Postmortem Specificity of Troponin for Acute Miocard Infarction Diagnosis throug Qualitative Dosing from Pericardial Fluid

2018 ◽  
Vol 69 (9) ◽  
pp. 2482-2486
Author(s):  
Iuliana Hunea ◽  
Simona Irina Damian ◽  
Carmen Corina Radu ◽  
Sorin Moldoveanu ◽  
Tatiana Iov
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Disease ◽  
Cardiac Death ◽  
Troponin I ◽  
Troponin T ◽  
Morphological Changes ◽  
Pericardial Fluid ◽  
Histological Changes ◽  
Lethal Arrhythmia ◽  
Myocardial Lesions

Cardiac disease is the leading cause of death, and sudden cardiac death occupies the first place in sudden deaths of natural causes. Sudden cardiac death due to lethal arrhythmia may be the first manifestation of a cardiac disease, such cases becoming suspect dead, thus forensic cases. The autopsy performed in such cases may reveal important cardiovascular disease but not obvious macroscopic or histological changes of acute myocardial infarction (IMA), except for cases of survival for several hours after the onset of the symptomatology. Biochemical markers were used to test for myocardial lesions in the absence of morphological changes. Methods for determining myoglobin, CK-MB, troponin T (cTn T), troponin I (cTn I) were introduced to the clinic to diagnose the condition of patients with chest pain as early as the 1990s. The lack of pathognomonic elements in corps investigations, where part of the analysis cannot be carried out, requires verification of the value of the investigations that can be carried out, with reference to the biochemical in the present case, in establishing the diagnosis with certainty.

scholarly journals Diagnostic Application of Postmortem Cardiac Troponin I Pericardial Fluid/Serum Ratio in Sudden Cardiac Death

Diagnostics ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 614
Author(s):  
Diana Hernández-Romero ◽  
María del Rocío Valverde-Vázquez ◽  
Juan Pedro Hernández del Rincón ◽  
José A. Noguera-Velasco ◽  
María D. Pérez-Cárceles ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sudden Cardiac Death ◽  
Cardiac Troponin ◽  
Cardiac Death ◽  
Troponin I ◽  
Sampling Site ◽  
Pericardial Fluid ◽  
Cardiac Troponin I ◽  
Control Group ◽  
Complementary Method

In approximately 5% of unexpected deaths, establishing a conclusive diagnosis exclusively on the basis of anatomo-pathological findings in a classic autopsy is difficult. Postmortem biomarkers have been actively investigated as complementary indicators to help to reach valid conclusions about the circumstances of death. Several studies propose either the pericardial fluid or peripheral veins as a location for troponin determination, but the optimum sampling site is still a matter of debate. Our objective was to evaluate the association between the ratio of troponin values in the pericardial fluid and serum (determined postmortem) and the diagnosis of acute myocardial infarction (AMI) in the context of sudden cardiac death. We included 175 forensic cases. Two groups were established: AMI deaths (48; 27.4%) and the control group (127; 72.6%). The cardiac Troponin I (cTnI) values in the pericardial fluid and the troponin ratio were found to be associated with the cause of death. Univariate regression analyses showed that both age and the cTnI ratio were significantly associated with the diagnosis of AMI death. In a multivariate analysis, adjusting for confounding factors, the age and cTnI ratio were independent predictors of death from myocardial infarction. We performed a receiver operating characteristic (ROC) curve for the cTnI ratio for AMI death and selected a cut-off point. Our biomarker was found to be a valuable and highly effective tool for use in the forensic field as a complementary method to facilitate diagnosis in nonconclusive autopsies.

A Study of Various Morphologic Variables and Troponin I in Pericardial Fluid as Possible Discriminators of Sudden Cardiac Death

1999 ◽  
Vol 20 (4) ◽  
pp. 333-337 ◽  
Author(s):  
Stephen J. Cina ◽  
William C. Thompson ◽  
Joseph R. Fischer ◽  
Daniel K. Brown ◽  
Jack M. Titus ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Troponin I ◽  
Pericardial Fluid

scholarly journals Diagnostic Roles of Postmortem cTn I and cTn T in Cardiac Death with Special Regard to Myocardial Infarction: A Systematic Literature Review and Meta-Analysis

2019 ◽  
Vol 20 (13) ◽  
pp. 3351 ◽  
Author(s):  
Zhipeng Cao ◽  
Mengyang Zhao ◽  
Chengyang Xu ◽  
Tianyi Zhang ◽  
Yuqing Jia ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Forensic Medicine ◽  
Cardiac Troponin ◽  
Cardiac Death ◽  
Troponin I ◽  
Troponin T ◽  
Heart Diseases ◽  
Meta Analysis ◽  
Pericardial Fluid ◽  
Diagnostic Biomarkers

Background: Cardiac troponin I (cTn I) and cardiac troponin T (cTn T) are currently widely used as diagnostic biomarkers for myocardial injury caused by ischemic heart diseases in clinical and forensic medicine. However, no previous meta-analysis has summarized the diagnostic roles of postmortem cTn I and cTn T. The aim of the present study was to meta-analyze the diagnostic roles of postmortem cTn I and cTn T for cardiac death in forensic medicine, present a systematic review of the previous literature, and determine the postmortem cut-off values of cTn I and cTn T. Methods: We searched multiple databases for the related literature, performed a meta-analysis to investigate the diagnostic roles of postmortem cardiac troponins, and analyzed the receiver operating characteristic (ROC) curve to determine their postmortem cut-off values. Results and Conclusions: The present meta-analysis demonstrated that postmortem cTn I and cTn T levels were increased in pericardial fluid and serum in cardiac death, especially in patients with acute myocardial infarction (AMI). We determined the postmortem cut-off value of cTn I in the pericardial fluid at 86.2 ng/mL, cTn I in serum at 9.5 ng/mL, and cTn T in serum at 8.025 ng/mL.

scholarly journals Prognostic implications of troponin T variations in inherited cardiomyopathies using systems biology

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Rameen Shakur ◽  
Juan Pablo Ochoa ◽  
Alan J. Robinson ◽  
Abhishek Niroula ◽  
Aneesh Chandran ◽  
...  
Keyword(s):  
Heart Failure ◽  
Systems Biology ◽  
Sudden Cardiac Death ◽  
Risk Stratification ◽  
Clinical Data ◽  
Cardiac Death ◽  
Troponin T ◽  
Management Options ◽  
Familial Cardiomyopathy ◽  
The Impact

AbstractThe cardiac troponin T variations have often been used as an example of the application of clinical genotyping for prognostication and risk stratification measures for the management of patients with a family history of sudden cardiac death or familial cardiomyopathy. Given the disparity in patient outcomes and therapy options, we investigated the impact of variations on the intermolecular interactions across the thin filament complex as an example of an unbiased systems biology method to better define clinical prognosis to aid future management options. We present a novel unbiased dynamic model to define and analyse the functional, structural and physico-chemical consequences of genetic variations among the troponins. This was subsequently integrated with clinical data from accessible global multi-centre systematic reviews of familial cardiomyopathy cases from 106 articles of the literature: 136 disease-causing variations pertaining to 981 global clinical cases. Troponin T variations showed distinct pathogenic hotspots for dilated and hypertrophic cardiomyopathies; considering the causes of cardiovascular death separately, there was a worse survival in terms of sudden cardiac death for patients with a variation at regions 90–129 and 130–179 when compared to amino acids 1–89 and 200–288. Our data support variations among 90–130 as being a hotspot for sudden cardiac death and the region 131–179 for heart failure death/transplantation outcomes wherein the most common phenotype was dilated cardiomyopathy. Survival analysis into regions of high risk (regions 90–129 and 130–180) and low risk (regions 1–89 and 200–288) was significant for sudden cardiac death (p = 0.011) and for heart failure death/transplant (p = 0.028). Our integrative genomic, structural, model from genotype to clinical data integration has implications for enhancing clinical genomics methodologies to improve risk stratification.

scholarly journals Hypertrophy, Fibrosis, and Sudden Cardiac Death in Response to Pathological Stimuli in Mice With Mutations in Cardiac Troponin T

Circulation ◽  
2004 ◽  
Vol 110 (15) ◽  
pp. 2102-2109 ◽  
Author(s):  
Alexander H. Maass ◽  
Kaori Ikeda ◽  
Silke Oberdorf-Maass ◽  
Sebastian K.G. Maier ◽  
Leslie A. Leinwand
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Troponin ◽  
Cardiac Death ◽  
Troponin T ◽  
Cardiac Troponin T

scholarly journals Cardiac Troponins are Among Targets of Doxorubicin-Induced Cardiotoxicity in hiPCS-CMs

2019 ◽  
Vol 20 (11) ◽  
pp. 2638 ◽  
Author(s):  
Michaela Adamcova ◽  
Veronika Skarkova ◽  
Jitka Seifertova ◽  
Emil Rudolf
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Early Recognition ◽  
Morphological Changes ◽  
Cancer Therapeutics ◽  
Diagnostic Strategies ◽  
Human Cardiomyocytes ◽  
Induced Pluripotent ◽  
Cardiac Troponins

Modern diagnostic strategies for early recognition of cancer therapeutics-related cardiac dysfunction involve cardiac troponins measurement. Still, the role of other markers of cardiotoxicity is still unclear. The present study was designed to investigate dynamics of response of human cardiomyocytes derived from induced pluripotent stem cells (hiPCS-CMs) to doxorubicin with the special emphasis on their morphological changes in relation to expression and organization of troponins. The hiPCS-CMs were treated with doxorubicin concentrations (1 and 0.3 µM) for 48 h and followed for next up to 6 days. Exposure of hiPCS-CMs to 1 µM doxorubicininduced suppression of both cardiac troponin T (cTnT) and cardiac troponin I (cTnI) gene expression. Conversely, lower 0.3 µM doxorubicin concentration produced no significant changes in the expression of aforementioned genes. However, the intracellular topography, arrangement, and abundance of cardiac troponin proteins markedly changed after both doxorubicin concentrations. In particular, at 48 h of treatment, both cTnT and cTnI bundles started to reorganize, with some of them forming compacted shapes extending outwards and protruding outside the cells. At later intervals (72 h and onwards), the whole troponin network collapsed and became highly disorganized following, to some degree, overall changes in the cellular shape. Moreover, membrane permeability of cardiomyocytes was increased, and intracellular mitochondrial network rearranged and hypofunctional. Together, our results demonstrate complex effects of clinically relevant doxorubicin concentrations on hiPCS-CM cells including changes in cTnT and cTnI, but also in other cellular compartments contributing to the overall cytotoxicity of this class of cytostatics.

Morphological characteristic and assessment of changesin the main structural components of the histohematological barrier of the thyroid tissue in cases of the sudden cardiac death from alcoholic cardiomyopathy

2017 ◽  
Vol 8 (5) ◽  
pp. 30-34
Author(s):  
Olga V. Sokolova ◽  
Orazmurad D. Yagmurov ◽  
Ruslan A. Nasyrov
Keyword(s):  
Sudden Cardiac Death ◽  
Thyroid Gland ◽  
Cardiac Death ◽  
Morphological Changes ◽  
Cytotoxic Action ◽  
Structural Components ◽  
Alcoholic Cardiomyopathy ◽  
Endothelial Lining ◽  
Gland Tissue ◽  
Thyroid Gland Tissue

A retrospective analysis of acts of forensic medical autopsies from the archive of St. Petersburg GBUS BSME and a histological study of thyroid gland tissue in 188 cases (95 women and 93 men) were carried out with statistical processing of the obtained results for the purpose of studying and assessing the morphological changes in the main components of the histohematological barrier of thyroid gland tissue in cases of the sudden cardiac death from alcoholic cardiomyopathy. The decrease in the weight of the thyroid gland in the investigated cases and the revealed morphological signs, indicative of a decrease in the memory function of the thyroid gland were found and can be caused by the prolonged toxic effect of ethanol and its metabolites. Morphological changes in the endothelial lining of the vessels of the microcirculatory bed are caused both by the direct cytotoxic action of ethanol and its metabolites and by the action of mediators, the release of which occurs as a result of stimulation of the reactive cells, which leads to swelling, deformation and increased activity of endothelial cell membranes with the expansion of intercellular spaces and the development of increased permeability of the endothelial lining, which, in its turn, contributes to disruption of electrolyte transport and nutrients transport with changes trophism thyroid gland tissue, which is a substrate for the appearance of dystrophic and necrobiotic processes in main structural components of the histogematogenous barrier of the thyroid gland. The revealed morphological changes in thyroid gland tissue in cases of death from alcoholic cardiomyopathy have a non-specific nature and should be considered in conjunction with other visceral manifestations that are a reflection of alcohol intoxication during the chronic alcoholism.

scholarly journals Features of morphological changes of the liver’s tissue in cases of sudden cardiac death because of alcoholic cardiomyopathy

2017 ◽  
Vol 8 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Olga V Sokolova ◽  
Ruslan A Nasyrov
Keyword(s):  
Sudden Cardiac Death ◽  
Liver Tissue ◽  
Cardiac Death ◽  
Morphological Changes ◽  
Alcohol Intoxication ◽  
The Body ◽  
Alcoholic Cardiomyopathy ◽  
Endothelial Lining ◽  
Inflammatory Reactions ◽  
Morphological Criteria

A retrospective analysis of acts of forensic autopsies from the archives of St Petersburg GBOOSE BSME and histological examination of liver tissue in an amount of 152 cases (78 women and 74 men) with a statistical processing of the results for studying and evaluating the morphological changes of liver’s tissue in cases of sudden cardiac death from alcohol cardiomyopathy. Identified in the course of the study morphological changes in the endothelial lining of the microvasculature showed that in addition to direct cytotoxic effects of ethanol and its metabolites in the basis of damage to the endothelial lining of the microvasculature are the cellular responses associated with exposure to mediators, the release of which is due to irritation of reactive cells, which entails a swelling deformation and increased activity endothelial cell membranes with the expansion of intercellular spaces. The development of increased permeability of the endothelial lining of transport contributes to a violation of electrolytes and nutrients to the changes of the liver’s tissue trophism, which is a substrate for the occurrence of degenerative processes and necrobiotic major structural components of the body. In turn, a direct toxic effect of ethanol and its metabolites on the wall microvascular contributes to ischemia and necrosis of the hepatocytes with the development of severe inflammatory reactions in the surrounding liver tissue, which in turn is the direct cause of the disturbances regeneration nature and excessive proliferation connective tissue with the subsequent restructuring of the vascular bed. Identified and described the morphological criteria of changes in liver’s tissue in cases of death from alcoholic cardiomyopathy should be considered in conjunction with other visceral manifestations, being a reflection of the alcohol intoxication in chronic alcoholism.

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