Key result
Active and passive fixation ventricular pacemaker leads resulted in similar extents of myocardial micro-damage, with median high-sensitive Troponin T levels increasing by 0.009 ng/ml and 0.008 ng/ml, respectively.
Why the study?
Does an active (screw-in) fixation ventricular lead compared to a passive (tined) fixation lead influence the magnitude of hsTnT release in patients undergoing pacemaker implantation?
RCT (n=326)
Open-label
1:1 ratio stratified for single and dual chamber pacemaker implantations using varying block sizes
Yes
Does an active (screw-in) fixation ventricular lead compared to a passive (tined) fixation lead influence the magnitude of hsTnT release in patients undergoing pacemaker implantation?
The choice between active or passive fixation ventricular leads does not significantly influence the extent of myocardial injury as measured by hsTnT release during pacemaker implantation.
Either fixation type acceptable without injury trade-off; confirms RCT equivalence in myocardial micro-damage.
Fixation of the pacemaker leads during pacemaker implantation leads to an increase of cardiac Troponin T (cTnT) that can be interpreted as a sign of minimal myocardial damage. This trial evaluates whether the mechanism type of lead fixation influences the magnitude of cTnT release. Patients having a de-novo cardiac pacemaker implantation or a lead revision were centrally randomized to receive either a ventricular lead with an active (screw) or passive (tine) fixation mechanism. High-sensitive Troponin T (hsTnT) was determined on the day of the procedure beforehand and on the following day. 326 Patients (median age (IQR) 75.0 (69.0-80.0) years, 64% male) from six international centers were randomized to receive ventricular leads with an active (n = 166) or passive (n = 160) fixation mechanism. Median (IQR) hsTnT levels increased by 0.009 (0.004-0.021) ng/ml in the group receiving screw-in ventricular leads and by 0.008 (0.003-0.030) ng/ml in the group receiving tined ventricular leads (n.s.). In conclusion pacemaker implantations are followed by a release of hsTnT. The choice between active or passive fixation ventricular leads does not have a significant influence on the extent of myocardial injury and the magnitude of hsTnT release.
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Blažek et al. (2018) conducted an RCT in Symptomatic bradycardia requiring pacemaker implantation (n=326). Active (screw-in) ventricular pacemaker lead vs. Passive (tined) ventricular pacemaker lead was evaluated on Absolute difference of serum high-sensitive Troponin T (hsTnT) levels before and after pacemaker implantation (OR 1.15, 95% CI 0.36-4.13, p=0.506). Active and passive fixation ventricular pacemaker leads resulted in similar extents of myocardial micro-damage, with median high-sensitive Troponin T levels increasing by 0.009 ng/ml and 0.008 ng/ml, respectively.
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