increased risk of vascular disease. The purpose of this study was to investigate the association between four genetic variations of PON SNPs and carotid atherosclerosis (CA) in Korean stroke patients. Methods: Acute stroke patients with cardioembolism, other etiologies, and undermined etiologies were excluded to avoid mistaking embolic occlusive lesion for true atherosclerotic lesion. We included 656 subjects who met the inclusion criteria among acute ischemic stroke patients. One hundred and eighty-six subjects had LAA subtype of stroke, and 468 had SVO stroke. All subjects were categorized four subgroups based on the angiographic findings as follows: (1) the No ECIC+ICIC group (those without significant stenosis in the intracranial and extracranial carotid arteries); (2) the ECIC group (those with significant stenosis in the extracranial carotid arteries, but with no significant stenosis in the intracranial carotid arteries); (3) the ICIC group (those with significant stenosis in the intracranial carotid arteries, but with no significant stenosis in the extracranial carotid arteries); and (4) the ECIC+ICIC group (those with significant stenosis in the intracranial and extracranial carotid arteries). All enrolled patients were genotyped with the four genetic variations of PON SNPs (PON1 L55M, PON1 Q192R, PON2 A1148G, and PON2 C311S). Results: There were no significant associations between the four PON SNPs of each subgroups according to CA. In cases of LAA stroke, patients with CA had a significantly higher frequency of the PON2 148 AA and PON2 311 CC genotype than those without CA (p=0.021). Conclusion: We found an association between PON SNPs and carotid atherosclerosis in LAA stroke. But there was no significant difference in distributions of PON SNPs between intracranial CA and extracranial CA.