Myocardial injury occurs earlier than myocardial inflammation in acute experimental viral myocarditis

Lim, Byung-Kwan; Shin, Jae-Ok; Choe, Seong-Choon; Choi, Si Wan; Jeong, Jin‐Ok; Seong, In‐Whan; Kim, Duk Kyung; Jeon, Eun‐Seok

doi:10.1038/emm.2005.7

Cited by 17 publications

(11 citation statements)

References 20 publications

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“…The absence of increased serum cTnI concentrations and the lack of histologic evidence of cardiomyocyte degeneration differentiate the condition described here from the findings in models of myocarditis, in which increases in serum cTn are associated with cardiomyocyte damage (Bachmaier et al 1995;Lim et al 2005;Smith et al 1997). As reported here, normal serum concentrations of cTnI in monkeys with myocardial mononuclear cell infiltrates imply that cardiomyocyte damage, not cellular infiltration, is responsible for the serum cTnI increases seen in animal models of myocarditis.…”

Section: Discussionsupporting

confidence: 58%

Myocardial Mononuclear Cell Infiltrates Are Not Associated with Increased Serum Cardiac Troponin I in Cynomolgus Monkeys

et al. 2012

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Myocardial mononuclear cell infiltrate is a spontaneous cardiac finding commonly identified in laboratory cynomolgus monkeys. The infiltrates are predominantly composed of macrophages with lesser lymphocytes and are not typically associated with histologically detectable cardiomyocyte degeneration. These infiltrates are of concern because they confound interpretation of test article-related histopathology findings in nonclinical safety toxicology studies. The interpretation of safety studies would be simplified by a biomarker that could identify myocardial infiltrates prior to animal placement on study. We hypothesized that monkeys with myocardial mononuclear cell infiltrates could be identified before necropsy using an ultrasensitive immunoassay for cardiac troponin I (cTnI). Serum cTnI concentrations in monkeys with myocardial infiltrates were not higher than those in monkeys without infiltrates at any of the sampling times before and on the day of necropsy. Increased serum cTnI levels are not suitable for screening monkeys with myocardial mononuclear cell infiltrates before placement in the study.

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Section: Discussionsupporting

confidence: 58%

Myocardial Mononuclear Cell Infiltrates Are Not Associated with Increased Serum Cardiac Troponin I in Cynomolgus Monkeys

et al. 2012

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“…35 It was reported that the serum cardiac troponin concentration was an earlier marker of myocardial injury after virus infection than was the histologic finding of inflammation. 25 The increase of serum cTnI and reduction or loss of cTnI expression in tissue are roughly related to disease severity, probably reflecting the extent of inflammatory and degenerative changes of the myocardium. In humans, maintenance of high serum concentrations of cTnI was considered an indication of a poor prognosis in advanced heart failure.…”

Section: Discussionmentioning

confidence: 99%

Determination of Cardiac Troponin I in the Blood and Heart of Calves with Foot-and-Mouth Disease

Tunca

Sözmen

Erdoğan³

et al. 2008

J VET Diagn Invest

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Abstract. The current study was designed to determine the changes of the cardiac troponin I (cTnI) expression in blood and tissue during the myocardial degeneration in calves with foot-and-mouth disease (FMD). Seventeen crossbred calves presenting pathological signs for FMD confirmed by viral analysis were studied. A biochemistry panel and immunohistochemistry were performed on 17 diseased calves and 7 calves used as controls. Creatine kinase (CK), CK-myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analyzed for both groups. Cardiac troponin I levels were measured by a commercially available enzyme-linked immunosorbent assay kit. Mean cTnI (14.8 6 1.9 ng/ml) concentration and CK (573 6 407 U/l), CK-MB (238 6 37 U/l), AST (84 6 7), and LDH (298 6 29 U/l) activities were higher in FMD cases compared with controls. Immunohistochemistry revealed loss or depletion of cTnI expression in myocardium of all cases. None of the 7 controls showed loss of cTnI expression. Increased serum cTnI concentration correlated with myocardial injury and loss of cTnI immunolabeling in cardiomyocytes of calves with FMD.

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“…However, because each pony had a normal prechallenge cTnI, and the CON ponies did not have variations in cTnI over the same duration of time, the transient increases suggested that they were associated with viral challenge. Definitive proof of cause and effect would have required endomyocardial biopsies, but cardiac troponins have been used to follow both clinical and experimentally induced viral myocarditis in people and laboratory animals 12,17,18 …”

Section: Discussionmentioning

confidence: 99%

“…Cardiac troponin I (cTnI) concentrations are increased in a number of human cardiac diseases, including viral myocarditis 12,16,17 . Both cTnI and cardiac troponin T (cTnT) have been used to monitor viral myocarditis in people, 12,17 and cTnT has been shown to correlate well with viral infection in the heart, and to precede the development of histologically confirmed inflammation in a mouse model of myocarditis 18 . In this experimental model, cTnT concentrations increased by day 3 after infection, persisted at day 7, and had returned to normal by day 14.…”

mentioning

confidence: 99%

Cardiac Troponin I Concentrations in Ponies Challenged with Equine Influenza Virus

Durando

Birks

Hussey

et al. 2011

Veterinary Internal Medicne

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Background: Myocarditis is thought to occur secondary to equine influenza virus (EIV) infections in horses, but there is a lack of published evidence. Hypothesis/Objectives: We proposed that EIV challenge infection in ponies would cause myocardial damage, detectable by increases in plasma cardiac troponin I (cTnI) concentrations. Animals: Twenty‐nine influenza‐naïve yearling ponies: 23 were part of an influenza vaccine study (11 unvaccinated and 12 vaccinated), and were challenged with 108 EID50 EIV A/eq/Kentucky/91 6 months after vaccination. Six age‐matched healthy and unvaccinated ponies concurrently housed in a separate facility not exposed to influenza served as controls. Methods: Heparinized blood was collected before and over 28 days after infection and cTnI determined. Repeated measures analysis of variance, chi‐square, or clustered regression analyses were used to identify relationships between each group and cTnI. Results: All EIV‐infected ponies developed clinical signs and viral shedding, with the unvaccinated group displaying severe signs. One vaccinated pony and 2 unvaccinated ponies had cTnI greater than the reference range at 1 time point. At all other times, cTnI was <0.05 ng/mL. All control ponies had normal cTnI. There were no significant associations between cTnI and either clinical signs or experimental groups. When separated into abnormal versus normal cTnI, there were no significant differences among groups. Conclusions and Clinical Importance: This study demonstrated no evidence of severe myocardial necrosis secondary to EIV challenge with 108 EID50 EIV A/eq/Kentucky/91 in these sedentary ponies, but transient increases in cTnI suggest that mild myocardial damage may occur.

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Myocardial injury occurs earlier than myocardial inflammation in acute experimental viral myocarditis

Cited by 17 publications

References 20 publications

Myocardial Mononuclear Cell Infiltrates Are Not Associated with Increased Serum Cardiac Troponin I in Cynomolgus Monkeys

Myocardial Mononuclear Cell Infiltrates Are Not Associated with Increased Serum Cardiac Troponin I in Cynomolgus Monkeys

Determination of Cardiac Troponin I in the Blood and Heart of Calves with Foot-and-Mouth Disease

Cardiac Troponin I Concentrations in Ponies Challenged with Equine Influenza Virus

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