Hongmei Dong

Background: The classic symptoms of coronary atherosclerotic disease (CAD), such as chest pain, are easily recognized in clinical practice. However, atypical manifestations like convulsive syncope can lead to misdiagnosis or delayed diagnosis, resulting in a poor prognosis. Case Presentation: We report an unusual case of a 36-year-old male who experienced recurrent convulsive episodes over 2 days. Initially, on the first day, the patient was diagnosed with epilepsy in the outpatient department, although the electroencephalogram revealed no abnormalities. He was admitted the following day after experiencing a recurrence of the same symptoms. Further investigation revealed severe hyperthyroidism and an electrocardiogram showing a short PR interval and T-wave inversions. The patient ultimately succumbed to sudden cardiac arrest after the final convulsive episode, with ventricular tachycardia documented on electrocardiogram monitoring. Post-mortem examination confirmed severe CAD, left ventricular hypertrophy, and thyroid hyperplasia. Conclusion: The most likely explanation for the patient’s clinical presentation is a fatal arrhythmia arising from the synergistic effects of severe CAD, left ventricular hypertrophy, and hyperthyroidism, ultimately leading to cardiogenic syncope and sudden cardiac death. This case highlights that arrhythmias secondary to CAD can mimic epilepsy-like seizures and, therefore, need to be carefully distinguished from epilepsy.

Carcass decomposition is a natural process that is characterized by a series of chemical transformations. During postmortem degradation, macromolecules are broken down into smaller molecules. Because proteins constitute a large proportion of the dry cell mass, protein degradation is the dominant postmortem decomposition process. Currently, the characteristics of protein degradation postmortem are largely unknown. Metabolomics enables the quantitative analysis of all metabolites within organisms or cells and has been used to investigate metabolite changes during physiological and pathological processes. Recently, forensic researchers have also applied metabolomics to postmortem challenges. In this study, we used targeted metabolomics with gas chromatography–mass spectrometry (GC–MS) to quantitatively analyze amino acid changes in rat myocardial tissue and assess protein degradation with the postmortem interval (PMI). First, the GC–MS method was validated and yielded satisfactory results. Quantitative analysis revealed good correlations between the concentrations of 14 amino acids (alanine, glycine, valine, leucine, isoleucine, proline, methionine, phenylalanine, tryptophan, glutamine, tyrosine, glutamic acid, histidine, and arginine) and early PMI. Among the 14 amino acids, the concentrations of nearly all neutral nonpolar amino acids consistently increased during the 0–6 days postmortem, while that of glutamic acid increased up to 10 days postmortem. Higher ambient temperatures increased the rate of protein degradation. A total of 9 amino acids (alanine, glycine, valine, leucine, isoleucine, phenylalanine, tryptophan, tyrosine, and glutamic acid) that exhibit regular increases at different temperatures during specific PMI show potential as biomarkers for PMI estimation.

Cardiac rupture in blunt cardiac injuries, though uncommon, can be fatal. A particularly rare occurrence is blunt cardiac rupture of the left ventricle without external chest injury. Herein, we report a case of cardiac rupture without external chest injuries in a 21-year-old man who died after a physical altercation. The cause of death was attributed to cardiac rupture caused by blunt force. We analysed the differential diagnoses of cardiac rupture with intact pericardium, including cardiac diseases, blunt chest injury, cardiopulmonary resuscitation, and Takotsubo cardiomyopathy. Additionally, we discussed the relevant factors for cardiac rupture in this case, including sudden enormous force, cardiac cycle, chest wall compliance, and alcohol consumption. Furthermore, we highlighted that no explicable cause other than cardiac rupture accounted for the death.

Recently, the incidence and mortality of heat stroke (HS) have risen catastrophically. However, postmortem diagnosis of HS is challenging owing to the lack of characteristic morphological markers. Liver damage can often serve as a direct cause of death in HS. Therefore, this study aimed to identify protein biomarkers in the liver and to evaluate their utility as diagnostic biomarkers for HS. The morphological and biochemical tests of HS rats models revealed hydropic degeneration, hepatocyte necrosis, and impaired liver function. 283 differentially expressed proteins between the HS and control groups were screened by proteomic analysis. Subsequently, HSPA4, GGCX, and CYP2B6 were selected as candidate biomarkers based on Proteomic results, Western blotting and immunohistochemistry results in HS rats. These three candidate biomarkers were further validated as diagnostic protein biomarkers for HS death based on the immunohistochemistry results of 29 human cases. Finally, receiver operating characteristic analysis indicated that the combination of HSPA4, GGCX and CYP2B6 provided optimal diagnostic efficacy for HS, with an area under the curve of over 0.999. In conclusion, we propose that the integrating morphological findings, liver function analysis, and protein biomarkers (HSPA4, GGCX, and CYP2B6) in liver could be used for HS diagnosis in forensic practices.

Nitrous oxide (N₂O) abuse is becoming increasingly popular worldwide. Moreover, the use of N₂O combined with other substances, such as alcohol, is also common. Accidental deaths associated with N₂O abuse are rare in forensic practice, with most fatal cases involving continuous inhalation equipment or exposure in a confined space. In contrast, the inhalation of N₂O using balloons is traditionally regarded as a relatively safe method. In this report, we present an unusual fatal case of a 16-year-old girl who died after drinking alcohol and inhaling N₂O from balloons. The decedent was found in a prone position with the nose and mouth compressed against the bed. Cyanosis of nails, pulmonary and cerebral edema, and the positive expression of HIF-1α in lung, myocardium and brain, were indicative of asphyxiation. Toxicological analysis revealed a peripheral blood ethanol concentration of 140 mg/dL and cardiac blood N₂O concentration of 74.5 μL/mL. N₂O was also positively detected in the lungs, stomach contents, gastric air, and the brain. In conclusion, we determined that the decedent died from accidental asphyxia related to N₂O inhalation, prone positioning, and alcohol consumption. We also investigated chronic N₂O abuse from a forensic perspective. This report aims to help forensic pathologists manage similar cases. It also reminds N₂O abusers of potential dangers.