主动脉瓣病变伴根部严重狭小的外科治疗

主动脉瓣置换手术人工瓣膜瓣开面积与患者的体表面积匹配影响手术的远期临床疗效,因此,对于主动脉根部狭小患者,常需行主动脉窦部或瓣环加宽以置换直径较大的人工瓣膜.从1998年1月到2007年12月,我们共实施21例小主动脉根部加宽和主动脉瓣置换手术,取得了满意的临床效果.现报道如下.

AIM:NLRP3 inflammasome was identified as the cellular machinery responsible for activation of inflammatory processes .The present study investigated whether the activation of NLRP 3 inflammasomes contributes to hyperhomocysteinemia ( HHcy)-induced in-flammation and atherosclerosis .METHODS:ApoE-/-mice were fed regular diet , high fat ( HF) diet or HF plus high methionine (HM) diet for 10 weeks.NLRP3 shRNA or scramble shRNA viral suspension was injected twice at the 2nd and the 6th weeks after HFHM treatment.The whole aortas and aortic root sections were stained with Oil Red O for atherosclerotic lesion .Plasma lipids, ho-mocysteine ( Hcy) , IL-1βand IL-18 levels were measured .We also examined the effect of Hcy on NLRP 3 inflammasomes activation in THP-1 differentiated macrophages in the presence or absence of NLRP 3 siRNA, caspase-1 inhibitor Z-WEHD-FMK, or antioxidant N-acetyl-L-cysteine ( NAC) .RESULTS:HFHM treatment induced HHcy in ApoE-/-mice.Increased plasma levels of IL-1βand IL-18, aggravated macrophage infiltration into atherosclerotic lesion , and accelerated development of atherosclerosis were detected in HHcy mice, which were associated with the activation of NLRP 3 inflammasomes.Silencing the NLRP3 gene significantly suppressed NLRP3 inflammasomes activation , reduced plasma levels of proinflammatory cytokines , attenuated macrophage infiltration , and improved HHcy-induced atherosclerosis .Moreover, we found that Hcy activated NLRP3 inflammasomes and promoted subsequent production of IL-1βand IL-18 in macrophages, which were blocked by NLRP3 gene silencing, Z-WEHD-FMK, or NAC.CONCLUSION:These data suggest that the activation of NLRP 3 inflammasomes contributes to HHcy-induced inflammation and atherosclerosis .Hcy activates NLRP3 inflammasomes in reactive oxygen species dependent pathway in macrophages .