Cytotoxin-Associated Gene-A-Seropositivity and Interleukin-1 Polymorphisms Influence Adverse Cardiovascular Events.
Cytotoxin-Associated Gene-A-Seropositivity and Interleukin-1 Polymorphisms Influence Adverse Cardiovascular Events.
复制标题
细胞毒素相关基因 A 血清阳性和白细胞介素 1 多态性影响不良心血管事件。
DOI:
10.1016/j.ijcha.2020.100498
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发表时间:
2020
影响因子:
2.9
通讯作者:
and Tsujita K.
中科院分区:
文献类型:
--
作者:
Tabata N;SuetaD;Arima Y;Okamoto K;Shono T;Hanatani S;Takashio S;Oniki K;Saruwatari J;Sakamoto K;Kaikita K;Sinning JM;Werner K;Nickenig G;Sasaki Y;Fukui T;and Tsujita K.
AimsAlthough the bacterial virulent factor of cytotoxin-associated gene-A (CagA)-seropositivity and the host genetic factors ofinterleukin (IL)-1polymorphisms have been suggested to influenceHelicobacter pylori (HP)-related diseases, the underlying mechanisms of the association betweenHPinfection and acute coronary syndrome (ACS) remain unknown.Methods and resultsAmong 341 consecutive ACS patients, the clinical outcomes after ACS included composite cardiovascular events within the 2-year follow-up period.A significantly higher probability of primary outcomes was observed inHPpositive patients than inHPnegative patients. There were no significant differences in the rate of cardiovascular events betweenHPpositive andHPnegative patients in the absence of anIL-polymorphism, while there were significant differences in the presence of anIL-polymorphism. There were significant differences in the rate of cardiovascular events among CagA positive, CagA negative/HPpositive and CagA negative/HPnegative patients. Moreover, via immunohistochemical staining, aortic CagA positive cells were confirmed in the vasa vasorum in CagA positive patients, whereas they could not be identified in CagA negative patients.ConclusionsThe bacterial virulence factor CagA and host geneticIL-1polymorphisms influence the incidence of adverse cardiovascular events, possibly through infection of atherosclerotic lesions.Registration:University Hospital Medical Information Network (UMIN)-CTR (http://www.umin.ac.jp/ctr/).Identifier:UMIN000035696.