Effect of matrix metalloproteinase and their inhibitors on atrial myocardial structural remodeling

To explore the expression of matrix metalloproteinase and tissue inhibitor of metalloproteinase of atrial myocardial structure of rheumatic and coronary heart disease.

Fifty patients with rheumatic heart disease (RHD) undergoing artificial mitral valve replacement surgery were selected: 20 with sinus rhythm and 30 with atrial fibrillation. Another 40 patients with coronary artery disease (CAD) undergoing coronary artery bypass surgery were selected: 22 with myocardial infarction (MI) and 18 with unstable angina. During thoractomy, samples of the right auricle were taken and immunohistochemical staining and fluorescence quantitative PCR were performed to test matrix metalloproteinase (MMP) 1, MMP-3, MMP-7, MMP-9, tissue inhibitor of metalloproteinase (TIMP) 1, TIMP-2, TIMP-3 and TIMP-4 expression of the samples.

In RHD, the left and right atrial diameters of the atrial fibrillation group were significantly larger than those of the sinus rhythm group (P < 0.01), but there was no significant difference between the left ventricular diastolic diameter and the left ventricular ejection. The immunohistochemical staining and real-time (RT)-PCR show that the expression of MMP-3, MMP-7, MMP-9, TIMP-1, TIMP-2, TIMP-3 and TIMP-4 were significantly increased in the atrial fibrillation group compared with the sinus rhythm group (all P < 0.01). The difference in MMP-1 of the two groups was not statistically significant. In CAD patients, the left and right atrial diameters and left ventricular diameter of the MI group were significantly larger than those of the unstable angina group (P < 0.01), but the left ventricular ejection fraction was obviously lower than that of the unstable angina group (P < 0.05). Immunohistochemical staining and RT-PCR show that the expression of MMP-3, MMP-9, TIMP-1 TIMP-2, TIMP-3, TIMP-4 were significantly increased in MI group compared with the unstable angina (P < 0.01, P < 0.01, P < 0.05, P < 0.05, P < 0.01 and P < 0.01, respectively).

The expression of MMPs and TIMPs increased in RHD patients and MI patients. Regulating the expression and activity of MMPs and TIMPs may be an important clinical treatment and method to prevent, and even reverse, atrial remodeling.