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目的:研究基质金属蛋白酶抑制剂(TMPs)与心脏瓣膜病(瓣膜病)慢性心房颤动(房颤)患者心房肌间质纤维化的关系。方法:开胸换瓣的手术病人45例,慢性房颤患者27例,窦性心律患者18例,术中取左心耳组织,采用半定量逆转录-聚合酶链反应(RT-PCR)测定Ⅰ型胶原、Ⅲ型胶原、TMP1、TMP2、TMP3、TMP4的mRNA表达水平。结果:与窦性心律组比较,慢性房颤组Ⅰ型胶原的mRNA表达水平上调(P<0.05),TMP1、TMP3的mRNA表达水平下调(P<0.05)。TMP1的mRNA表达水平与Ⅰ型胶原的mRNA表达水平、左心房内径呈负相关(r=-0.309,P=0.039;r=-0.533,P=0.002);TMP3的mRNA表达水平与Ⅰ型胶原的mRNA表达水平、左心房内径呈负相关(r=0.356,P=0.031;r=-0.535,P=0.002)。结论:心房肌TMP1以及TMP3的基因转录表达水平下调引起Ⅰ型胶原转录水平的上调,可能是瓣膜病房颤患者心房肌间质纤维化的分子基础。
AIM: To investigate the relationship between matrix metalloproteinase inhibitors (TMPs) and atrial fibrosis in patients with valvular heart disease (AF) and chronic atrial fibrillation (AF). Methods: 45 patients with open thoracotomy, 27 patients with chronic atrial fibrillation, 18 patients with sinus rhythm and left atrial appendage were taken from the patients. RT-PCR was used to detect the expression of Ⅰ Type collagen, type Ⅲ collagen, TMP1, TMP2, TMP3, TMP4 mRNA expression levels. Results: Compared with sinus rhythm group, mRNA expression of type Ⅰ collagen in chronic atrial fibrillation group was up-regulated (P <0.05), and mRNA expression of TMP1 and TMP3 was down-regulated (P <0.05). The mRNA expression level of TMP1 was negatively correlated with the mRNA expression of type Ⅰ collagen and the diameter of left atrium (r = -0.309, P = 0.039; r = -0.533, P = 0.002) mRNA level and left atrial diameter were negatively correlated (r = 0.356, P = 0.031; r = -0.535, P = 0.002). CONCLUSION: The down-regulation of TMP1 and TMP3 gene transcription in atrial myocardium leads to the up-regulation of type Ⅰ collagen transcription, which may be the molecular basis of atrial fibrosis in patients with valvular atrial fibrillation.