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Pacemaker Implantation Associated Myocardial Micro-Damage: A Randomised Comparison between Active and Passive
Patrick Blažek1, Jerko Ferri-Certić2, Hrvoje Vražić3
1Deutsches Herzzentrum München, Klinik für Herz- und Kreislauferkrankungen, Abteilung für Elektrophysiologie, Fakultät für Medizin der Technischen Universität München, Munich, Germany. blazek@dhm.mhn.de.
Pacemaker lead fixation can cause minor heart muscle damage, indicated by cardiac Troponin T (cTnT) release. This study found no significant difference in cTnT levels between active (screw) and passive (tine) fixation methods.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Biomarkers
Background:
- Pacemaker lead implantation can cause minimal myocardial injury, evidenced by an increase in cardiac Troponin T (cTnT).
- The mechanism of lead fixation (active vs. passive) may influence the extent of this myocardial release.
Purpose of the Study:
- To evaluate whether the type of ventricular lead fixation mechanism impacts the magnitude of cardiac Troponin T release post-pacemaker implantation.
Main Methods:
- A randomized trial involving 326 patients undergoing de-novo pacemaker implantation or lead revision.
- Patients received either active (screw) or passive (tine) fixation ventricular leads.
- High-sensitive Troponin T (hsTnT) levels were measured before the procedure and the following day.
Main Results:
- Both active and passive fixation methods resulted in an increase in hsTnT levels.
- Median hsTnT increase was 0.009 ng/ml for screw-in leads and 0.008 ng/ml for tined leads.
- The difference in hsTnT release between the two fixation types was not statistically significant (n.s.).
Conclusions:
- Pacemaker implantation is associated with a release of hsTnT, indicating minor myocardial injury.
- The choice between active (screw) and passive (tine) fixation for ventricular leads does not significantly alter the extent of myocardial injury or hsTnT release.
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