Data on the development of left ventricular dysfunction after permanent pacemaker implantation are available. Myocardial collagen deposition is a well-known mechanism that occurs in left ventricular remodelling. This gave us reason to dynamically monitor the levels of the main molecules involved in collagen synthesis, PIPC (carboxy-terminal propeptide of type I procollagen) and PIIINP (amino-terminal propeptide of type III procollagen).
PIPC and PIIINP levels were studied using enzyme-linked immunoassays in plasma from 45 patients (25 men, 20 women, 72.1 ± 9 years) and 46 controls (24 men, 22 women, 71.9 ± 8.7 years) without known cardiovascular diseases (except arterial hypertension, conduction disorder, indication for the procedure) at baseline (immediately before PPM implantation for patients), at 12 and 24 weeks.
There was no difference in baseline levels of PICP and PIIINP between patients and controls (p > 0.05, Table abstract). At week 12, PICP levels increased significantly in patients compared to baseline in controls (p < 0.05, Table abstract). At week 24, values continued to increase and were again significantly higher than baseline in the controls (p < 0.001, Table abstract). At the 12-week follow-up visit, PIIINP values in patients were significantly higher than those at baseline in controls (p < 0.001, Table abstract). At week 24, the values of the patients were still higher than those of the controls, but the difference was not significant (p > 0.05, Table abstract).
This study showed early activation of collagen synthesis < 6 months after PPM (permanent pacemaker) implantation. Due to the selection of patients without concomitant cardiovascular pathology, we have reason to assume that it is a result of the procedure itself and a serious prerequisite for increased collagen deposition in the myocardium.