Detection of myocardial injury due to defibrillation threshold checking after insertion of implantable cardioverter/defibrillators

Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
Acta cardiologica (Impact Factor: 0.65). 04/2013; 68(2):167-72. DOI: 10.2143/AC.68.2.2967274
Source: PubMed


Possible myocardial damage caused by defibrillation threshold (DFT) control and its extent after insertion of implantable cardioverter/defibrillators (ICD) is still a matter for debate. This study aimed to identify the effect of DFT checking during ICD implantation, compared with permanent pacemaker (PPM) implantation, on the magnitude of myocardial damage as assessed by cardiac troponin-T (cTNT) and CK-MB.
A total of 133 candidates for ICD implantation were enrolled in the ICD group (mean age 60.66 +/- 12.25 years; males 111 [83.5%]) as well as 130 candidates in the PPM group (mean age 69.56 +/- 12.86 years; males 64 [49.2%]). DFT was controlled in all of the ICD patients. Serum levels of cTNT and CK-MB were measured at baseline plus 8 and 24 hours following the procedure. The results were adjusted for age, gender, and other confounding factors. The amount of cTNT rise after 8 and 24 hours in the ICD group was significantly higher than in the PPM group (p < 0.001 for both). These differences remained significant after adjustment for confounding factors. The level of CK-MB rise after 8 and 24 hours was also significantly higher in the ICD group, although it lost its significance after adjustment for age, gender and other confounding variables. There was no significant relationship between the amount of energy delivered and enzyme elevation.
Elevation of cTNT and CK-MB after the ICD implantation was significantly higher than that after the PPM implantation and may be attributed to the DFT testing shock and resulting myocardial injury.

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Available from: Akbar Shafiee, Oct 13, 2015
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    ABSTRACT: Background Multiple shocks of the implantable cardioverter defibrillator (ICD) can cause myocardial injury, contributing to the progression of underlying heart disease. The aim was to evaluate if the elevation of troponin I after multiple ICD shocks has impact on the prognostic of these patients. Methods We evaluated patients with multiple ICD shocks (> 3 shocks) in the last 24 hours. Troponin I was measured around 12 hours after the last shock. After this episode, these patients were followed and events of death or heart failure hospitalization were recorded. Results Twenty-six patients were included in the study. Elevation of troponin I occurred in 16 patients (62%), who had received a higher number of shocks (14 ± 9 vs. 7 ± 4, p = 0.03) and greater cumulative total voltage (455 ± 345 J vs. 141 ± 62 J, p = 0.03) compared to the group without elevation of this biomarker. We observed a positive correlation between troponin I and number of shocks (r = 0.70; p = 0.0001). Patients with troponin I elevation after multiple ICD shocks had higher risk of death or heart failure hospitalization (hazard ratio (HR): 7.0; 95% confidence interval (IC) 1.2 to 16.0; p = 0.03) compared with the group without elevation of this biomarker. After adjustment for age, gender and number of shocks, the elevation of this biomarker remained as predictor of these events (HR:16.0; 95% CI 1.7 to 151.0; p = 0.02). Conclusion Large proportion of patients with multiple ICD shocks have troponin I elevation, and these patients have higher risk of death or hospitalization due to heart failure.
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