Recognition of Early Myocardial Infarction by Immunohistochemical Staining with Cardiac Troponin‐I and Complement C9*

Jasra, Shashi K.; Badian, Cherryl; Macri, Iain; Ra, Paul

doi:10.1111/j.1556-4029.2012.02172.x

Cited by 27 publications

(20 citation statements)

References 20 publications

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“…Thus, cTnI egress got the same degree at the periphery as at the center of the lesions in the last of a very long obstructed time. This phenomenon perhaps resembles the most clinical evidence more likely (Fishbein et al, 2003;Jasra et al, 2012;Jia et al, 2015;Tunca et al, 2008).…”

Section: Discussionsupporting

confidence: 77%

A cardiac troponin I study in a minimally invasive myocardial infarction canine model

Mikrani¹,

Liang²,

Naveed³

et al. 2019

JAB

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Cardiac troponin I (cTnI) is an important biomarker of acute myocardial infarction (MI) in animals and human beings. Nevertheless, no immunohistochemical study has been reported about the pattern of myocardial cTnI egression in a minimally invasive model. The present study intended to establish a minimally invasive model of MI and to evaluate the distribution of cTnI. Twelve Mongrel dogs were divided into 2 groups (n = 6): experimental and sham-operated group. Three incisions were made on the left thoracic wall, left anterior descending (LAD) of coronary artery was identified and titanium nips were clamped by video-assisted thoracoscopy surgery (VATS). Series of electrocardiograms (ECG) and biochemical analyses of blood samples-oxidatively modified proteins (OMP), creatine kinase (CK), and cTnI were performed. Furthermore, Masson's trichrome staining was used to observe the histopathology of cardiac myocytes, while immunohistochemistry was done to observe cTnI egression from myocardium. ECG showed elevated ST-segment, whereas OMP, CK and cTnI level increased remarkably and declined to baseline subsequently in the model group throughout study period. Masson's trichrome staining of model group showed a large amount of collagen deposition in the fibrotic area as compared to control group. In immunohistochemical staining, no loss of cTnI staining was observed in non-necrotic myocardium, meanwhile, a great loss was observed in necrotic myocardium. An exception was the myocardium of cardiac apex, where loss of cTnI was visible even in non-necrotic myocardium. All these results revealed that loss of cTnI occurs not only in the necrotic myocardium but also in so-called non-necrotic myocardium of minimally invasive MI model through VATS.

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Section: Discussionsupporting

confidence: 77%

A cardiac troponin I study in a minimally invasive myocardial infarction canine model

Mikrani¹,

Liang²,

Naveed³

et al. 2019

JAB

View full text Add to dashboard Cite

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“…12 The CCC9 can be detected in the AMI cases where the patient died within 6 hours. 13 The CBN is also a well-established feature of early myocardial ischemia. 12 On the basis of these reports and our studies, we concluded that CBN appeared in the very early phases of ischemia and that CBN would become coagulation necrosis in prolonged ischemia.…”

Section: Discussionmentioning

confidence: 99%

Classification of Contraction Bands Using Immunohistochemistry

Morita

Furukawa²,

Nishi³

2015

American Journal of Forensic Medicine &Amp; Pathology

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Pathological contraction bands (CBs) are a type of necrosis pattern found in the myocardium. The composition of CB is not well studied. This is because CBs have diverse forms and can be observed in various causes of death. In pathology fields, CBs are classified artifactual CB and CB necrosis. We have identified different forms of CB by examining the expression and distribution of complement component C9 (CCC9) and Sirtuin1 by immunohistochemistry in the myocardium of patients who died because of different causes of death. We used cardiac tissues with CB from 30 forensic autopsy cases in our department from the last 2 years. We excluded the cases that had very little CB. We found that our CB classification based on expression levels of both CCC9 and Sirtuin1 correlated well with the agonal situation, including high temperature, myocardial infarction, cardiopulmonary resuscitation, and hypothermia. On the basis of these results, we here advocate a classification scheme based on immunohistochemistry. Furthermore, we found that CB necrosis could be detected using immunostaining with CCC9. Using our classification scheme, it will be possible to more accurately research each type of CB and the causative mechanisms.

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“…CC9 is useful for detecting acute myocardial damage. When abnormalities are not detected in HE staining in acute myocardial infarction within 6 h of onset, positive findings of CC9 are observed (Jasra et al 2012). Furthermore, SIRT1, which modulates cellular adaptation to hypoxia by targeting hypoxia-inducible factor α, is also useful for detecting damaged myocytes.…”

Section: Discussionmentioning

confidence: 99%

Complement C9 expression is associated with damaged myocardial cells in pediatric sudden death cases of fulminant myocarditis

Uno

Hitosugi

Nakamura

et al. 2020

Egypt J Forensic Sci

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Background Because disease progression is so fast in sudden death of acute fulminant myocarditis, damage of myocardial cells is not evident in routine hematoxylin and eosin staining. To understand damage to myocardial cells and the mechanism of sudden death, immunohistochemical staining was performed for two forensic autopsy cases. Case presentation The patients were a healthy 5-year-old girl and 8-year-old boy. They suddenly died within 2 days of appearance of flu-like symptoms. An autopsy showed accumulation of yellowish-clear pericardial fluid containing fibrin deposits, fluid blood in the heart, and congestion of visceral organs. Histologically, minor necrosis or degeneration of myocardial cells with mainly lymphocytic infiltration was observed sometimes in tissue sections. Immunohistochemically, positive complement C9 staining and negative sirtuin 1 staining were found. These findings suggested wide damage of myocardial cells, even in regions with no marked changes in myocardial cells with hematoxylin and eosin staining. These areas corresponded to those with strong accumulation of lymphocytes. Conclusions Immunohistochemistry for complement C9 and sirtuin 1 might become a new tool for evaluating damage of myocardial cells of fulminant acute myocarditis.

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Recognition of Early Myocardial Infarction by Immunohistochemical Staining with Cardiac Troponin‐I and Complement C9*

Cited by 27 publications

References 20 publications

A cardiac troponin I study in a minimally invasive myocardial infarction canine model

A cardiac troponin I study in a minimally invasive myocardial infarction canine model

Classification of Contraction Bands Using Immunohistochemistry

Complement C9 expression is associated with damaged myocardial cells in pediatric sudden death cases of fulminant myocarditis

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