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Revista chilena de cardiología

versión On-line ISSN 0718-8560


SAAVEDRA, Nicolás et al. Genetic polymorphisms of APOA5 are associated with hypertriglyceridemia and hyperglycemia in Chilean subjects with coronary artery disease and controls. Rev Chil Cardiol [online]. 2010, vol.29, n.1, pp.19-27. ISSN 0718-8560.

Background: Several genetic variants have been linked to the development ofcoronary heart disease and/or their riskfactors, including the S19Wand-1131T> C polymorphisms ofthe gene that encodes apolipoprotein A5 (APOA5). Thus, the objective ofthis study was to investígate the possible association between S19W and -1131T>C genetic variants ofAPOA5 and coronary disease in Chilean individuáis. Methods: We evaluated 425 not related subjects; 209 patients with coronary artery disease (CAD) confirmed by angiography (stenosis→ 70%,), aged between 33 and 74 years, and 216 control individuáis (30 to 68 years). The genotyping of S19W and -1131T>C polymorphisms of APOA5 gene was evaluated by PCR-RFLP. Results: The genotype distríbution of S19W polymorphism of APOA5 gene in CAD patients (SS: 80%,, SW: 19%, WW: 1 %>) and controls (SS: 82%,, SW: 17%, WW: 1 %>) was similar (p = NS). In the same way the genotype distríbution of-1131T>C genetic variantin CAD subjects (TT: 56%,, TC: 37%,, and CC: 7%>) and controls (TT: 63%,, TC: 30%, and CC: 7%o) was equivalent (p = NS). The Odds ratios related to the mutant alleles 19W (1.12, 95%, Cl, 0.72 - 1.74, p = NS) and -1131C (1.19, 95%, Cl, 0.87 -1.63, p = NS) confirms the absence of association. On the otherhand, the triglycerides and fasting glucose concentrations were significantly higher in subjects carrying the alleles 19W and -1131C, in both groups, CAD patients and controls (p <0.05). Conclusion: The observed association between genetic variants of APOA5 and higher serum levéis of triglycerides and glucose, in both groups, suggesting that these polymorphisms could be contribute to the development ofdiabetic dyslipidemia, a known risk factor for coronary artery disease.

Palabras clave : Coronary artery disease; APOA5 gene; Cardiovascular risk factors.

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