Why the study?
Do specific gene polymorphisms (eNOS, MTHFR, TNF-α) increase the risk of myocardial infarction and cardiovascular events in patients with atherosclerosis?
Do specific gene polymorphisms (eNOS, MTHFR, TNF-α) increase the risk of myocardial infarction and cardiovascular events in patients with atherosclerosis?
Specific genetic polymorphisms in eNOS, MTHFR, and TNF-α are associated with a significantly higher risk of myocardial infarction and cardiovascular events, suggesting potential utility for genetic screening in atherosclerosis.
Hypothesis-generating for genetic screening in atherosclerosis; prospective validation required before clinical adoption.
The development of atherosclerosis is a multifactorial process. The purpose of the study was to examine three genetic polymorphisms playing a role in the metabolic processes underlying the disease. We compared the data of 348 atherosclerotic non-diabetic patients with 260 atherosclerotic diabetic patients and 384 healthy controls. We analyzed the prevalence of myocardial infarction and stroke in three different groups of patients carrying different polymorphisms. It was proved that if the mutant TT eNOS Glu298ASP variant is present, a significantly higher number of myocardial infarctions can be observed than in patients carrying heterozygote GT or normal GG genotype. We proved that in the case of MTHFR 677CT heterozygote variants, the occurrence of myocardial infarction is significantly higher and the difference is also significant in case of the 677TT homozygote variant. It was verified that among patients with the mutant TNF-α AA genotype the occurrence of cardiovascular events was significantly higher. Screening the genetically high risk groups on the long run should be considered as an early detection opportunity that may give better chances for prevention and treatment. Understanding the inflammatory mechanisms of the atherosclerosis may give new therapeutical targets to pharmacologists.
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Gábor Szabó (2013) studied this question.
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