Association of the genetic and traditional risk factors of ischaemic heart disease with STEMI and NSTEMI development

缺血性心脏病的遗传和传统风险因素与 STEMI 和 NSTEMI 发展的关系

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作者:Diana Žaliaduonytė-Pekšienė, Vaiva Lesauskaitė, Rasa Liutkevičienė, Vytenis Tamakauskas, Vilius Kviesulaitis, Giedrė Šinkūnaitė-Maršalkienė, Sandrita Šimonytė, Simonita Mačiulskytė, Eglė Tamulevičiūtė-Prascienė, Olivija Gustienė, Abdonas Tamošiūnas, Remigijus Žaliūnas

Conclusions

Genetic polymorphisms of MMP-3 5A/6A and ACE I/D along with conventional ischaemic heart disease risk factors increase the risk of the occurrence of STEMI, while having no influence on the pathogenesis of NSTEMI.

Methods

Five hundred and twenty-three patients with acute coronary syndromes (393 with ST elevation myocardial infarction (STEMI) and 130 with non-ST elevation myocardial infarction (NSTEMI)) comprised the study group. The control group consisted of 645 subjects free from symptoms of ischaemic heart disease and stroke. Genetic polymorphisms of MMP-2 (-735) C/T, MMP-2 (-1306) C/T, MMP-3 (-1171) 5A/6A, MMP-9 (-1562) C/T and ACE I/D were evaluated using polymerase chain reaction.

Results

Patients with acute coronary syndromes more often had ID or II genotype than DD genotype of ACE ( P = 0.04) and 5A5A or 5A6A genotype than 6A6A genotype of MMP-3 ( P = 0.02) in comparison to the control group. The genotypes of other matrix metalloproteinase genes did not differ between the groups. 5A5A and 5A6A genotypes of MMP-3 (odds ratio (OR) 1.5; P = 0.021), II and ID genotypes of ACE (OR 1.7; P = 0.006) along with traditional ischaemic heart disease risk factors such as smoking (OR 4.9; P = 0.001), hypertension (OR 2.0; P = 0.001), diabetes mellitus (OR 2.9; P = 0.001) and dyslipidaemia (OR 2.1; P = 0.001) increased the risk of STEMI. However, the polymorphism of MMP-3 5A/6A and ACE I/D was not associated with the occurrence of NSTEMI. Conclusions: Genetic polymorphisms of MMP-3 5A/6A and ACE I/D along with conventional ischaemic heart disease risk factors increase the risk of the occurrence of STEMI, while having no influence on the pathogenesis of NSTEMI.

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