Pacemaker Implantation Associated Myocardial Micro-Damage: A Randomised Comparison between Active and Passive Fixation Leads

Blažek, Patrick; Ferri-Certic, Jerko; Vražić, Hrvoje; Lennerz, Carsten; Grebmer, Christian; Kaitani, Kazuaki; Karch, Martin R.; Starčević, Boris; Semmler, Verena; Kolb, Christof

doi:10.1038/s41598-018-23209-5

Cited by 8 publications

(7 citation statements)

References 29 publications

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“…The results above suggest that the myocardial damage of this new pacing mode is clearly existing. The previous studies have shown that the damage caused by traditional RVP is not clinically significant 15 . Different from the traditional RVP, the ventricular lead of LBBAP needs to penetrate into the interventricular septum to reach the left ventricular endocardium 16 .…”

Section: Discussionmentioning

confidence: 99%

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing

Chen

et al. 2021

RIC

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Background: Different from the traditional right ventricular pacing, the left bundle branch area pacing (LBBAP) is accomplished with deeper lead implantation and more attempts. However, myocardial damage is unclear in LBBAP. Objective: The objective of the study was to observe the change of troponin T and explore possible factors associated with greater myocardial damage in LBBAP. Methods: Patients with an indication for pacemaker implantation underwent attempts for LBBAP by transventricular septal method. Levels of troponin T were determined before operation, 12 h and 1 week after the operation. Parameters of intraoperation and follow-up were recorded and analyzed. Results: In total, successful LBBAP was achieved in 126 patients. The levels of troponin T increased significantly at 12 h after the operation compared with those before operation (96.45 ± 11.07 [69.06] vs. 16.59 ± 1.84 [11.92] ng/L, p < 0.001), while there were no significant differences between pre-and post-operative levels at 1 week. Correlation and regression analysis showed that only the number of attempts was an independent factor related to the change of troponin T. During 1 year of follow-up, LBBAP was safe and feasible with few complications. Conclusions: Myocardial damage of LBBAP was clinically significant. The number of attempts was an independent factor related to the myocardial damage. (REV INVEST CLIN. [AHEAD OF PRINT]

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Section: Discussionmentioning

confidence: 99%

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing

Chen

et al. 2021

RIC

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“…As all implanted leads in this study were active fixation leads, we are not able to comment about myocardial micro-damage caused by ATP and passive fixation leads. However, in a recent study, the type of pacemaker lead fixation (active versus passive fixation leads) did not significantly influence the extent of myocardial injury 25 . Due to ethical and logistical reasons, postoperative blood samples were taken the next morning.…”

Section: Discussionmentioning

confidence: 79%

Myocardial Minimal Damage After Rapid Ventricular Pacing – the prospective randomized multicentre MyDate-Trial

Semmler

Deutschmann

Haller

et al. 2020

Sci Rep

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therapy of choice for the primary and secondary prevention of sudden cardiac death is the implantation of an implantable cardioverter defibrillator (ICD). Whereas appropriate and inappropriate ICD shocks lead to myocardial microdamage, this is not known for antitachycardia pacing (ATP). In total, 150 ICD recipients (66 ± 12 years, 81.3% male, 93.3% primary prevention, 30.0% resynchronization therapy) were randomly assigned to an ICD implantation with or without intraoperative ATP. In the group with ATP, the pacing maneuver was performed twice, each time applying 8 impulses 6 Volt x 1.0 milliseconds to the myocardium. High sensitive Troponin T (hsTnT) levels were determined prior to the implantation and thereafter. There was no significant difference in the release of hsTnT between the two randomization groups (delta TnT without ATP in median 0.010 ng/ml [min. −0.016 ng/ml-max. 0.075 ng/ml] vs. with ATP in median 0.013 ng/ml [min. −0.005-0.287 ng/ml], p = 0.323). Setting a hsTnT cutoff of 0.059 ng/dl as a regularly augmented postoperative hsTnT level, no relevant difference between the two groups regarding the postoperative hsTnT levels above this cutoff could be identified (without ATP n = 10 [14.7%] vs. with ATP n = 16 [21.9%], p = 0.287). There was no significant difference in the release of high sensitive troponin between patients without intraoperative Atp compared to those with intraoperative ATP. Hence, antitachycardia pacing does not seem to cause significant myocardial microdamage. This may further support its use as a painless and efficient method to terminate ventricular tachycardia in high-risk patients.

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“…Accordingly, we hypothesized that the bradycardia‐dependent increase in the pacing threshold observed in the early phase after pacemaker implantation was associated with Phase 4 depolarization in the damaged myocardium, caused by factors such as inflammation and edema due to lead‐contact and could be improved by the administration of ATP, which increases the resting membrane potential and activates sufficient Na + current (Figure 3). Indeed, Blazek et al 6 suggested that pacemaker‐lead implantation‐induced myocardial microdamage, either with an active or passive fixation lead, could be monitored by using the high‐sensitive troponin T level as an index.…”

Section: Discussionmentioning

confidence: 99%

“…resting membrane potential and activates sufficient Na + current (Figure 3). Indeed, Blazek et al 6 suggested that pacemaker-lead implantation-induced myocardial microdamage, either with an active or passive fixation lead, could be monitored by using the highsensitive troponin T level as an index.…”

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confidence: 99%

Rate‐dependent pacing failure after pacemaker implantation: Novel insights into the mechanism of using adenosine

Ohe

Oginosawa

Yamagishi

et al. 2020

Cardiovasc electrophysiol

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An 82-year-old woman received pacemaker implantation for sick sinus syndrome. Two days after the implantation, electrocardiography showed 2:1 atrial pacing failure, followed by a bradycardia-dependent increase in the atrial pacing threshold during a pacemaker examination. However, transient 1:1 atrial pacing capture recovered by adenosine triphosphate (ATP) administration, which was performed to evaluate the bradycardia-dependent pacing failure mechanism. We considered this phenomenon to be caused by Phase 4 depolarization and avoided replacing this atrial lead. Three weeks later, the atrial pacing threshold had improved. We report the potential role of Phase 4 depolarization in a bradycardia-dependent increase in pacing threshold by using ATP.

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Pacemaker Implantation Associated Myocardial Micro-Damage: A Randomised Comparison between Active and Passive Fixation Leads

Cited by 8 publications

References 29 publications

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing

Quantification of Acute Myocardial Damage Secondary to Implantation of Electrodes for the Left Bundle Branch Area Pacing

Myocardial Minimal Damage After Rapid Ventricular Pacing – the prospective randomized multicentre MyDate-Trial

Rate‐dependent pacing failure after pacemaker implantation: Novel insights into the mechanism of using adenosine

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