Factors underlying elevated troponin I levels following pacemaker primo-implantation

Abstract

Background. Cardiac troponins are routinely used as markers of myocardial damage. Originally, they were only intended for use in diagnosing acute coronary syndromes; however, we now know that raised serum troponin levels are not always caused by ischemia. There are many other clinical conditions that cause damage to cardiomyocytes, leading to raised levels of troponin. However, the specificity of cardiac troponins towards the myocardium is absolute. Our work focuses on mechanical damage to the myocardium and on monitoring the factors that raise the levels of cardiospecific markers after primo-implantation of a pacemaker with an actively fixed electrode. Aims. (i) To determine whether the use of a primo-implanted pacemaker with an electrode system with active fixation will raise troponin levels over baseline. (ii) To assess whether troponin I elevation is dependent on procedure complexity. Methods. We enrolled 219 consecutive patients indicated for pacemaker primo-implantation; cardiospecific marker values (troponin I, CKMB, myoglobin) were determined before the implantation procedure and again at 6-and 18-h intervals after the procedure. We monitored duration of cardiac skiascopy, number of attempts to place the electrode (active penetration into the tissue) and intervention range (single-chamber versus dual-chamber pacing), and we assessed the clinical data. Results. The average age of the enrolled patients was 78.2 ± 8.0 years (median age, 80 years); women constituted 45% of the group. We implanted 128 dual-chamber and 91 single-chamber devices with an average skiascopic time of 38.6 ± 22.0 s (median, 33.5 s). Troponin I serum levels increased from an initial 0.03 ± 0.07 μg/L (median, 0.01) to 0.18 ± 0.17 μg/L (median, 0.13) and 0.09 ± 0.18 μg/L (median, 0.04) at 6 and 18 h, respectively. The differences were statistically significant (P < 0.001 or P < 0.001). We confirmed a correlation between troponin increase and duration of skiascopy (P < 0.001). We also demonstrated a correlation between increased troponin I and number of attempts to place a pacemaker electrode (penetration into the tissue) at 6 h (P < 0.001) post-implantation. Conclusion. We detected slightly elevated troponin I levels in patients with primo-implanted pacemakers using electrodes with active fixation. We demonstrated a direct correlation between myocardial damage (number of electrode penetrations into the myocardium) and troponin I elevation, as well as between complexity (severity) of the implantation procedure (indicated by prolonged skiascopy) and raised troponin I. The described phenomenon demonstrates the loss of the diagnostic role of troponin I early after pacemaker primo-implantation in patients with concomitant chest pain.

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

“…Permanent pacemaker implantation is accomplished by transvenous insertion of endocardial leads. A number of studies have demonstrated that the mechanical effect of lead fixation on the myocardium may cause local injury, as evidenced by raised levels of plasma troponin and inflammatory biomarkers 1,2 . It is reported that transvenous insertion of the leads is followed by a sequence of cardiac histopathological changes, leading eventually to the formation of a fibrous connective tissue scar 3 .…”

Biomarkers of Myocardial Injury and Inflammation after Permanent Pacemaker Implantation: The Lead Fixation Type Effect

“…Rapid increase and decrease in cardiac troponin plasma levels are characteristic of reversible myocardial mechanical injury, especially due to the physical contact between lead and endocardium, resulting in direct cardiomyocyte destruction during the implantation procedure [1,2] . A small percentage of troponin is found in the myocyte cytoplasm in a soluble free form, which is released into the circulation under such circumstances [5] . A rapid troponin washout occurs within 24 hours, as there is no obstructive myocardial blood flow [3,4,6] .…”

“…Permanent pacemaker implantation is accomplished by transvenous insertion of endocardial leads, whose stability is secured and maintained using either active or passive fixation. A number of studies have demonstrated that the mechanical effect of both lead fixation types on the myocardium may lead to local injury, as evidenced by raised levels of plasma troponin and inflammatory biomarkers [1][2][3][4][5][6][7][8][9]12] . However, data are scarce regarding the association of the lead fixation type (active or passive) with the extent of myocardial injury, the subsequent systemic inflammatory response, and the possible clinical significance of cardiac biomarkers elevation, as clinical adverse events or abnormal change in pacing parameters.…”