Detection of myocardial injury due to defi brillation threshold checking after insertion of implantable cardioverter/defi brillators

Davoodi, Gholamreza; Mohammadi, Vahid; Shafiee, Akbar; Kazemisaeid, Ali; Sadeghian, Saeed; Vasheghani‐Farahani, Ali; Yaminisharif, Ahmad

doi:10.1080/ac.68.2.2967274

Cited by 14 publications

(12 citation statements)

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“…Although cTnI increased in both DFT+ and DFT− groups in our study, DFT+ patients had higher levels of cTnI release compared to the DFT− group, likely associated with the defibrillation shock. Our results, similar to other studies, 13,15,16 contrast with those of Furniss et al 14 who used a control group with DFT only (at time of ICD generator change) and found no troponin elevation associated with defibrillation. This discrepancy may be related to the lower number of patients included in their study, as well as the lower energy delivered with a single shock.…”

Section: Troponin Increasesupporting

confidence: 90%

Acute Effects of Implantable Cardioverter‐Defibrillator Shocks on Biomarkers of Myocardial Injury, Apoptosis, Heart Failure, and Systemic Inflammation

Brewster

Sexton

Dhaliwal

et al. 2017

Pacing Clinical Electrophis

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Background ICD shocks are potentially associated with myocardial injury, altered hemodynamics, apoptosis and inflammatory signaling. Their precise cellular impact can be explored after defibrillation testing (DFT) via biomarkers. We evaluated changes in biomarkers after ICD shocks during DFT. Methods We prospectively enrolled outpatients presenting for first implantation of a cardiac device. Biomarkers indicative of myocardial injury, inflammation and apoptosis were measured before and after implantation, and compared between patients receiving DFT (DFT+) to those not (DFT−). Results Sixty-three patients were enrolled, 40 in the DFT+ group and 23 in the DFT− group. Average levels of troponin I, hsCRP, Calprotectin, NTproBNP, and sFas increased by >50% after cardiac device implantation compared to baseline. Increase in troponin never exceeded 50 fold upper limit of normal (2ng/mL). Troponin trended higher in the DFT+ group at 8 hours (median 0.18 ng/mL, IQR 0.11–0.48) versus the DFT− group (0.10 ng/mL, IQR 0.06–0.28, P=0.0501); NTproBNP had a similar trend (p=0.0581). sFas significantly increased in the DFT+ group from baseline (median 4663 pg/mL, IQR 2908–5679) to 24 hours (5039 pg/mL, IQR 3274–6261; p=0.0338) but not in the DFT− group (p=0.4705). Conclusion DFT testing is associated with acutely increased plasma levels of troponin and sFas, a biomarker of apoptosis, along with a trend towards higher NTproBNP.

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Section: Troponin Increasesupporting

confidence: 90%

Acute Effects of Implantable Cardioverter‐Defibrillator Shocks on Biomarkers of Myocardial Injury, Apoptosis, Heart Failure, and Systemic Inflammation

Brewster

Sexton

Dhaliwal

et al. 2017

Pacing Clinical Electrophis

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“…11 Davoodi et al found that DFT test shock might result in myocardial injury. 12 In the Sham'a et al study, troponin elevation occurred in most of patients after inappropriate ICD shock because of lead fracture. 13 Therefore, it was proven that ICD shock causes myocardial damage, and the severity of the myocardial damage is related to the defibrillation energy.…”

Section: Discussionmentioning

confidence: 98%

Decreased Defibrillation Threshold and Minimized Myocardial Damage With Left Axilla Implantable Cardioverter Defibrillator Implantation

Noro

Zhu

Enomoto

et al. 2016

Circ J

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“…"Catecholamine overload" (ref. [27][28][29] or direct mechanical damage [30][31][32][33][34][35][36][37][38][39] during skiascopy of the heart (during pacemaker implantation) can be a marker of procedure complexity and may positively correlate with troponin levels 31 . Left ventricular failure 40 , right ventricular failure [41][42][43] , or the disparity between physiological degradation of the myocardium and insufficient elimination of its fragments (renal insufficiency) (ref.…”

Section: Methodsmentioning

confidence: 99%

“…In a study by Davoodi 34 , troponin T levels were compared between patients undergoing pacemaker versus ICD primo-implantations. The group of patients undergoing ICD implantations had higher levels of troponin T. In this case, the aetiology of this phenomenon is polyfactorial.…”

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confidence: 99%

Factors underlying elevated troponin I levels following pacemaker primo-implantation

Hnátek¹,

Táborský²,

Malý³

et al. 2016

BIOMED PAP

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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.

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Detection of myocardial injury due to defi brillation threshold checking after insertion of implantable cardioverter/defi brillators

Abstract: 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.

Cited by 14 publications

References 0 publications

Acute Effects of Implantable Cardioverter‐Defibrillator Shocks on Biomarkers of Myocardial Injury, Apoptosis, Heart Failure, and Systemic Inflammation

Acute Effects of Implantable Cardioverter‐Defibrillator Shocks on Biomarkers of Myocardial Injury, Apoptosis, Heart Failure, and Systemic Inflammation

Decreased Defibrillation Threshold and Minimized Myocardial Damage With Left Axilla Implantable Cardioverter Defibrillator Implantation

Factors underlying elevated troponin I levels following pacemaker primo-implantation

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