Clinical performance of CLS was very satisfactory in the large cohort studied.

Abstract:Background: Since the late 1990s, a growing number of clinical studies have indicated that long-term permanent right ventricular (RV) apical pacing will induce severe complications such as development of heart failure, increased burden of atrial fi brillation leading to decreased quality of life. Aim of the study: To investigate whether cardiac resynchronization therapy (CRT) using biventricular (BiV) pacing can prevent the development of left ventricular (LV) dysfunction, LV remodelling, worsening of the clinical status and quality of life in chronically RV paced patients with normal LV ejection fraction (EF). Methods and results:A total of 127 patients with Class I indication for permanent cardiac pacing and without established indication for CRT were subjected to 6 months of RV and BiV pacing in a patient-blinded, randomized crossover trial. Treatment effects of BiV pacing were evaluated for LV function, LV remodelling and clinical status. Conclusion: BiV pacing, compared to RV pacing, did not change LV function and quality of life in patients with the absence of LV dysfunction or remodelling, standard bradycardia pacing indications in a pilot phase (12-month follow-up) of the TUGENDHAT trial. The fi nal report will be published after 60-month follow-up termination (Tab. 5, Fig. 3, Ref. 30). Full Text in PDF www.elis.sk. Key words: BiV and RV pacing, LV remodelling, heart failure, atrial fi brillation, quality of life. Results of several trials have supported the fact that right ventricular (RV) apical pacing might lead to adverse clinical outcomes in patients with standard pacing indications. Nevertheless, RV apical pacing continues to be practiced by many physicians because of its easy accessibility and relative stability over time (1, 2). The optimal mode and site of pacing remain undefi ned.The detrimental effect of RV pacing is probably most important in patients with pre-existing left ventricular (LV) dysfunction and may lead to worsening of heart failure (3, 4). In RV pacing, the sequence of electrical activation resembles the activation pattern in left bundle branch block (LBBB). This asynchronous electrical pattern is accompanied by abnormal dyssynchronous mechanical interactions within the LV (5). Experimental data suggested that biventricular (BiV) pacing might preserve myocardial performance better than RV apical pacing in patients with atrioventricular (AV) block and normal systolic function (6). The underlying mechanism may be a signifi cant reduction in LV systolic dyssynchrony, as shown by Cojoc et al (7). In the majority of patients with severe LV dysfunction and severe clinical heart failure associated with either LBBB-or RV pacing-induced dyssynchrony, BiV pacing improves clinical status, reduces mortality and morbidity, reduces heart failure (HF) hospitalizations, reverses LV remodelling and improves LV function (8, 9). Therefore, BiV pacing is nowadays recommended in patients with ventricular dyssynchrony (QRS > 120 ms), severe LV dysfunction [LV ejection fraction (LVEF) < 0.35] ...

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.