Informace o publikaci

Association of polymorphisms in the endocannabinoid system genes with myocardial infarction and plasma cholesterol levels

Název česky Asociace polymorfizmů v genech endokanabinoidního systému s infarktem myokardu a plazmatickou hladinou cholesterolu
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CHMELÍKOVÁ Monika PÁCAL Lukáš ŠPINAROVÁ Lenka VAŠKŮ Anna

Rok publikování 2015
Druh Článek v odborném periodiku
Časopis / Zdroj Biomedical Papers
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
Doi http://dx.doi.org/10.5507/bp.2014.043
Obor Ostatní lékařské obory
Klíčová slova chronic heart failure; endocannabinoid system; fatty acid amide hydrolase; cannabinoid receptor; myocardial infarction cholesterol
Popis Aims. The aim of this study was to investigate the relationship between selected symptoms of chronic heart failure (myocardial infarction, plasma cholesterol level) and single nucleotide polymorphisms (SNPs) in the FAAH and CNR1 genes. Methods. A case – control study involving 155 patients with chronic heart failure and 169 age- and sex-matched healthy subjects. We detected SNPs 385 C/A (rs324420) in the FAAH and 1359 G/A (rs1049353) in the CNR1 genes using the polymerase chain reaction and restriction analysis. Genotype and allele frequencies were compared between patients and controls as well as between patients with and without myocardial infarction. Results. No significant differences in genotype or allelic frequencies between patients and controls were found (P > 0.05). Carriers of the FAAH A allele had a 2.37-fold increase in the risk of myocardial infarction (odds ratio 2.37, 95% confidence interval 1.36-6.93, P = 0.01). Homozygous carriers of genotype AA of CNR1 SNP 1359 had significantly higher plasma cholesterol levels than carriers of GG and GA genotypes in patients (P = 0.04). Conclusions. The study results suggest a role for allele A of the FAAH 385 variant as a risk factor for myocardial infarction. Genotype AA of CNR1 1359 variant probably affects plasma cholesterol levels. Pharmacological intervention in this system could modify the therapeutic approach to certain cardiovascular disorders.

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