**6. Correlation between postmortem cardiac troponin and histological evidence of cardiomyocyte necrosis**

At postmortem, the diagnosis of myocardial infarction is typically assessed by gross macroscopic anatomy further confirmed by microscopic histology and immunohistochemical analysis. Defining AMI in a medico-legal autopsy is a clinical challenge for the forensic pathologist as detection can only be made 4–6 hours after the onset of cardiac ischemia. Histological changes indicative of AMI include oedema, congestion, haemorrhage, inflammation cytoplasmic vacuoles, contraction band alterations, fibrosis and necrosis. Immunohistochemical analysis at postmortem has focused on a number of markers of cellular damage, including C5b-9, myoglobin, CK-MB, fibronectin myosin heart-type fatty acid binding protein and desmin [30].

*Use of Cardiac Troponin for the Diagnosis of Cardiac Pathology in Postmortem Samples Taken… DOI: http://dx.doi.org/10.5772/intechopen.111799*

**Figure 4.**

*Cardiac troponin T (cTnT) degradation patterns (Western blotting) in (a) fatal burn; (b) myocardial infarction; (c) electrocution; (d) asphyxiation (source: Adapted from (a) [25]; b–d [26]).*

A number of studies have evaluated postmortem cTn concentrations in relation to evidence of cardiomyocyte necrosis (**Figure 6**). Ortmann and colleagues identified antigen depletion in the detection of early ischemic cardiac lesions in 8 cases of AMI, 8 cases of sudden cardiac death and 12 cases of acute exogenic hypoxia due to hanging or carbon monoxide poisoning. Strong evidence of immunohistochemical depletion

#### **Figure 5.**

*Meta-analysis of pericardial fluid and serum cardiac troponin I, cTnI; or cardiac troponin T, cTnT; in the investigation of cardiac death and acute myocardial infarction, AMI (source: data extracted from [28]).*

of cTnT was evident in all eight cases of AMI, in 50% of sudden cardiac death and in 1 (8%) of acute exogenic hypoxia, with 42% demonstrating weak loss and 50% demonstrating negative results (no loss of cTnT staining) [30].

Martinez Diaz and colleagues have demonstrated immunohistological changes in cTn in AMI or multiple trauma compared to other causes of death. PCF cTnI, myoglobin and CKMB were all significantly higher in AMI or multiple trauma cases compared to other causes of death. Serum concentrations of cTnI myoglobin and CKMB were not significantly different between the two groups [31]. Immunohistological analysis was performed by the authors with the analysis of troponin C and cTnT staining. 86% of cases demonstrated strong positive TnC with expression differing in isolated cells demonstrating contraction band necrosis but with significantly less intensity in the area of the infarction. cTnT staining was less evident in only 46% of cases in focal areas of the tissue.

Campobasso et al. [34] compared 4 immunohistochemical markers as early indicators of myocardial ischemia in 18 sudden cardiac deaths (4 AMI,4 coronary deaths, 8 acute cardiac deaths compared to 6 cases of acute traumatic death gunshot wounds with immediate lethal head injury). The authors stained paraffin-embedded myocardial tissue and immunohistochemically stained the tissue for C5b-9, fibronectin, myoglobin and cTnI. Diffuse depletion of cTnI was evident in all AMI deaths, in 75% of acute cardiac deaths, with 50% of coronary deaths demonstrating limited cellular foci depletion and normal distribution in all six cases of acute traumatic death. Whilst the staining patterns were significantly different between the cardiac and non-cardiac deaths, the authors concluded that no single marker was able to detect early myocardial ischemia and the combination of all four markers was useful in demonstrating evidence of myocardial ischemia and/or necrosis [34].

More recently, Amin and co-workers stained histological sections from ischemic and non-ischemic cardiac tissue for cTnT, myoglobin and caspase-3, demonstrating cTnT detection in normal myocardium and loss in necrotic tissue. The loss of cTnT was non-uniform with greater loss at the periphery compared to the central regions of infarcted tissue [35].

*Use of Cardiac Troponin for the Diagnosis of Cardiac Pathology in Postmortem Samples Taken… DOI: http://dx.doi.org/10.5772/intechopen.111799*

#### **Figure 6**

*Immunohistochemical staining of cardiac troponin: (A) TnC in isolated cells with evidence of necrosis ×325; (B) TnC in contraction band necrosis ×300; (C) TnC in infarction zone ×200; (D–F) TnC in myocardium from sudden cardiac death due to coronary atherosclerosis. Brown expression (arrow) increases with PMI where (D) 1st PMI, (E) 2nd PMI, (F) 3rd PMI; (G–I) TnC in myocardium from sudden cardiac death due to myocardial infarction. Brown expression (arrow) increases with PMI where (G) 1st PMI, (H) 2nd PMI, (I) 3rd PMI; (J–L) cTnI immunohistochemical staining of the anteriolateral right ventricle in (J) non-ischemic cardiac tissue demonstrating no depletion in cTnI ×10; (K) 1 hour of LAD ligation demonstrating cTnI depletion in the subendocardial region [square box] ×10; (L) magnified box area from section K ×40. (M–O) cTnT immunohistochemical staining of the anteriolateral right ventricle in (M) non-ischemic cardiac tissue demonstrating no depletion in cTnT ×10; (N) 1 hour of LAD ligation demonstrating cTnT depletion in the subendocardial region [square box] ×10; (O) magnified box area from section N ×40 (sources: adapted from (A–C) [31]; (D–I) [32]; (J–O) [33]).*
