TY - CONF
T1 - Cytokine Polymorphism in Takotsubo Cardiomyopathy
AU - Vaccarino, Loredana
AU - Novo, Salvatore
AU - Balistreri, Carmela Rita
AU - Novo, Giuseppina
AU - Scola, Letizia
AU - Assennato, Pasquale
AU - Lio, Domenico
PY - 2014
Y1 - 2014
N2 - IMIN11. Cytokine Polymorphism in Takotsubo CardiomyopathyP. Di Gangi1, L. Scola1, S. Giambanco1, M. Bova1, G. Santini1, L.Vaccarino1, C. R. Balistreri1, D. Lio1, P. Assennato1, S. Novo1, G. Novo11University of Palermo, Palermo, ItalyBackground: Takotsubo (TT) cardiomyopathy is characterised by anacute left ventricular dysfunction triggered by emotional or physicalstresses. Clinically, the syndrome is characterised by acute symptomsmimicking acute infarction without relevant electrocardiographic andbiochemical markers of myocardial damage changes. Stressful eventsinducing an excess catecholamine release and myocardial β-adrenergicreceptors (β-AR) seem to play a major role in TT. Accordingly, we havereported that the L41Q polymorphism of the G protein-coupled receptorkinase 5 (GRK5), which, leads to β-arrestin recruitment and mediates β-AR desensitisation might play a role in TT susceptibility. Extendedsympathetic activation may influence the pro-inflammatory cytokinesecretion triggering b-adrenergic receptors of the immuno system cells. Inturn, IL-1, IL-6, TNF-α stimulating the synthesis and release of CRH andnorepinephrine might magnify the activation of the sympathetic system. Inthis view, we have analyzed the role that polymorphisms of inflammatorycytokines 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 controlsusing KASPar SNP genotyping method. Statistical analysis of data wasperformed using dominant, codominant, and recessive models.Results: Analysis of the genotypic and allelic frequencies does not allowthe detection of relevant differences in polymorphism frequencies in TTpatients.Conclusions: Because of the low number of patients, further studies arenecessary to understand the role of cytokine polymorphisms in Takotsubocardiomyopathy. Work is in progress to recruit and analyse a larger groupof patients.
AB - IMIN11. Cytokine Polymorphism in Takotsubo CardiomyopathyP. Di Gangi1, L. Scola1, S. Giambanco1, M. Bova1, G. Santini1, L.Vaccarino1, C. R. Balistreri1, D. Lio1, P. Assennato1, S. Novo1, G. Novo11University of Palermo, Palermo, ItalyBackground: Takotsubo (TT) cardiomyopathy is characterised by anacute left ventricular dysfunction triggered by emotional or physicalstresses. Clinically, the syndrome is characterised by acute symptomsmimicking acute infarction without relevant electrocardiographic andbiochemical markers of myocardial damage changes. Stressful eventsinducing an excess catecholamine release and myocardial β-adrenergicreceptors (β-AR) seem to play a major role in TT. Accordingly, we havereported that the L41Q polymorphism of the G protein-coupled receptorkinase 5 (GRK5), which, leads to β-arrestin recruitment and mediates β-AR desensitisation might play a role in TT susceptibility. Extendedsympathetic activation may influence the pro-inflammatory cytokinesecretion triggering b-adrenergic receptors of the immuno system cells. Inturn, IL-1, IL-6, TNF-α stimulating the synthesis and release of CRH andnorepinephrine might magnify the activation of the sympathetic system. Inthis view, we have analyzed the role that polymorphisms of inflammatorycytokines 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 controlsusing KASPar SNP genotyping method. Statistical analysis of data wasperformed using dominant, codominant, and recessive models.Results: Analysis of the genotypic and allelic frequencies does not allowthe detection of relevant differences in polymorphism frequencies in TTpatients.Conclusions: Because of the low number of patients, further studies arenecessary to understand the role of cytokine polymorphisms in Takotsubocardiomyopathy. Work is in progress to recruit and analyse a larger groupof patients.
UR - http://hdl.handle.net/10447/99776
M3 - Other
SP - 31
EP - 31
ER -