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LETIZIA SCOLA

Cytokine Polymorphism in Takotsubo Cardiomyopathy

  • Autori: Di Gangi, P.; Scola, L.; Giambanco, S.; Bova, M.; Santini, G.; Vaccarino, L.; Balistreri, C.; Lio, D.; Assennato, P.; Novo, S.; Novo, G.
  • Anno di pubblicazione: 2014
  • Tipologia: Proceedings (TIPOLOGIA NON ATTIVA)
  • OA Link: http://hdl.handle.net/10447/99776

Abstract

IMIN11. Cytokine Polymorphism in Takotsubo Cardiomyopathy P. Di Gangi1, L. Scola1, S. Giambanco1, M. Bova1, G. Santini1, L. Vaccarino1, C. R. Balistreri1, D. Lio1, P. Assennato1, S. Novo1, G. Novo1 1University of Palermo, Palermo, Italy Background: Takotsubo (TT) cardiomyopathy is characterised by an acute left ventricular dysfunction triggered by emotional or physical stresses. Clinically, the syndrome is characterised by acute symptoms mimicking acute infarction without relevant electrocardiographic and biochemical markers of myocardial damage changes. Stressful events inducing an excess catecholamine release and myocardial β-adrenergic receptors (β-AR) seem to play a major role in TT. Accordingly, we have reported that the L41Q polymorphism of the G protein-coupled receptor kinase 5 (GRK5), which, leads to β-arrestin recruitment and mediates β- AR desensitisation might play a role in TT susceptibility. Extended sympathetic activation may influence the pro-inflammatory cytokine secretion triggering b-adrenergic receptors of the immuno system cells. In turn, IL-1, IL-6, TNF-α stimulating the synthesis and release of CRH and norepinephrine might magnify the activation of the sympathetic system. In this view, we have analyzed the role that polymorphisms of inflammatory cytokines might play in the pathogenesis of TT. Methods: We analysed ADRB-1 (rs1801253), IL–1A (rs1800587), IL-1B (rs16944), (rs1143634), IL-6 (rs1800795), TNF-α(rs1800629), TGF- β(rs1800471), IL-10 (rs1800872), (rs1800871), (rs1800896), MAL (rs8177374) and TLR-4 polymorphisms in 25 TT patients and 100 controls using KASPar SNP genotyping method. Statistical analysis of data was performed using dominant, codominant, and recessive models. Results: Analysis of the genotypic and allelic frequencies does not allow the detection of relevant differences in polymorphism frequencies in TT patients. Conclusions: Because of the low number of patients, further studies are necessary to understand the role of cytokine polymorphisms in Takotsubo cardiomyopathy. Work is in progress to recruit and analyse a larger group of patients.