Introduction: The gene of inducible nitric oxide synt-hase (iNOS), located on chromosome 17 (17q11.2-12) is involved in a wide range of pathologies. It forms nitric oxide that has a key role in immune response. iNOS is expressed rapidly by the action of pro-inflammatory stimuli and has been shown to be involved in complex immunomodulatory, cardiovascular and metabolic mechanisms.

Objective: The study of iNOS gene polymorphism in young people with non-lesion arrhythmias, with and without dyslipidemia.

Methods: T he study was conducted on 180 subjects, 18-45 years of age, divided into 3 groups, 2 of them with cardiac arrhythmias, with and without dyslipi-demia and a control one. The polymorphism of iNOS rs2297518 (26096597G>A) gene was identified using Real Time Chain Polymerization reaction, by multi-plying double-stranded DNA fragments, with visu-alization by florescence. With the help of a TaqMan probe, 2 alleles (mutant/wild): G (guanine) and A (ala-nine) and 3 genotypes: homozygous-AA/GG and hete-rozygous-AG were identified.

Results: Genotyping of iNOS rs2297518 showed mo-nonucleotide variants. The data respected the Hardy-Weinberg balance. Patients in the dyslipidemia group had a higher proportion of AG genotype at the expense of the GG genotype, compared to the group with ar-rhythmias, but without dyslipidemia, the differences being even greater in the control group. Genotypic distribution also marked differences in arrhythmia types: in sinus bradycardia: predominant GG (66.67%), AG (16.67%), and AA (22.66%). In atrial fibrillation: 65%-AG, 34%-GG and 1%-AA, predominantly AG ge-notype. In supraventricular paroxysmal tachycardia: 63.64%-AG, 34.36%-GG and 2%-AA, significantly pre-dominating AG genotype. For sinus tachycardia, atrial/ ventricular extrasystoles: 57.14%-AG, 34.29%-GG, and 5.71%-AA.

Conclusions: 1. The research of polymorphisms of ge-nes involved in the pathogenesis of cardiovascular, me-tabolic diseases represents innovative methods. 2. The-re are links between arrhythmias, dyslipidemia and pre-dominance of the genotypic variant, iNOS rs2297518 polymorphism representing higher cardiovascular risk for AG and GG genotypes compared to AA.