Cardiac troponin I. A marker with high specificity for cardiac injury.

Adams, Jesse E.; Bodor, G.; Dávila‐Román, Víctor G.; Delmez, James A.; Apple, Fred S.; Ladenson, Jack H.; Jaffe, Allan S.

doi:10.1161/01.cir.88.1.101

Cited by 1,041 publications

(576 citation statements)

References 41 publications

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“…1: 1A8 ϭ 110.2 Ϯ 11.6 mg compared with IgG ϭ 140.0 Ϯ 11.0 mg, p Ͻ 0.01 and Expt. 2: 1A8 ϭ 113.6 Ϯ 2.8 mg compared with IgG ϭ 149.6 Ϯ 15.8 mg, p Ͻ 0.01; n ϭ 5 mice per group); however, no differences were noted in levels of cardiac troponin I, a marker of myocardial injury (29,30), in serum from neutropenic or control mice at day 7 postinfection (data not shown).…”

Section: Virus Replication and Spread In Neutropenic Mice Following Imentioning

confidence: 91%

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Tate

Deng

Jones

et al. 2009

The Journal of Immunology

283

308

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The clinical response to influenza infection ranges from mild disease to severe pneumonia and it remains unclear whether the inflammatory response to infection is protective or pathogenic. We have defined a novel role for neutrophils in ameliorating lung injury during influenza infection, thereby limiting development of severe disease. Infection of neutrophil-depleted mice with influenza virus HKx31 (H3N2) led to rapid weight loss, pneumonia, and death. Neutropenia was associated with enhanced virus replication in the respiratory tract; however, viral titers were declining at the time of death, leading us to investigate other factors contributing to mortality. In addition to thymic atrophy, lymphopenia, and viremic spread, depletion of neutrophils led to exacerbated pulmonary inflammation, edema, and respiratory dysfunction. Thus, while it is well established that neutrophils contribute to lung injury in a range of pathological conditions, reduced numbers or impaired neutrophil function can facilitate progression of mild influenza to severe clinical disease.

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Section: Virus Replication and Spread In Neutropenic Mice Following Imentioning

confidence: 91%

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Tate

Deng

Jones

et al. 2009

The Journal of Immunology

283

308

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“…Myocardial necrosis is signified by increased level of cTn.Cardiac troponin I (cTnI), in particular, is not expressed by injured or regenerating skeletal muscle, and is, therefore, exquisitely specific for myocardial injury. 8 In general, cTnI and cTnT provide comparable information, except in renal failure, where cTnT is more likely to be elevated. 9 Troponin elevation after myocardial necrosis occurs within 2-3 hours, reaches its peak in 24 hours, and remains elevated for 1 to 2 weeks.…”

Section: Troponin Assessmentmentioning

confidence: 98%

A Review of Causes and Systemic Approach to Cardiac Troponin Elevation

Patil

Vaidya

Bogart

2011

Clinical Cardiology

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The first American College of Cardiology/European Society of Cardiology task force published recommendations for a universal definition of myocardial infarction (MI) in 2000 based on the measurement of troponin (Tn). Although this rapid and highly sensitive blood test is certainly valuable in the appropriate setting, its widespread use in variety of clinical scenarios may lead to the detection of Tn elevation in absence of thrombotic acute coronary syndrome. In 2007, the joint European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Heart Federation task force proposed a new definition for acute MI based on detection of Tn and associated clinical evidence. The goal of this article is to review the universal definition of acute MI and to differentiate type 1 MI, type 2 MI, and non–acute coronary syndrome Tn elevations. The prognosis and a clinical approach to this differential diagnosis will be developed. © 2011 Wiley Periodicals, Inc.The authors have no funding, financial relationships, or conflicts of interest to disclose.

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“…[19][20][21][22][23][24][25][26][27][28][29] Cardiac troponin I also remains elevated longer, usually up to 10-14 days.20 Recently it has also been shown that cTnI is an important prognostic indicator in patients presenting with unstable angina, even when CK-MB is not e l e~a t e d . l~\~&~~ Our study supports that notion.…”

Section: Why Use Cardiac Troponin I?mentioning

confidence: 99%

A Prospective Study of an Algorithm Using Cardiac Troponin I and Myoglobin as Adjuncts in the Diagnosis of Acute Myocardial Infarction and Intermediate Coronary Syndromes in a Veteran's Hospital

Maisel

Templin

Love

et al. 2000

Clinical Cardiology

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summaryBackground: Accurate and cost-effective evaluation of acute chest pain has been problematic for years. The high prevalence of missed myocardial infarctions (MI) has led to conservative triage behavior on the part of physicians, leading to expensive admissions to coronary care units. New algorithms are sorely needed for more rapid and accurate triage of patients with chest pain to appropriate treatment settings.Hypothesis: We sought to test an algorithm for rapid diagnosis of MI and acute coronary syndromes using cardiac troponin I (cTnI) and myoglobin as adjuncts to creatine kinase (CK)-MB. We hypothesized our algorithm would be both sensitive and specific at early time points, and would allow safe stratification of patients not ruling in by conventional CK-MB criteria.

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Cardiac troponin I. A marker with high specificity for cardiac injury.

Abstract: Elevations of cTnI are highly specific for myocardial injury. Use of cTnI should facilitate distinguishing whether elevations of MBCK are due to myocardial or skeletal muscle injury.

Cited by 1,041 publications

References 41 publications

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

Neutrophils Ameliorate Lung Injury and the Development of Severe Disease during Influenza Infection

A Review of Causes and Systemic Approach to Cardiac Troponin Elevation

A Prospective Study of an Algorithm Using Cardiac Troponin I and Myoglobin as Adjuncts in the Diagnosis of Acute Myocardial Infarction and Intermediate Coronary Syndromes in a Veteran's Hospital

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