Dynamics of matrix metalloproteinases and procollagen type-1 N-terminal propeptide following right ventricular outflow tract reconstruction: the protective mechanism of restrictive physiology.

OBJECTIVE

Right ventricular outflow tract reconstruction frequently leads to long-term pulmonary failure and ventricular dilation. This study aims to investigate the dynamics of matrix metalloproteinase-2, matrix metalloproteinase-9, and procollagen type-1 N-terminal propeptide in predicting postoperative remodelling and to evaluate the "protective" potential of restrictive right ventricular physiology.

METHODS

This prospective comparative cohort study included 20 patients undergoing right ventricular outflow tract reconstruction (Research Group) and 20 patients undergoing atrial or ventricular septal defect repair via transatrial approach (Control Group). Biomarker levels were measured using ELISA at preoperative, early postoperative (24-48 hours), and 6-month intervals. Right ventricular geometry was assessed with cross-sectional snapshots at 6 months and 10 years. Right ventricular dilation was defined as right ventricular end-diastolic volume index > 150 ml/m2 or diameter z-score > 2, while preserved geometry was defined as right ventricular end-diastolic volume index < 100 ml/m2 or diameter z-score < 1.5.

RESULTS

Early postoperative biomarker increases were similar (p = 0.310) but differed significantly at 6 months. In the study group, matrix metalloproteinase-2 (p < 0.001) and procollagen type-1 N-terminal propeptide (p = 0.001) levels remained significantly elevated, independent of pulmonary regurgitation severity (p > 0.05). Ten years later, restrictive physiology was observed in 10 patients (50%), representing a progression compared to the 8 patients identified at 6 months.

CONCLUSION

Persistent elevation of matrix metalloproteinase-2 and procollagen type-1 N-terminal propeptide reflects an active "remodeling" process. Restrictive physiology is associated with the "Biological Banding" mechanism. By increasing myocardial stiffness, this adaptive process is linked to protecting the right ventricle from irreversible dilation under chronic volume overload.