Cardiac troponin levels following implantable cardioverter defibrillation implantation and testing

Furniss, Guy; Shi, B.; Jiménez, Alejandro; Harding, Scott; Larsen, Peter

doi:10.1093/europace/euu306

Cited by 13 publications

(17 citation statements)

References 20 publications

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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%

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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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Section: Methodsmentioning

confidence: 99%

“…In a 2015 study published by Furniss 38 , increased levels of troponin T in patients undergoing simple ICD implantations both with and without discharge therapy were observed. There were no differences in troponin T elevation between the two groups and no differences in the dependence on total energy applied during test discharge.…”

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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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“…There was a significant correlation between the number of leads implanted and the percent change in hs-cTnT (r = 0.51, p = 0.01), but no correlation between the number of shocks (r = 0.26, p = 0.25) or the total delivered energy (r = 0.24, p = 0.30) and percent change in hs-cTnT levels. 36 This suggests that, although device implantation and lead deployment may cause an increase in hs-cTn levels, ICD shocks alone do not appear to cause hs-cTn elevation. In addition, the prognostic implication of elevated hs-cTn in ICD patients has yet to be investigated and warrants future examination.…”

Section: Sudden Cardiac Death and Cardiac Arrestmentioning

confidence: 99%

“…In a prospective study, Furniss et al 36 examined hs-cTn levels and electrocardiogram changes during ICD implantation without defibrillation threshold testing (DFT), ICD implantation with DFT, and DFT as a standalone procedure. There was no significant change in hs-TnT levels in a group of patients undergoing defibrillation testing alone compared with baseline levels, while hs-TnT was significantly higher in patients undergoing implantation alone (median increase 96%, p = 0.005) and in patients undergoing implantation and testing (median increase 161%, p = 0.005).…”

Section: Sudden Cardiac Death and Cardiac Arrestmentioning

confidence: 99%

High-Sensitivity Troponin as a Biomarker in Heart Rhythm Disease

McCarthy

Yousuf

Alonso

et al. 2017

The American Journal of Cardiology

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Biomarkers are important prognostic tools in various cardiovascular conditions, including coronary artery disease and heart failure. Although their utility in cardiac electrophysiology (EP) is less established, biomarkers may guide EP clinical practice by identifying patients at risk for developing arrhythmias and their complications, in addition to augmenting therapeutic decisions by targeting appropriate pharmacologic and interventional therapies to patients who may benefit most. In this review, we focus on the prognostic role of high-sensitivity cardiac troponin (hs-cTn) assays—which detect subclinical cardiac myocyte damage—in cardiac arrhythmias and their sequelae. We review the current literature on hs-cTn and its impact on various arrhythmia disease states and also provide suggestions for future research in this field. In conclusion, although the utility of hs-cTn assays remains at an investigational stage in cardiac EP, studies to date have suggested value as a prognostic biomarker in atrial fibrillation and as a screening marker for patients at high risk of sudden cardiac death (both in the general population and among those with hypertrophic cardiomyopathy).

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“…Implantation of ICD leads has been associated with release of troponin, but there is no clear evidence that ICD shocks alone cause myocardial injury. In fact, Guy et al [70] studied 32 patients who underwent a total of 34 procedures and found that implantable cardioverter defibrillator implantation and testing is associated with release of cardiac troponin and is correlated to the number of ventricular lead deployments during the procedure. Secondly, they also noted that implantable cardioverter defibrillator testing conducted as a stand-alone procedure does not result in the release of cardiac troponin [70].…”

Section: Defibrillator Shocksmentioning

confidence: 99%

A Review of Cardiac and Non-Cardiac Causes of Troponin Elevation and Clinical Relevance Part I: Cardiac Causes

2017

JCCR

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IntroductionCardiac troponin T (cTnT) and troponin I (cTnI) are cardiac regulatory proteins that control the calcium mediated interaction between actin and myosin [1]. The troponin complex consists of three subunits: troponin C, troponin I, and troponin T. This complex is located on the myofibrillar thin (actin) filament of striated (skeletal and cardiac) muscle. The cardiac isoforms troponin T and I are only expressed in cardiac muscle [1].In the year 2007 a consensus statement from the Joint European Society of Cardiology and The American College of Cardiology committees redefined myocardial infarction (MI) as an elevation of cTnT or cTnI in conjunction with clinical evidence of myocardial ischemia [2]. They recommended highsensitivity cardiac troponin assays to rule out MI using a 3-hour pathway based on the 99 th percentile of the normal reference range [2]. Cardiac troponins are detected in the serum by the use of monoclonal antibodies to epitopes of cTnI and cTnT. These antibodies are highly specific for cardiac troponin but do not react with skeletal muscle troponins [3,4]. Troponin assays are quite sensitive and can detect <1 g of myocardial necrosis; therefore, the diagnosis of myocardial infarction requires that cTn must be above the 99 th percentile upper reference limit for the specific assay being used [5]. Some studies have reported that the 99 th percentile reference limit differs between men and women when measured with high-sensitivity assays for cardiac troponin [6].An elevation of cTn indicates the presence of, but not the underlying reason for, myocardial injury. Elevated troponins have been noted in several clinical conditions in addition to acute myocardial infarction (AMI). These conditions include pulmonary embolism, sepsis, heart failure, myocarditis, myocardial contusion, critical illness, cardio-toxic chemo, defibrillator shocks, atrial fibrillation, and end stage renal disease. Elevated cTnT and cTnI almost always imply a poor prognosis regardless of the mechanism by which troponins were released from cardiac myocytes into circulation. Ottani et al. found that the odds ratio for death and MI was 3.44-fold at 30 days in the cTnT-positive group compared to patients with unstable angina who did not have elevated troponins [7].The aim of this article is to highlight different conditions in which elevated troponins have been commonly noted, and to discuss the suggested mechanisms for elevated troponins in these patients. It is still unclear how to manage troponin elevation in clinical conditions other than AMI, but it is important to note the differential diagnosis for elevated troponins and the clinical significance of troponin elevation in each setting. Troponin elevation reflects acute or chronic myocardial damage but is not exclusive for ACS, thus causing some problems with interpretation of results. Differentiating elevated troponins due to non-coronary diseases is challenging; however, this differentiation is paramount in order to provide timely and appropriate treatment. This is a t...

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Cardiac troponin levels following implantable cardioverter defibrillation implantation and testing

Abstract: Implantation of ICD leads was associated with release of troponin, but we did not observe any evidence that ICD shocks alone cause myocardial injury.

Cited by 13 publications

References 20 publications

Factors underlying elevated troponin I levels following pacemaker primo-implantation

Factors underlying elevated troponin I levels following pacemaker primo-implantation

High-Sensitivity Troponin as a Biomarker in Heart Rhythm Disease

A Review of Cardiac and Non-Cardiac Causes of Troponin Elevation and Clinical Relevance Part I: Cardiac Causes

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