【摘要】 从机制上讲心房颤动一直以来都是临床上难以攻克的常见心律失常,机制未明,治疗自然无从谈起,目前持续房颤的治疗仍然是对症、预防栓塞等保守疗法,疗效差.随着人们对房颤机制的不断深入探索,发现房颤时心房肌细胞内氧化物质增多,如活性氧(ROS)等,而清除这些氧化物质可使房颤发生率明显降低,进一步研究发现这些氧化物质增多时可出现心房肌组织结构改变,最终可出现心房肌细胞凋亡.故推测氧化应激可能通过某些途径诱导心房肌细胞凋亡,进而促进房颤发生与维持,但具体机制尚需进一步研究明确.更多还原

【Abstract】 Atrial fibrillation is a common clinical arrhythmia and has always been difficult to conquer from the mechanism, its pathogenesis is not clear, and there is almost no therapy. At present, the treatment of atrial fibrillation is still conservative therapy, such as symptomatic treatment, embolism prevention and so on, but the curative effect is poor.With the deep exploration of the mechanism of atrial fibrillation, people find the increase of oxidizing substances in the atrial muscle cells during atrial fibrillation, such as reactive oxygen species(ROS)and so on, and remove the oxidizing substances can obviously decrease the incidence of atrial fibrillation. Further studies find that the increase of these oxidizing substances can change atrial muscle organization structure, and in the end, the atrial myocytes apoptosis appear. So it is speculated that oxidative stress may induced atrial myocyte apoptosis by some pathways, thus promote and maintain atrial fibrillation, but the specific mechanism still needs further research.更多还原