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Cintra R, Moura FA, Carvalho LS, et al. TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction. BBA Clin. 2016;5:159-65doi: 10.1016/j.bbacli.2016.03.010.
Cintra, R., Moura, F. A., Carvalho, L. S., Daher, M., Santos, S. N., Costa, A. P., Figueiredo, V. N., Andrade, J. M., Neves, F. A., Silva, J. C., Sposito, A. C. (2016). TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction. BBA clinical, 5159-65. https://doi.org/10.1016/j.bbacli.2016.03.010
Cintra, Riobaldo, et al. "TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction." BBA clinical vol. 5 (2016): 159-65. doi: https://doi.org/10.1016/j.bbacli.2016.03.010
Cintra R, Moura FA, Carvalho LS, Daher M, Santos SN, Costa AP, Figueiredo VN, Andrade JM, Neves FA, Silva JC, Sposito AC. TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction. BBA Clin. 2016 Apr 02;5:159-65. doi: 10.1016/j.bbacli.2016.03.010. eCollection 2016 Jun. PMID: 27213136; PMCID: PMC4865630.
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BBA Clin. 2016 Apr 02;5:159-65. doi: 10.1016/j.bbacli.2016.03.010. eCollection 2016 Jun.

TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction.

BBA clinical

Riobaldo Cintra, Filipe A Moura, Luiz S F Carvalho, Mauricio Daher, Simone N Santos, Ana P R Costa, Valeria N Figueiredo, Joalbo M Andrade, Francisco A R Neves, Jose C Quinaglia E Silva, Andrei C Sposito,

Affiliations

  1. Cardiology Division, Faculty of Medical Sciences, State University of Campinas (Unicamp), Campinas, SP, Brazil.
  2. Health Science School, University of Brasília (UnB), Brasília, DF, Brazil.
  3. Health Science School, University of Brasília (UnB), Brasília, DF, Brazil; Hospital de Base do Distrito Federal, Brasília, DF, Brazil.

PMID: 27213136 PMCID: PMC4865630 DOI: 10.1016/j.bbacli.2016.03.010

Abstract

BACKGOUND: The favorable effects of insulin during myocardial infarction (MI) remain unclear due to the divergence between mechanistic studies and clinical trials of exogenous insulin administration. The rs7903146 polymorphism of the transcription factor 7-like 2 (TCF7L2) gene is associated with attenuated insulin secretion.

METHODS: In non-diabetic patients with ST-elevation MI (STEMI), using such a model of genetically determined down-regulation of endogenous insulin secretion we investigated the change in plasma insulin, C-peptide, interleukin-2 (IL-2), C-reactive protein (CRP), and nitric oxide (NOx) levels between admission (D1) and the fifth day after MI (D5). Coronary angiography and flow-mediated dilation (FMD) were performed at admission and 30 days after MI, respectively. Homeostasis Model Assessment estimated insulin secretion (HOMA2%β) and insulin sensitivity (HOMA2%S).

RESULTS: Although glycemia did not differ between genotypes, carriers of the T-allele had lower HOMA2%β and higher HOMA2%S at both D1 and D5. As compared with non-carriers, T-allele carriers had higher plasma IL-2 and CRP at D5, higher intracoronary thrombus grade, lower FMD and NOx change between D1 and D5 and higher 30-day mortality.

CONCLUSION: In non-diabetic STEMI patients, the rs7903146 TCF7L2 gene polymorphism is associated with lower insulin secretion, worse endothelial function, higher coronary thrombotic burden, and higher short-term mortality.

GENERAL SIGNIFICANCE: During the acute phase of MI, a lower capacity of insulin secretion may influence clinical outcome.

Keywords: Endothelial function; Mortality; Myocardial infarction; TCF7L2 polymorphism

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