Factors underlying elevated troponin I levels following pacemaker primo-implantation.

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.

Optimizing the pacing site in the ventricular septum by fluoroscopy and morphology of the paced QRS complex.

AIMS: To analyze the paced QRS duration in various septal positions of the right ventricular leads and with different paced QRS vectors. To use the results to assess parameters suggesting the optimal site for right ventricular pacing. METHODS AND RESULTS: A total of 609 patients with leads implanted in the right ventricular septum were classified using fluoroscopy in the lateral view (the primary pacing site), and in the anteroposterior view (the secondary pacing site), according to the QRS vector in leads I and III. Significantly shortened paced QRS was found in the primary pacing site with the true septal compared with the anteroseptal site, with the vector being negative or isoelectric in lead I plus positive in lead III. In secondary pacing sites, no significant difference in pacing QRS duration was found between RVOT-HS, RVOT-LS, mid-septum and inferior-septum. CONCLUSIONS: For optimization of the pacing site in the ventricular septum, the following are significant: the primary site based on the lateral view, and the paced QRS vector in leads I and III.