摘要
目的探讨风湿性心脏病(风心病)心房纤颤(房颤)患者的心房结构和细胞凋亡的变化与房颤发病机制之间的关系。方法选择接受外科换瓣手术的风心病患者共43例,分为3组,其中窦性心律15例(A组),阵发性房颤8例(B组),慢性房颤20例(C组)。在手术中取左心房组织,应用TUNEL法检测各组患者左心房肌细胞凋亡的情况,计算其凋亡指数(AI):应用电镜观察左心房肌细胞的超微结构的变化。结果C组的AI为24.6%±9.1%,与A组和B组的比较明显升高(P〈0.01)。且AI分别与左心房内径、房颤持续时间呈明显正相关(P〈0.05-P〈0.006)。在B组和C组中,在电镜下见肌节长短不一,结构模糊;线粒体肿胀,大小不一,闰盘扭曲,肌浆网肿胀、破裂,以C组更为明显。结论慢性房颤时左心房肌细胞凋亡增加和其超微结构的变化在房颤的发生和持续存在中起重要的作用。
Objective To investigate the relationship between the changes of apoptosis,ultrastructure and the mechanism of atrial fibrillation(AF) in rheumatic heart disease(RHD) patients with AF. Methods A total of 43 patients with RHD who required valve-replacement were included, of patients 15 with regular sinus rhythm(group A), 8 with paroxysmal AF(groupB) and 20 with chronic AF(group C). The apeptosis index(AI) was measured by TUNEL The ultrastructure was observed with electron microscope. Results The AI of group C patients was significantly increased to 24.6 % ± 9.1% (P 〈 0.01 ) ,and AI was positively related to the left atrial dimension and duration of AF respectively. With electron microscope,the disorganized sarcomere,enlarged mitochondria,fragmentation of sarcoplasmic reticulum,and tortuous intercalated disc were found in group B and C, particularly in group C. Conclusion It is demonstrated that the increased atrial myocyte apeptosis and ultrastructure changes may play an important role on the onset and sustaining of AF.
出处
《生物医学工程与临床》
CAS
2007年第5期355-358,共4页
Biomedical Engineering and Clinical Medicine
关键词
风湿性心脏病
心房纤颤
超微结构
细胞凋亡
rheumatic heart disease
atrial fibrillation
ultrastructure
apoptosis