Associations between N-terminal procollagen type III, tissue inhibitors of matrix metalloproteinase and atrial fibrillation in patients with mitral stenosis

The N-terminal procollagen types III (PIIINP) play an important role in triggering the remodeling process. In fact, the relationship between PIIINP and atrial fibrillation (AF) in patient mitral valve diseases is unresolved. This study aimed to assess relationships among serum PIIINP and atrial fibrillation remodeling in patients with mitral stenosis. One hundred and seventeen patients MS were screened for AF (51 without AF and 66 with AF) in the cardiology department of La Rabta Hospital. Plasma levels of PIIINP and TIMP-1-2 were measured by ELISA sandwich assay. Multiple linear regression analysis by the backward method was used. PIIINP ( P = 0.013), TIMP-1 ( P = 0.033) and TIMP-2 ( P = 0.049) were significantly lower in patients with AF compared to patients without AF. The serum levels of the following biomarkers protected the occurrence of AF according of ROC curves analysis: PIIINP (AUC = 0.625; 95% CI: 0.509–0.742; P = 0.039; cut-off =236.7 pg/mL; sensitivity (Se) 60%, specificity (Sp) 66%) and TIMP-1 (AUC = 0.631 (95% CI 0.514–0.748); P = 0.033; cut-off = 36.8 ng/mL; Se 75%, Sp 60%). The correlation analysis showed that PIIINP significantly negatively correlated with end-diastolic volume (EDV) ( r = −0,353; P = 0.05) and with the mitral valve area ( r = −0,338; P = 0.048). TIMP-1 correlated positively Wilkins score ( r = 0,432; P = 0.015) and PIIINP ( r = 0,229; P = 0.021). In patients without AF, no correlation is found between these biomarkers and clinical parameters. Multiple linear regression analysis by the backward method was used for detection of significant biomarkers that influenced the occurrence of AF. In fact, the PIIINP ( P = 0.047) and TIMP1 ( P = 0.030) have a significant negative effect on occurrence of AF. Our findings to suggest that significant decrease in plasma levels of PIIINP may be an indication of AF in patients with mitral stenosis.