基质金属蛋白酶及其抑制剂在风湿性二尖瓣狭窄合并心房纤颤中的作用

心房纤颤是临床上较为普遍的一种心律失常，心房纤颤时可加重风湿性二尖瓣瓣膜狭窄的程度。房颤对心脏瓣膜的破坏主要表现为细胞外基质正常结构被破坏，胶原沉积增多，各型胶原比例失调和排列紊乱。影响细胞外基质代谢的最主要的酶类是基质金属蛋白酶（matrix metalloproteinases，MMPs） 和金属蛋白酶内源性组织抑制剂（tissue inhibitors of metalloproteinases，TIMPs）。心房纤颤时MMPs、TIMPs 平衡失调使心脏瓣膜破坏，Ⅰ型和Ⅲ型胶原沉积增多，排列紊乱。MMP 9 和TIMP 2 是心房纤颤发生后MMPs 和TIMPs 中表达最具有意义的指标。本文通过对心房纤颤后心脏瓣膜组织中MMP 9 和TIMP 2 异常表达的研究进行综述，以了解心房纤颤对风湿性二尖瓣瓣膜影响的程度。

Effect of matrix metalloproteinases and tissue inhibitors of metalloproteinases on rheumatic mitral valve stenosis with atrial fibrillation

Atrial fibrillation is a common clinical arrhythmia, which could aggravate the rheumatic mitral valve stenosis. The pathomechanism for the mitral valve with atrial fibrillation includes the destruction of the structures of extracellular matrix and the deposition and disproportion of collagen. Matrix metalloproteinases （MMPs） and tissue inhibitors of metalloproteinases （TIMPs） are the main enzymes that affect the extracellular matrix’s metabolism. The disequilibrium between MMPs and TIMPs with atrial fibrillation make the extracellular matrix of atrial muscle degradation, type Ⅰ and Ⅲ collagen deposition and disarrangement. According to current findings, matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 2 are the most significant indicators in their terms. This study reflects that atrial fibrillation will aggravate the rheumatic mitral valve stenosis by analyzing the relationship between the abnormal expression of MMP 9 and TIMP 2.