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Immunostaining by complement C9: a tool for early diagnosis of myocardial infarction and application in forensic
M D Piercecchi-Marti1, H Lepidi, G Leonetti
1Service de Médecine Légale, CHU Timone, Marseille, France.
Insights
Diagnosing early myocardial infarction is challenging. Immunohistochemical analysis of complement C9 expression in heart tissue shows high sensitivity and specificity, aiding forensic pathology in identifying infarction within 12 hours post-mortem.
Area of Science:
- Forensic Pathology
- Immunohistochemistry
- Cardiovascular Pathology
Background:
- Early diagnosis of myocardial infarction (MI) presents significant challenges for forensic pathologists, particularly within the initial 12 hours.
- Histological examination may not reveal definitive signs of ischemic damage in cases of sudden cardiac death attributed to MI.
Purpose of the Study:
- To evaluate the utility of complement C9 expression as a biomarker for early myocardial infarction in forensic investigations.
- To determine the sensitivity and specificity of immunohistochemical C9 detection in identifying myocardial damage.
Main Methods:
- An immunohistochemical procedure was employed to assess complement C9 expression in 121 formalin-fixed, paraffin-embedded heart samples.
- Samples were categorized into four groups: confirmed MI with histological damage, MI based on ECG but without clear histological damage, severe coronary disease without clear cause of death, and controls without MI or coronary disease.
- Controlled putrefaction studies were conducted to assess C9 staining specificity in relation to tissue autolysis.
Main Results:
- Complement C9 expression was detected in all 33 cases with confirmed histological ischemic damage.
- Positive C9 staining was observed in 17 out of 20 cases with ECG-diagnosed MI but no clear histological damage.
- Controls and cases with severe coronary disease without MI showed minimal to no C9 deposition, indicating high specificity.
Conclusions:
- Immunohistochemical evaluation of complement C9 expression is a highly sensitive and specific marker for early myocardial infarction.
- This method is valuable in forensic medicine for diagnosing MI, especially when the survival period after myocyte damage exceeds one hour.
Abstract:
Before the first 12 hours, diagnosis of early myocardial infarctions is always difficult for forensic pathologists. We tested complement C9 expression in 121 formalin-fixed and paraffin-embedded heart samples by an immunohistochemical procedure. The heart specimens were separated into four groups: 33 cases in group 1 with typical ischemic damages histologically located, 20 cases in group 2 with death related to myocardial infarction on the basis of ischemic presentation on electrocardiogram but no obvious histological ischemic damage, 35 cases in group 3 with severe coronary disease without cause of death found at the autopsy, and 33 cases in group 4 without sign of myocardial infarction and without coronary disease. In the first group, all 33 heart samples showed a well-defined C9 expression in the necrotic areas. The second group in 17 of 20 cases showed positive areas for C9 expression. In the other three heart specimens, only few stained cells were observed whereas the painful symptoms had begun less than 1 h before death. The third group showed C9 immunopositive areas in six of 35 cases, few stained cells in 8 cases, and no C9 deposition in the 21 other cases. The last group showed no staining area. To avoid nonspecific C9 staining due to tissue autolysis, we studied C9 expression during a controlled putrefactive process in four cases included in group 1; staining was found only in infarcted myocardial areas, and was observed up to ten days. Specificity of C9 expression was evaluated to be 100% [89.4 to 100%] and sensitivity to be 85% [62.11 to 96.79%]. In conclusion, evaluation of immunohistochemical expression of C9 appears to be a highly sensitive and specific marker of early myocardial infarction, useful in forensic medicine if survival is more than 1 h after the beginning of myocyte damage.