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.
Cardiac resynchronization therapy (CRT) has been shown to reduce mortality in selected patients with heart failure (HF) [1], however its impact on ventricular arrhythmias (VAs) remains controversial. Several randomized controlled studies have demonstrated that while CRT significantly reduces mortality and HF progression, patients remain at increased risk of VAs [2,3]. Some data also indicate that left ventricular (LV) lead pacing alone could impose a potential proarrhythmic risk [4,5].Global scar burden and myocardial viability at the LV lead position play an important role in CRT response and VA occurrence [6][7][8][9]. A high LV pacing threshold (PT) at resynchronization device implantation may be a contributing factor to the adverse CRT outcome and could indicate a regional myocardial scar [10]. In addition, our previous study demonstrated that lower regional viability in the vicinity of the LV lead pacing site could be associated with increased risk of malignant tachyarrhythmias [11].In this analysis, we sought to determine the relationship between LVPT and myocardial viability at the LV lead position. We also hypothesized that high LVPT would be associated with potential occurrence of VAs.
MethodsThe study complies with the Declaration of Helsinki. The study protocol was approved by The National Medical Ethics Committee and all patients gave a written informed consent before entering the study.
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