Background: Biochemical analyses of N-terminal pro-brain natriuretic peptide (NT-proBNP), cardiac troponin T (cTnT), and creatine kinase MB (CK-MB) have been reported to be valuable for the auxiliary diagnosis of sudden cardiac death (SCD) in previous forensic studies. Aims and Objectives: The present study aimed to evaluate the diagnostic efficiency of combined analyses of NT-proBNP, cTnT and CK-MB in the pericardial fluid for forensic diagnosis of SCD caused by ischemic heart disease. Materials and Methods: Levels of NT-proBNP, cTnT, and CK-MB in the pericardial fluid of 132 medicolegal autopsy cases were obtained through electrochemiluminescence method. Results: NT-proBNP, cTnT, and CK-MB levels were significantly elevated in SCD cases (P < 0.05). Receiver-operating characteristics (ROC) analysis showed that NT-proBNP, cTnT, and CK-MB have diagnostic value for the diagnosis of SCD: NT-proBNP, cutoff value of 2236 pg/ml; cTnT, cutoff value of 199.51 ng/ml; CK-MB: cutoff value of 2742.5 ng/ml, and the combined analyses of these three biomarkers have better diagnostic efficiency than each single biomarker alone. Moreover, the causes of SCD were sub-divided into acute ischemic heart disease, acute myocardial infarction (AMI), and recurrent myocardial infarction subgroups for further analysis, which revealed that the ratio of cTnT/CK-MB could be used to distinguish AMI with the cutoff value of 0.1085 estimated by ROC analysis. Conclusion: These observations suggested that the postmortem biochemical analyses of NT-proBNP, cTnT, and CK-MB in the pericardial fluid may assist to diagnose SCD in forensic practice, and the combined analyses of multiple biomarkers have better diagnostic efficiency than each single biomarker alone. On the basis of the postmortem biochemical analyses of NT-proBNP, cTnT and CK-MB, combining the ratio of cTnT/CK-MB could be used to distinguish AMI.

Background: Accumulated studies have demonstrated that Kruppel-like factor 5 (KLF5), a transcription factor, plays an important role in regulating cell proliferation and tissue remodeling through the expression of its downstream genes. KLF5-related factors are expected to be involved in the healing process after myocardial injury or myocardial ischemic changes, especially for the forensic diagnosis of myocardial ischemic physiopathology. Aim and Objectives: This study aimed to explore the discrimination ability and applicability of KLF5-related factors in SCD caused by MI compared with other causes of death to provide further insights into the forensic diagnosis of myocardial ischemic pathology. Materials and Methods: The relative quantification of F-Box and WD Repeat Domain Containing 7 (FBW7), KLF5, factor-binding protein (FGFBP) 1, and FGFBP2 messenger RNAs (mRNAs) in myocardial tissue samples was performed using real-time fluorescence quantitative reverse transcription polymerase chain reaction. KLF5 and FGFBP1/2 protein levels were examined using immunohistochemistry (IHC). The forensic autopsy cases (27 in total, autopsy within 72 h postmortem) included seven cases of acute myocardial infarction and 10 cases of acute myocardial ischemia. There were 10 cases in the control group, including four cases of traffic injury one case of injury by fall from height, one case of electric death, and four cases of blunt force injury. Results: Characteristic results were found in myocardial samples from three groups of deaths: KLF5 and FGFBP1 mRNA levels were significantly elevated in the infarction and ischemia groups, while FBW7 mRNA levels were significantly decreased. FBW7 is an important ubiquitin ligase that can mediate the degradation of KLF5 protein. In addition, FBW7 and FGFBP2 mRNA levels were decreased in the infarction group compared with the ischemia group. The IHC results were consistent with the observed mRNA expression patterns. Conclusions: Quantitative detection of FBW7, KLF5, FGFBP1, and FGFBP2 mRNA transcripts in myocardial tissues supports the pathophysiological study of myocardial ischemic diseases and provides molecular pathological evidence for forensic discrimination of death causes.

Postmortem imaging (PMI) technology known as virtual autopsy or virtopsy is regarded as a useful method of noninvasive or minimally invasive autopsy in forensic practice. Postmortem computed tomography is applicable to traumatic investigation, acute hemorrhage, pulmonary parenchyma disease, calcification (calculus, atherosclerosis), and gas accumulation. Postmortem magnetic resonance (PMMR) has been proven to have advantages in soft tissue identification. Cardiac death is one of the keys and difficult points in forensic practice. With the introduction and development of PMCT angiography and PMMR, it was proved to be a very promising tool in the investigation of cardiac death, including vascular cavities and ischemic myocardium. This article reviewed the applications of the latest PMI and its related technologies in forensic cardiac pathology, including advantages, limitations, and development prospects.

Sudden cardiac death (SCD) is an unexpected cardiac death that is instantaneous or occurs within a short period of time after onset of symptoms, in a person in a stable state of health. SCD has either a certain etiology (for example, cardiac tamponade or fresh occlusive coronary thrombus), or has one or more morphologic substrates that increase the risk of electrical instability that in turn can lead to a fatal arrhythmia. The latter group of SCD has been assigned as either highly probable or uncertain etiologies, according to guidelines of the Association of European Cardiovascular Pathology. This review describes definitive causes and potential underlying substrates for SCD.

Sudden cardiac death (SCD) is a common cause of death due to the high prevalence and mortality of cardiovascular disease (CVD). Currently, the forensic identification of SCD relies on traditional histomorphological examination, lacking stable biomarkers with high specificity and sensitivity. Previous studies have shown that exosomes (Exos) are ideal vectors and the application of Exos provides novel insight as the diagnostic biomarkers and treatment of CVD, and is hot research filed in biomedicine. This review briefly describes the biology of Exos, including the biogenesis of Exos and the mechanisms of action. The research progresses on Exos multi-omics, i.e., genomics, proteomics and metabolomics, and their roles in the diagnosis of different types of CVD, especially coronary heart disease and cardiomyopathy, are summarized. In addition, the current difficulties of applications of Exos in forensic identification of SCD and the prospective forensic applications in the future are highlighted. The aim of this review is to summarize the current advances of Exos in CVD in a disease-oriented manner, and to provide a reference for future forensic pathological identification of SCD, as well as the early diagnosis of SCD in clinic.

Sudden cardiac death (SCD), accounting for a substantial part of the forensic autopsy, is a leading cause of mortality worldwide. Lethal arrhythmia due to sodium channel diseases is recognized as one of the most prevalent etiologies of SCD. In these disorders, defective cardiomyocytes, including the pacemaker and the working cardiomyocytes, would manifest as abnormal electrical activity and morphology, thereby predisposing individuals to SCD. It is always a problem for forensic pathologists to adjudicate a sudden death caused by sodium channel diseases since structural changes in those cases are often inconspicuous. With the advent of the molecular autopsy, forensic pathologists can conduct targeted gene testing to identify the risk of SCD for family members of the probands. This review aims to discuss the relationship between SCD and sodium channel diseases, clarify the underlying mechanisms, and provide prophylactic suggestions for the relatives of SCD patients at risk.

Here, we report a case of acute attack of coronary heart disease (CHD). A 47-year-old pregnant woman with gestational hypertension developed sudden-onset chest tightness, palpitations, dyspnea, and cyanosis of the face and lips after admission. Her blood pressure was 180/110 mmHg and her blood oxygen saturation was 45% at that time. After cardiopulmonary resuscitation, a weak heartbeat was restored, but oxygen saturation did not increase significantly. Therefore, she was transferred to the intensive care unit; however, she died after 21 days of admission. Autopsy findings revealed that a foreign body was embedded in the esophagus near the right piriform, and her heart weighed 392 g; histopathological examination revealed CHD, thrombosis in the lumen of the right coronary artery, cardiomyocyte hypertrophy, vascular hyaline degeneration in arterioles, neutrophils in the bronchiole and alveolar. All the tested samples yielded negative toxicological results. Clinical status and autopsy findings were not compatible with a diagnosis of peripartum cardiomyopathy. The patient's sudden death was attributed to CHD, and esophageal foreign-body impaction was considered to be concomitant phenomenon. Our findings might help in increasing the awareness between esophageal foreign-body impaction and sudden cardiac death and they can also help in clarifying that understanding the primary cause of death is the key to resolving an iatrogenic medical tangle.

Identification of sudden cardiac death (SCD) with a structurally normal heart remains an important challenge in forensic pathology. Long QT syndrome (LQTS) is known as an inherited or acquired channelopathy, which is characterized with prolonged QT interval, and is likely to cause SCD in young adults. In this circumstance, no specific pathological change in the heart can be found anatomically or histologically in the LQTS victims. Thus, postmortem LQTS diagnosis is mainly based on clinical manifestations and genetic testing. Here, we reported a 26-year-old woman who was found dead at home with a history of unexplained syncope. Her clinical records and an electrocardiograph (ECG) obtained 3 months before her death showed a QTc interval of 539 ms which implicates the diagnosis of LQTS. Although the autopsy and pathological examination findings lacked specificity, we noticed enhanced lipofuscin accumulation in cardiomyocytes, which might be related to LQTS. After excluding potential diseases and injuries, we made the postmortem diagnosis as LQTS according to ECG, clinical history, and forensic postmortem findings. In conclusion, we provided clinical and pathological features of an SCD case due to LQTS, which might enrich the understanding of forensic postmortem SCD diagnosis with nonstructural cardiac diseases.