Troponin T elevation after implanted defibrillator discharge predicts survival

Blendea, Dan; Blendea, Mihaela C; Banker, Jeffrey; McPherson, Craig A.

doi:10.1136/hrt.2008.162677

Cited by 18 publications

(14 citation statements)

References 30 publications

(40 reference statements)

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“…Miranda et al [68] revealed that patients with cTnI elevation after multiple ICD shocks had higher risk of death or heart failure hospitalization (hazard ratio, 7.0; 95% confidence interval, 1.2-16.0; P = .03) compared with patients without elevation of this biomarker [68]. Blandea et al [69] in a prospective observational study of 174 patients (mean (SD) age 68 (12) years, 32 women) who received spontaneous (n = 66) or induced (n = 108) ICD discharges found that elevation of cTnT after ICD discharge, even when it occurs after device testing, is a risk factor for mortality that is independent of other clinical factors that predict survival in such patients [69]. The shocks may be an epiphenomenon or marker of underlying disease progression; however, it cannot be excluded that shocks cause direct myocardial damage.…”

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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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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“…Myocardial damage induced by ICD shocks may contribute to worsening HF. 11,12 This is suggested by the adverse impact on prognosis of inappropriate shocks. In the MADIT-II study, however, inappropriate shocks did not increase the risk of adverse outcomes.…”

Section: Prognostic Importance Of Appropriate Icd Shocksmentioning

confidence: 99%

“…Large shock field strengths destroy cardiac myocytes causing biomarker release, which increases with shock strength and proximity to recent MI. 11,12,18 The severity of post-resuscitation myocardial depression increases with shock strength, and is inversely related to survival. 19 Repetitive shocks may cause cardiovascular collapse and death due to electromechanical dissociation.…”

Section: Possible Mechanisms For Increased Risk Of Negative Outcomes mentioning

confidence: 99%

Prognostic Significance of Implantable Cardioverter-Defibrillator Shocks

Blendea¹,

Dadu²,

McPherson³

2011

Cardiac Defibrillation - Prediction, Prevention and Management of Cardiovascular Arrhythmic Events

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“… Electrical shock by itself may cause harm by direct myocardial injury, 25,26 stunning, or indirectly by catecholamine release 27 The ICD treated arrhythmia (atrial or ventricular) may cause clinical deterioration and death. Atrial arrhythmias with rapid ventricular response may signify high adrenergic tone, inadequate beta blockade, or decompensate heart failure.…”

mentioning

confidence: 99%

“…1. Electrical shock by itself may cause harm by direct myocardial injury, 25,26 stunning, or indirectly by catecholamine release. 27 2.…”

mentioning

confidence: 99%

Prognostic Significance of Implantable Defibrillator Shock: Are All Shocks Created Equal?

Freedberg

Feldman

2012

Cardiovasc electrophysiol

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Troponin T elevation after implanted defibrillator discharge predicts survival

Abstract: Elevation of troponin T after ICD discharge, even when it occurs after device testing, is a risk factor for mortality that is independent of other common clinical factors that predict survival in such patients.

Cited by 18 publications

References 30 publications

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

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

Prognostic Significance of Implantable Cardioverter-Defibrillator Shocks

Prognostic Significance of Implantable Defibrillator Shock: Are All Shocks Created Equal?

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