[Alterations in gene expression of calcium handling proteins in patients with chronic atrial fibrillation].
OBJECTIVE
To discuss the role of calcium-overloading in initiation and maintenance of atrial fibrillation (AF).


METHODS
The right atrial appendages were obtained from 14 patients with AF and 12 patients with sinus rhythm. The mRNA expression of proteins influencing the calcium homeostasis was measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and normalized to the mRNA level of glyceraldehyde-3- phosphate dehydrogenase. The left atrial diameter (LAD), mitral valvular area (MVOA), and systolic pulmonary arterial pressure were obtained by echocardiography before surgery.


RESULTS
Compared to sinus rhythm group, the mRNA levels of L-type calcium channel alc, sarcoplasmic reticulum (SR), calcium adenosine triphosphatase (Ca2+ -ATPase), and ryanodine receptor type-2 (R(Y) R2) were significantly decreased (P < 0.01); the mRNA level of inositol triphosphate receptor type-1 (IP3R1) was significantly increased (P < 0.05). No changes in the mRNA expression of phospholamban and calsequestrin were observed between two groups (P > 0.05). Correlations were found between MVOA and mRNA levels of LVDC-Calc, SR Ca2+ -ATPase (r = 0.719, P = 0.004; r = 0.625, P = 0.017). The mRNA level of SR Ca2+ -ATPase was negatively correlated with LAD (r = -0.573, P = 0.032).


CONCLUSIONS
Calcium loading may be responsible for the occurrence and maintenance of AF, and abnormal regulation in the mRNA expression may be the molecular mechanism of intracellular Ca2+ overload. The progressive nature of AF involves structural change.
Tang
Bao-peng
BP
Department of Cardiology, Department of Cardiac Surgery, the First Affiliated Hospital, Xinjiang Medical University, Urumqi 830054, China. tangbaopeng@hotmail.com
Xu
Guo-jun
GJ
Shabiti
Yilihamujing
Y
Yunus
Kurexi
K
Abutirehemen
Mulati
M
Cheng
Zu-Heng
ZH
D001146:Arrhythmia, Sinus / Q000378:metabolism; D001281:Atrial Fibrillation / Q000378:metabolism* / Q000473:pathology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000096:biosynthesis / Q000235:genetics; D002135:Calcium-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D000252:Calcium-Transporting ATPases / Q000096:biosynthesis / Q000235:genetics; D002908:Chronic Disease; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008943:Mitral Valve / Q000473:pathology; D009206:Myocardium / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis
D015220:Calcium Channels; D002135:Calcium-Binding Proteins; D012333:RNA, Messenger; D000252:Calcium-Transporting ATPases; D002118:Calcium