Qin Chaoyi, Gu Jun, Qian Hong, Liu Ruiqi, Xu Fei, Li Yajiao, Xiao Zhenghua, He Qian, Hu Jia, Meng Wei
Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, PR China.
Cardiology. 2016;135(4):228-235. doi: 10.1159/000446870. Epub 2016 Aug 17.
Acute aortic dissection (AD) is a lethal cardiovascular disease with severe inflammatory complications. Considering the proinflammatory properties of plasma mitochondrial DNA (mtDNA), we postulate that plasma mtDNA from activated platelets may be responsible for post-acute AD inflammatory responses.
We consecutively enrolled 68 patients with acute AD as well as matched hypertensive and healthy participants. Blood samples were collected on admission for blood routine tests, mtDNA assay, and inflammatory cytokine analysis. A computed tomography scan was used to evaluate the extent of dissections.
Our results demonstrate that plasma mtDNA, platelet activation, and inflammatory levels were remarkably higher in acute AD patients than in hypertensive or healthy participants. These parameters were also higher in the Stanford A group than in the Stanford B group (p < 0.05). Bivariate correlation analysis demonstrated positive associations between mtDNA and inflammatory levels (tumor necrosis factor-α: r = 0.577; interleukin-6: r = 0.632), mtDNA and platelet activation (r = 0.642), and platelet activation and the extent of dissection (r = 0.635).
Our study suggests that acute AD-induced tunica media exposure causes platelet activation, which leads to the initiation of inflammatory responses via the release of mtDNA into the circulation. Our study provides a novel fundamental basis and a potential therapeutic target for the prevention and treatment of post-AD inflammatory responses.
急性主动脉夹层（AD）是一种伴有严重炎症并发症的致命性心血管疾病。鉴于血浆线粒体DNA（mtDNA）的促炎特性，我们推测活化血小板释放的血浆mtDNA可能是急性AD后炎症反应的原因。
我们连续纳入了68例急性AD患者以及匹配的高血压患者和健康参与者。入院时采集血样进行血常规检查、mtDNA检测和炎症细胞因子分析。使用计算机断层扫描评估夹层的范围。
我们的结果表明，急性AD患者的血浆mtDNA、血小板活化和炎症水平显著高于高血压患者或健康参与者。这些参数在斯坦福A型组中也高于斯坦福B型组（p<0.05）。双变量相关性分析表明，mtDNA与炎症水平（肿瘤坏死因子-α：r=0.577；白细胞介素-6：r=0.632）、mtDNA与血小板活化（r=0.642）以及血小板活化与夹层范围（r=0.635）之间呈正相关。
我们的研究表明，急性AD引起的中膜暴露导致血小板活化，进而通过mtDNA释放到循环中引发炎症反应。我们的研究为AD后炎症反应的预防和治疗提供了新的基础和潜在的治疗靶点。
