Gene Expression of Atrial Calcium-Handling Proteins in Patients with Rheumatic Heart Disease and Atrial Fibrillation

• 来源期刊: 岭南心血管病杂志（英文版）
• 学科: 医学
• 关键词: Atrial fibrillation Calcium-handling protein,Rheumatic heart disease
• 年，卷（期）: 2003,（1）
• 页码范围: 11-16
• 页数: 6页
• 分类号: R54
• 语种: 英文

摘要

Objectives To investigate the gene expression of calcium-handling proteins inpatients with rheumatic heart disease (RHD) and atrialfibrillation (AF) . Methods A total of 50 patientswith rheumatic mitral valve disease were included.According to cardiac rhythm and duration of episode ofAF, patients were divided into four groups: sinusrhythm group, paroxysmal AF group, persistent AF forless than 6 months group and persistent AF for morethan 6 months group. Atrial tissue was obtained fromthe right atrial appendage, the right atrial free wall andthe left atrial appendage respectively during open heartsurgery. Total RNA was isolated and reversly tran-scribed into cDNA. In a semi -quantitative polymerasechain reaction the cDNA of interest and of glyceralde-hyde3 -phosphate dehydrogenase (GAPDH) were am-plified and separated by ethidium bromide - stained gelelectrophoresis. Multiple liner regress was used forcorrelation between the mRNA amount and age, sex,right atrial diameter (RAd) and left atrial diameter(LAd) Results The mRNA of L- type calciumchannelα1c subunit, of Ca2 + - ATPase and of ryanodinereceptor in patients with persistent AF for more than 6months were significantly decreased ( P all ＜ 0. 01 ). But no alterations of the mRNA levels for SR phos-pholamban and calsequestrin were observed in patientswith persistent AF for more than 6 months comparedwith patients with sinus rhythm, paroxysmal AF andpersistent AF for less than 6 months( P all ＞ 0.05) .There was no difference of the gene expression amongthe three atrial tissue sampling sites(P all ＞ 0.05). Age, gender, RAd and LAd had no significant effectson the gene expression of calcium- handling proteins( P all＞ 0. 05). Conclusions The mRNA expressionof calcium -handling proteins is down -regulated onlyin patients with RHD and long- term persistent AF.Such abnormalities may be related to the initiationand/or perpetuation of AF in the patients with RHD.