Pubblicato online: 16 mar 2024
Pagine: 8 - 16
Ricevuto: 09 giu 2023
Accettato: 17 lug 2023
DOI: https://doi.org/10.2478/amb-2024-0002
Parole chiave
© 2024 I. Yoncheva, published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
Introduction:
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).
Materials and Methods:
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.
Results:
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).
Conclusion:
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.