Key result
Single 65 J subcutaneous ICD shock does not significantly increase myocardial injury biomarkers.
Why the study?
ICD shocks are associated with increased risk of death and elevation of cardiac enzymes after defibrillation testing, but the impact of S-ICD shocks on acute cardiac damage in humans is unclear.
Does a single 65 J shock during S-ICD defibrillation testing cause acute cardiac damage as measured by circulating biomarkers in patients receiving an S-ICD?
Observational (n=30)
Does a single 65 J shock during S-ICD defibrillation testing cause acute cardiac damage as measured by circulating biomarkers in patients receiving an S-ICD?
A single 65 J shock during subcutaneous ICD defibrillation testing does not cause significant myocardial injury as measured by hs-CTnI and CK-MB mass, suggesting no long-term prognostic implications.
Answers are grounded in this paper and cite their sources.
No acute biomarker rise after single S-ICD shock; hypothesis-generating for myocardial safety and requires prospective confirmation.
Aims: Implantable cardioverter defibrillator (ICD) shocks are associated with a subsequent increased risk of death, and an elevation of cardiac enzymes has been measured after defibrillation testing (DFT). In an experimental swine study, subcutaneous ICD (S-ICD) shocks caused less myocardial damage than traditional ICD shocks. The aim of our study was to investigate the association between S-ICD shock and acute cardiac damage in humans, as evaluated by means of sensitive and highly specific circulating biomarkers. Methods and results: We calculated the variation in the serum levels of high-sensitivity cardiac troponin I (hs-CTnI) and creatine kinase-MB mass concentration (CK-MB mass), measured before and after an S-ICD shock delivered during intraoperative DFT. We also measured the degree of haemodynamic stress, as the variation in the serum levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and copeptin (CP), after the S-ICD shock. We analysed 30 consecutive patients who received an S-ICD and who underwent DFT by means of a single 65 J shock. The levels of biomarkers did not change from baseline to 1 h post-shock, i.e. hs-CTnI (from 0.029 ± 0.005 ng/mL to 0.030 ± 0.005 ng/mL, P = 0.079) and CK-MB mass (from 1.37 ± 0.17 ng/mL to 1.41 ± 0.18, P = 0.080) and remained stable 6 and 24 h after DFT. The plasma NT-proBNP did not change, whereas CP levels were significantly higher at 1 h post-shock evaluation. However, 6 h after DFT, the levels had returned to the baseline and remained stable at 24 h. Conclusion: The S-ICD shock did not seem to cause myocardial injuries. Although CP levels temporarily rose after DFT, they returned to basal levels within 6 h, which suggests that DFT does not have long-term prognostic implications. ICD shocks are associated with a subsequent increased risk of death, and an elevation of cardiac enzymes has been measured after DFT. We showed that serum levels of biomarkers of myocardial damage did not increase after high-energy DFT in patients who had undergone S-ICD device implantation. This suggests that S-ICD shock does not have long-term prognostic implications.
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D’Onofrio et al. (2017) conducted an observational in Patients implanted with a subcutaneous defibrillator (n=30). Subcutaneous ICD shock during defibrillation testing vs. Baseline (pre-shock) was evaluated on Variation in serum levels of high-sensitivity cardiac troponin I (hs-CTnI) and creatine kinase-MB mass concentration (CK-MB mass) (p=0.079). A single 65 J subcutaneous ICD shock during defibrillation testing did not significantly increase serum levels of hs-CTnI (P=0.079) or CK-MB mass (P=0.080) at 1 hour post-shock compared to baseline.
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