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Year : 2020  |  Volume : 6  |  Issue : 3  |  Page : 98-101

Troponin and its applications in forensic science

Department of Forensic Sciences, College of Criminal Justice, Naïf Arab University for Security Sciences, Riyadh, Kingdom of Saudi Arabia

Date of Submission16-Jan-2020
Date of Decision20-Feb-2020
Date of Acceptance09-Apr-2020
Date of Web Publication29-Sep-2020

Correspondence Address:
Sachil Kumar
Department of Forensic Sciences, College of Criminal Justice, Naïf Arab University for Security Sciences, Riyadh
Kingdom of Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jfsm.jfsm_3_20

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Troponin is used as the part of today's therapeutic sciences, but is also used in forensics. Studies on troponin and its use in forensic medicine have been retrieved from systematic internet search of databases “PubMed”, “Google Scholar,” “Medline,” and “Science Direct” with the last search performed in December 2019. A total of 38 publications have been reviewed that met the study criteria and have been cited in this article. Discussions on troponin often relate to its valuable attributes and particularly to its handiness as a diagnostic marker for different coronary heart disease. More specifically, it is a sensitive and specific indicators of damage to the heart muscle (myocardium).” Troponin was established in toxicological examinations as a biomarker of cardiovascular injury induced by drugs. Troponin degrades in a regular and predictable fashion and could be a reliable marker for determining the time and cause of death. In this review, the author outlines the potential application of troponin in forensic science.

Keywords: Cause of death, forensic medicine, postmortem interval, time since death, troponin

How to cite this article:
Kumar S. Troponin and its applications in forensic science. J Forensic Sci Med 2020;6:98-101

How to cite this URL:
Kumar S. Troponin and its applications in forensic science. J Forensic Sci Med [serial online] 2020 [cited 2022 Jul 4];6:98-101. Available from: https://www.jfsmonline.com/text.asp?2020/6/3/98/296569

  Introduction Top

The success of forensic investigations depends on establishing the correct timeline of events. Different methodologies use various chemical, biological, and physical indicators to estimate the time elapsed since death.[1] The common methods used in forensic medicine to determine postmortem interval (PMI) are based on the physical detection parameters.[2],[3] However, these methods do not give an exact PMI. Consequently, interest has now been focused on forensic pathology to estimate the PMI more accurately. This is largely based on biomedical research measuring changes in the chemical concentration of body fluids such as blood, spinal fluid, vitreous humor in the eye, and aqueous humor. These chemical changes are proportionate to the time between death and the disintegration of the body. However, these parameters can also be influenced by the factors such as preexisting disease, death cause, sample availability and pureness, survival period, and environmental factors.[4],[5] The parameters used to determine PMI typically include chloride concentration, potassium, aspartic amino transferase, nonprotein percentage and leukocyte cell changes, protein degradation during decomposition, and cardiac troponin (cTn) concentration. In addition to these studies, some work has also been done to investigate the pattern of degradation of DNA over time to figure out PMI.[6] Many methods to interpret PMI accurately have been studied and suggested, but only a few are included in the routine work.

At present, the term troponin is well known beyond the realm of clinical sciences. Discussions about troponin often relate to its functional characteristics and/or usefulness as a diagnostic marker or therapeutic target for various heart disorders, especially as a specific marker for myocardial infarction or the death of heart muscle cells.[7] They are very sensitive markers for detecting all types of myocardial injury and can distinguish myocardial and skeletal injuries. Moreover, they are an independent predictor of future cardiac events. Such markers are now commonly used in the clinical practice. The adverse prognostic risk associated with increased cTn was substantiated by multiple randomized studies and several meta analyses.[8]

cTns are biomarkers for human ischemic heart disease. Despite that, their value as biomarkers of cardiac injury due to causes other than ischemic heart disease, especially in drug development, is now being investigated. cTns have been established as a biomarker of choice for monitoring potential drug-induced myocardial injury in both clinical and preclinical studies. High levels of postmortem blood and pericardial cTnT may depend on the severity of myocardial damage caused by various causes of death.[9]

In this review, the author summarizes the possible applications of troponin in forensic science.

  Related Studies Identification Top

A systematic internet search of the databases “PubMed,” “Google Scholar,” “MEDLINE,” and “Science Direct” using the keywords of troponin, forensic pathology, forensic medicine, PMI, PMI, cause of death, and forensic science was performed for all related publications. During the last search in December 2019, broad search terms were used to help identify all relevant articles. A total of 38 articles that met our search criteria were included in this article. The following section describes all relevant studies.

  Troponin and Cause of Death Top

Establishing the conditions contributing to death are the significant task a pathologist performed in an autopsy. It is very important that law enforcement can prove without any doubt that the deceased has died from unnatural causes. The cause of death often seems to be quite obvious, particularly in mechanical injury. The cause of death is what has an effect; a combination of circumstances must precede and always lead to an effect.[10]

Sudden cardiac death (SCD) because of an intense myocardial localized necrosis includes a significant proportion of autopsy cases. In the America, the yearly rate of SCD in individuals aged 35–74 years is 191/100,000 in men and 57/100,000 in women; half of all SCDs happen in individuals with known or suspected coronary artery disease (CAD).[11] In the North-East of Italy, the general pervasiveness of SCD is 0.8/100,000 persons-year in the youthful, construct just upon after death audits.[12] Among young athletes, the occurrence of SCD turned out to be twice that in youthful nonathletes. The presence of heart diseases that cause a risk of SCD during vigorous exertion clarifies these figures.[13] Postmortem biochemical analysis of several biomarkers or indicators, for example, cTns, creatine kinase MB, and N-terminal proBNP play an important role in the postmortem diagnosis of cardiac death and may provide an auxiliary diagnosis basis for SCD.[14],[15]

In clinical practice, acute myocardial infarction (AMI) is diagnosed with the help of an electrocardiogram and specific serum biochemical markers utilized in the diagnosis of myocardial damage.[16],[17],[18] cTnT and cTnI specifically have been broadly contemplated, and proof of sensitivity and specificity in distinguishing AMI is entrenched.[18],[19],[20],[21]

Han et al. assessed the sensitivity and specificity of cTnT in the recognition of AMI at postmortem and found that while cTn is a sensitive marker, it is not particular as an analytic apparatus in the diagnosis of AMI at postmortem examination.[22] Gampon et al. utilized a commercial cTnT rapid assay for the diagnosis of delayed death from AMI in cases of SCD. They noted that femoral blood, in any case, produced less false positives and more accurate diagnoses. The assay turned out to be useful in criminological practice; however, more femoral blood tests ought to be examined.[23] Martínez Díaz et al. proposed that the immunohistochemical determination of cTnC and cTnT levels in myocardial tissue might be utilized as an index of myocardium damage.[24] Troponin has been set up as a biomarker for toxin-induced cardiac injury in toxicological investigations.

Remmer et al. noticed the findings of postmortem serum and pericardial fluid cTnT in different causes of death with reference to PMI and CAD. The outcomes proposed that cTnT levels may moreover help to distinguish cardiovascular death from poisoning and nonthoracic injury, notwithstanding recognizing cardiovascular and other diseases as a cause of death from suffocating and hypothermia.[25] González-Herrera et al. examined cTnT levels and their steadiness after death at different PMIs, assessing the practicality of the cTnT assay in the postmortem diagnosis of the cause of death. They assumed that determining cTnT by a highly sensitive pericardial fluid assay could provide legal pathologists with a correlative test when the cause of death is diagnosed.[26] Zhu et al. recommended that postmortem serum and pericardial cTnT levels should be increased depending on the severity of myocardial damage at death and related to pathological findings, although postmortem interference should be considered.[27] Ellingsen et al. completed an investigation on SCD and found that high postmortem serum concentration of cTnT reflects ongoing myocardial damage and may support the diagnosis of cardiac death in cases involving inadequate or uncertain postmortem morphological findings.[28] Hickson et al. concluded that cTnT makes an independent contribution beyond traditional risk markers to the prediction of end-stage renal disease (ESRD) and all-cause death in community-dwelling individuals.[29]

Davies et al. compared antemortem and after death cTn levels. The antemortem samples were obtained from the biochemistry laboratory of the medical institution after the death of each individual. The postmortem samples had been taken from different locations and under different circumstances in the early postmortem period. Different outcomes bearing little or no relation to the antemortem cTn level were obtained for all subjects. Four of the five subjects had raised antemortem troponin levels, albeit just a single subject had a cardiovascular related cause of death. From this, he inferred that postmortem blood is not a reasonable substrate for standard biochemical assays of cTns, which are intended for use on serum taken from living patients. Moreover, the outcomes also support the view that elevated cTns are a marker of serious morbidity and are not particular to cardiac damage as the major cause of morbidity or mortality.[30]

Khalifa et al. assessed the adequacy of the increase of postmortem cTnT in acute disease-related deaths using the immunoassay analyzer.[31] All cases of visual myocardial infarction had the increased levels of cTnT. The difference of the postmortem cTnT concentrations between resuscitated and nonresuscitated is not found significant. In noncardiac deaths, high cTnT concentrations were observed only in electrocution cases. The results of these tests could be used to facilitate the selection of cases that could be released after histological testing.

Kumar et al. assessed the effect of elapsed time on cTnT degradation and found that in case of death due to MI, the intact cTnT fragmented at a much faster rate than in burn, electrocution, control, poisoning, and asphyxia group. The postmortem troponin-T fragmentation reported in various causes of death reveals a sequential, time-dependent process with the potential to be used as and could be applied in future as a better method of evaluating cause of death.[32]

Apple et al. examined the prognostic value for all-cause cTnT and cTnI death using the European Society of Cardiology/Acute Coronary Syndrome and recommended troponin cutoff concentrations in the large cohort of patients with ESRD up to 3 years. They concluded that increases in cTnT and cTnI in patients with ESRD show a 2- to 5-fold increase in mortality, with an increased number of patients with cTnT.[33]

  Troponin and Postmortem Interval Top

The importance of determining the PMI is a supreme goal for medicolegal examination. Current innovations are dependent on posttemperature techniques like those shown in the 1800s. Biochemical markers for the PMI were investigated. Temperature remains a fundamental PMI marker after a number of tests and restrictions. In view of the subsequent degradation of a cTn, the approach described here is constructive.

After death, intracellular enzymes cause proteins to degrade into smaller fragments as time goes by. If this fragmentation is measurable and quantifiable, it can be a reliable PMI indicator. cTn has a distinctive temporal degradation profile after death, which is critical to its use in forensic medicine as a PMI marker. Several later reports focused on postmortem changes in cTn's as markers to build up the PMI.

Mathur et al. carried out an invivo study on rat myocardium samples to study cTnI's time degradation pattern using Western blotting and gold nanoparticles. cTn degrades to lower-molecular weight fragments over time and these changes were monitored using the UV Visible Spectrophotometer Gold nanoparticle conjugate based test. The method could detect time-dependent changes up to 96 h after death in cTnI and can be used to give a more accurate estimate of PMI.[34]

Sabucedo et al. examined the potential use of cTnI tissue as a PMI calculator by using a bovine model. The analysis included the extraction of protein, denaturation electrophoresis (SDS-PAGE) separation, and Western blot visualization using monoclonal antibodies specific to cTnI. The results showed a characteristic banding pattern between human bodies, a pseudo-linear relationship between the degraded cTnI percentage, and the time log since death (r > 0:95), and a qualitative band degradation pattern that makes it possible to estimate the PMI in a simple comparative analysis with a standard human heart of known PMI. The tissue cTnI degradation banding pattern is helpful in determining the early PMI (0–5 days).[35]

Kumar et al. showed a pseudo-linear relationship between the percentage of cTnT degradation and the time log since death (r > 0.95) that to be used to calculate the PMI.[36] In cases of burning and electrocution, Kumar et al. also noted postmortem cTnT fragmentation and uncovered a successive time varying process with the prospects of being used as a time since death calculator.[37]

Following the earlier work on the degradation of skeletal muscles in the porcine model, Pittner et al. estimated PMI by analyzing human postmortem skeletal muscle samples from 40 forensic cases. Western blot analysis was employed to examine the degradation behavior of cTn T, desmin, and tropomyosin. Study showed a characteristic protein degradation processes clearly associated with the temperature and PMI.[38]

  Conclusion Top

Troponins are delicate and specific cardiovascular markers with possibilities in forensic science and might be utilized to calculate PMIs, and moreover, to find out the manner and cause of death.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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