Cases Of Sudden Death Research Articles

Extra-cellular volume fraction analysis on cardiac CT is useful for predicting the prognosis of hypertrophic cardiomyopathy

Abstract Introduction Extra-cellular volume (ECV) fraction on magnetic resonance imaging (MRI) can evaluate the degree of myocardial fibrosis and has been reported to help diagnose and evaluate the prognosis of cardiomyopathy. In hypertrophic cardiomyopathy (HCM), ECV analysis on MRI is reported to help predict ventricular arrhythmias. However, the performance of cardiac MRI takes time, and there are also several contraindications. Cardiac computed tomography (CT) is more versatile than cardiac MRI and is also useful in screening coronary artery disease. ECV analysis on CT is now available, and a good correlation with ECV on MRI has been reported. We hypothesized that ECV on CT, a new fibrosis indicator, would be useful in predicting prognosis in HCM patients. Purpose To determine the utility of ECV analysis on CT to predict the prognosis in patients with HCM. Methods One hundred and three HCM patients (68 males, 66 ± 11 years old) who underwent cardiac CT using 320-row detector CT or 256-row detector CT, from 2008 to 2021 at our two hospitals were analyzed. We measured left ventricular (LV) ECV (LV-ECV) on CT and collected patient characteristics, transthoracic echocardiographic, and other CT findings. We investigated the relationship between these findings and the major adverse cardiac events (MACEs) (cardiac death, fatal arrhythmia, and heart failure hospitalization) after CT. Results All patients were followed for 64 ± 54 months after cardiac CT, and 15 patients (14.6%) had MACEs (ten heart failure hospitalization cases, two ventricular fibrillation cases, two sustained ventricular tachycardia cases, and one sudden cardiac death case). The patients with MACEs had a significantly higher LV-ECV, sudden cardiac death (SCD) risk score and lower LV ejection fraction (LVEF) than those without MACEs（42.0 ± 8.3% vs. 33.7 ± 6.1%, P < 0.001, 2.4 ± 0.39 vs 1.95 ± 0.16, P= 0.047, and 57.7 ± 11.9% vs. 66.7 ± 6.9%, P = 0.004). The percentage of dilated phase HCM was significantly higher in the patients with MACEs than those without MACEs (21% vs 0%, p=0.002). LV-ECV was the only significant predictor of MACEs based on the multivariate analysis by Cox proportional hazard model (hazard ratio 1.23, 95% confidence interval 1.09-1.41, P<0.001). The optimal threshold of LV-ECV to predict MACEs was 37.6% based on the receiver operating characteristic analysis. The sensitivity and specificity of LV-ECV to predict MACEs were 73% and 78% at the best cut-off, and the area under the curve was 0.79 (Figure A). The patients with LV-ECV ≥ 37.6% (30 patients) had significantly higher MACEs than those with LV-ECV < 37.6% during the follow-up periods (P < 0.001) (Figure B). Conclusion LV-ECV on CT of 37.6% is a good prognostic indicator in HCM cases. ECV analysis on CT helped predict MACEs in HCM cases.

Personalized prediction model specific for sudden cardiac death in the population: a machine learning study based on EHR

Abstract Background Predicting sudden cardiac death (SCD) in the general population remains a significant challenge, particularly at the individual level. SCD and myocardial infarction (MI) share similar pattern of characteristics and risk factors, making their specific prediction highly difficult. As a result, the current prediction models exhibit low specificity. Methods To estimate the specific risk of SCD over three months, we trained a machine learning model on electronic health record (EHR) data representing 8,566,229 drug prescriptions and 801,352 of hospital diagnoses up to five years prior to SCD. The data were obtained from a French cohort of 12,338 SCD and from a cohort of 12,338 controls from 2011 to 2015. We then validated the results on two external cohorts: one temporal cohort in the same area between 2016 and 2020 with 11,620 SCD cases and 11,620 controls and one geographical cohort from the USA with 892 SCD cases and 892 controls from 2013 to 2021. In order to address the specificity of our prediction model for SCD, SCD cases collected between 2016 and 2020 were also matched with a group of 35 000 controls who had myocardial infarction, with no SCD, following the same protocol as for the controls issued from the general population. Findings: The analysis reveals three distinct patterns of distribution for SCD cases, controls, and MI cases. We observed a semi linear increase of SCD cases over the deciles of predicted risk, and our model detected 24% (2,908) of SCD cases with a predicted risk exceeding 90% (highest decile). We observed the opposite among the controls that decreased linearly with increasing deciles of predicted risk: most of the controls were accurately identified in the lowest deciles, and there were only 214 controls (2%) in the highest decile. Interestingly, we observed a relatively stable distribution of MI cases across the deciles, with 10% of MI cases in the highest decile (Figure 1). Interpretation: We developed and validated a personalized prediction model that is able to identify subjects at high-risk for SCD specifically. Figure 1: Histogram of predicted risks for sudden cardiac death cases, controls and myocardial infarction cases in the validation cohort.Figure 1

The Role of Screening for Venous Thromboembolism in Pelvic Trauma Patients: A Single-Centre Retrospective Study

Background: Venous thromboembolism (VTE) is a severe complication following pelvic trauma. Thromboprophylaxis has reduced the risk of VTE in the pelvic trauma population; nevertheless, the risk remains high. A substantial pulmonary embolism has emerged as the unexpected cause of death among patients presenting with ‘minor pelvic fractures’. The purpose of this study was to analyse the single-centre experience with a surveillance protocol. We hypothesised that DVT surveillance with VUS and CTPA may reduce the perioperative mortality–morbidity rate in the subpopulation of patients with pelvic or acetabular fractures. Methods: This is a retrospective analysis of patients admitted with pelvic or acetabular fractures between January 2001 and December 2021. In April 2013, a screening protocol for VTE was introduced. This protocol included venous ultrasound and CTPA for patients with chest injuries. Patients from two groups—one screened for VTE and one without screening—were compared. Results: Of the 3186 patients with pelvic and/or acetabular fractures who were admitted, 1975 were not screened for VTE and 1211 underwent screening. There were more VTE cases in the screening group (5.62% vs. 0.86%, p < 0.001). Nine (0.46%) cases of sudden death occurred in the non-screening group, and all of them died with symptoms of acute PE. Since the screening was introduced, we have not encountered any deaths in the perioperative period (0.46 vs. 0, p = 0.02). Conclusions: The combined use of VUS and CTPA in chest-injured patients is a trustworthy means of screening for VTE, resulting in decreased mortality rates for those with pelvic and acetabular fractures by accurately diagnosing VTE during the perioperative phase.

Predictive value of coronary artery calcium score on radiological and autoptic findings in cases of sudden death

Calcium Artery Coronary Score (CACS) is a noninvasive examination of the coronary arteries in which the amount of calcium is calculated using cardiac Computed Tomography. The role of postmortem imaging in sudden death has been the subject of increasing interest in recent years, and previous studies have proposed a possible correlation between CACS and autopsy findings.The present study aims to establish a correlation between CACS, the presence of coronary artery opacification defects on Multi-Phase Post-Mortem Computed Tomography Angiography (MPMCTA), and the presence of coronary stenosis at autopsy, in order to verify whether CACS confirms its predictive value in terms of cardiac risk and can guide the decision to perform or not to perform MPMCTA.A cohort of 24 subjects who died suddenly was examined. Firstly, MPMCTA was performed, then autopsy was carried out. CACS was calculated, the detection of opacification defects on MPMCTA was investigated and the presence of coronary stenoses on autopsy was described.24 deceased individuals (53 years ± 11.7; 20 men) were evaluated. CACS has a positive predictive value of 0.78 and a negative predictive value of 0.73 in assessing the presence of radiological coronary artery opacification defects. The positive predictive value on stenosis relief is 0.88, while the negative predictive value on the same relief is 0.73.CACS is an appropriate additional tool in the evaluation of sudden death cases. Our results provided an encouraging contribution to the systematic application of CACS in cases of sudden death.

Некоторые факторы неблагоприятного прогноза на один год у пациентов с фибрилляцией предсердий

The aim of the study to determine factors of unfavorable influence on 12-months prognosis of life of patients with atrial fibrillation. Materials and methods of the study: The study included 183 patients (52.5% men) with atrial fibrillation (AF), with an average age of 66.2±10.0 years. Results of the study: It was found that 36% of patients had paroxysmal AF, 16% had persistent AF, and 48% had permanent AF. Non-valvular etiology of AF was identified in 85.3% of patients. Initially, 22% of patients were taking warfarin, while 37% were taking novel oral anticoagulants (NOACs). Based on the results of the one-year follow-up, patients were divided into two groups: group 1 with a favorable outcome (n=156) and group 2 (n=27) with an unfavorable outcome (total of 15 deaths, of which 11 were due to cardiovascular causes, including 6 cases of sudden death, 5 cases of chronic heart failure (CHF) decompensation requiring rehospitalization, 3 cases of ischemic stroke, including 1 fatal, and 4 cases of bleeding). Conclusion: A low initial rate of anticoagulant use was identified – 59%, including NOACs in 37%. High overall mortality (8.2%) and cardiovascular mortality (6.0%) were observed among AF patients over 12 months. Overall, an unfavorable prognosis was seen in 14.8% of patients.

Insights Of Cardiac Changes In Sudden Deaths In Kalaburagi District- An Autopsy Study.

Introduction: Sudden and unexpected death often arises as a complication of diverse cardiac ailments. The occurrence of sudden cardiac-related deaths is increasingly prevalent in both urban and rural settings. This surge presents a formidable challenge for forensic physicians tasked with conducting autopsies to ascertain the precise cause and manner of death, particularly in individuals previously considered healthy. Consequently, this study aims to shed light on infrequent lesions that may go unnoticed during the individual's lifetime, offering valuable insights into this phenomenon. Aims and Objectives of the study: 1) To study the demographic distribution of cardiac specimens of sudden death. 2) To study the histomorphology features in cardiac specimens in sudden death. 3) To grade the atherosclerotic lesions as per Modified American Heart Association Classification of Atherosclerotic Lesion. Materials and method: This is a retrospective study of 3 years from December 2020 to November 2023.The data of medicolegal autopsies was retrieved from the records of department of Pathology, Gulbarga Institute of Medical Sciences, Kalaburagi. A total of 371 medicolegal autopsy specimens were received in the department. Out of which 114 cardiac specimens (sent with other organs) of sudden death were studied. Results: Out of 114 cases of sudden death, 57% of the deaths occurred in outdoor location and remaining 43% occurred in hospitalized patients and homes. The commonest age group of sudden cardiac death was 31 to 40 years of age (27%). We found males were affected more commonly (84%) than females. The most common cause of sudden cardiac death is coronary artery disease (74.6%) followed by myocardial infarction (7.6%). Conclusion: The most common cause of sudden cardiac death is coronary artery disease, which is common in young males (age group 31-40 years).

Sudden death due to aortic rupture in New Zealand sheep

ABSTRACT Case history Over a period of 2 months in the spring and early summer of 2021, 13 cases of sudden death in cull ewes due to aortic rupture were diagnosed at a small number of New Zealand abattoirs. Clinical findings In 12/13 (92%) cases, a large blood clot was present in the thorax, and in one case the blood clot was seen in the tissues dorsal to the heart. There were no obvious signs of external trauma. The pluck (heart and lungs) or fixed aorta was submitted for histological examination in seven cases and in all of these, a tear in the aorta was found. Comparing the microscopic appearance of the proximal aorta in these seven cases to three clinically normal ewes from unaffected farms, the aortic wall thickness appeared thinner in the case ewes than the unaffected ewes. Subjectively, there was increased collagen in the tunica media in 3/7 and decreased elastin fibres in 5/7 case ewes compared to the control ewes. Further investigations on the index farm (where the first cases originated), found that the mean liver and serum Cu concentrations in 10 similarly aged, clinically normal ewes were within the normal reference range for New Zealand sheep. Similarly, the liver Cu concentrations of the seven case ewes were within the normal reference range. Diagnosis Aortic rupture due to an unknown aetiology. Clinical relevance Clinicians should be aware of this condition as a differential diagnosis for sudden death in older sheep and to assist the Ministry for Primary Industries in establishing the extent of this problem in New Zealand.

A Case of Sudden Death due to Massive Intraluminal Continuous Thrombosis from a Thoracic Stent Graft to Bilateral Femoral Arteries

A Case of Sudden Death due to Massive Intraluminal Continuous Thrombosis from a Thoracic Stent Graft to Bilateral Femoral Arteries

Interpretation of molecular autopsy findings in 45 sudden unexplained death cases: from coding region to untranslated region.

Sudden unexplained death (SUD) can affect apparently healthy adolescents and young adults with no prior clinical symptoms and no clear diagnostic findings at autopsy. Although primary cardiac arrhythmias have been shown to be the direct cause of death in the majority of SUD cases, the genetic predisposition contributing to SUD remains incompletely understood. Currently, molecular autopsy is considered to be an effective diagnostic tool in the multidisciplinary management of SUD, but the analysis focuses mainly on the coding region and the significance of many identified variants remains unclear. Recent studies have demonstrated the strong association between human disease and genetic variants in untranslated regions (UTRs), highlighting the potential role of UTR variants in the genetic predisposition to SUD. In this study, we searched for UTR variants with likely functional effects in the exome data of 45 SUD cases. Among 244 genes associated with cardiac diseases, three candidate variants with high confidence of pathogenicity were identified in the UTRs of SCO2, CALM2 and TBX3 based on a rigorous filtering strategy. A functional assay further validated the effect of these candidate variants on gene transcriptional activity. In addition, the constraint metrics, intolerance indexes, and dosage sensitivity scores of genes affected by the candidate variants were considered when estimating the consequence of aberrant gene expression. In conclusion, our study presents a practical strategy for UTR variant prioritization and functional annotation, which could improve the interpretation of molecular autopsy findings in SUD cohorts.

Fentanyl and Sudden Death-A Postmortem Perspective for Diagnosing and Predicting Risk.

Sudden, unexpected deaths are extremely difficult for families, especially when the victim is a child. Most sudden deaths occur due to cardiovascular issues, and a smaller number (approximately one-quarter) are attributed to other causes, such as epilepsy. The medicinal and non-medicinal use of the synthetic opioid fentanyl, which can cause breathing problems, is frequently involved in these deaths. It is also being found more often in autopsies of sudden death cases, and the number of overdose deaths from illicit drugs containing fentanyl is increasing. There are cases in which it is mixed with other drugs. A gene known as the KCNH2 gene or human ether-a-go-go-related gene (hERG), involved in the heart's electrical activity, can be related to abnormal heart rhythms. This gene, along with others, may play a role in sudden deaths related to fentanyl use. In response, we have examined the scientific literature on genetic variations in the KCNH2 gene that can cause sudden death, the impact of fentanyl on this process, and the potential benefits of genetic testing for the victims to offer genetic counseling for their family members.

Anatomical Ablation of the Atrioventricular Node.

Atrioventricular (AV) conduction ablation has been achieved by targeting the area of penetration of the conduction axis as defined by recording a His bundle potential. Ablation of the His bundle may reduce the possibility of a robust junctional escape rhythm. It was hypothesised that specific AV nodal ablation is feasible and safe. The anatomical position of the AV node in relation to the site of penetration of the conduction axis was identified as described in dissections and histological sections of human hearts. Radiofrequency (RF) ablation was accomplished based on the anatomical criteria. Specific anatomical ablation of the AV node was attempted in 72 patients. Successful AV nodal ablation was accomplished in 63 patients (87.5%), following 60 minutes (IQR 50-70 minutes) of procedure time, 3.4 minutes (IQR 2.4-5.5 minutes) of fluoroscopy time, and delivery of 4 (IQR 3-6) RF lesions. An escape rhythm was present in 45 patients (71%), and the QRS complex was similar to that before ablation in all 45 patients. Atropine was administered in six patients after the 10-min waiting period and did not result in restoration of conduction. In nine patients, AV conduction could not be interrupted, and AV block was achieved with ablation of the His after delivery of 12 (IQR 8-15) RF lesions. No cases of sudden death were encountered, and all patients had persistent AV block during a median 10.5 months (IQR 5-14 months) of follow-up. Anatomical ablation of the AV node is feasible and safe, and results in an escape rhythm similar to that before ablation.

Novel Immunohistochemical and Morphological Approaches in a Retrospective Study of Post-Mortem Myocarditis.

Background and Objectives: This study presents a retrospective analysis of 26 autopsy cases from a single centre, primarily focusing on forensic cases, with a majority of male individuals. Materials and Methods: We systematically analysed autopsy reports and cardiac tissue slides using haematoxylin-eosin stain and immunohistochemistry for CD3, CD163, and IL-6. The histological assessment evaluated key variables such as inflammation severity, necrosis, and background changes using a standardised grading system. Quantitative analysis of immunohistochemical markers was performed, calculating the percentage of positively stained cells within the inflammatory infiltrate. Results: The average age was 51.6 years, slightly skewed towards older males. The fatalities varied widely, with sudden death and drug abuse being the most common conditions linked to myocarditis findings on histological examination. A strong correlation was found between the severity of inflammation (measured by size within a myocardium section) and the scoring system based on the number of inflammatory foci per section (p ≤ 0.001). Most cases showed mild to minimal fibrosis, with some exhibiting moderate to severe fibrosis, arteriosclerosis, and myocyte hypertrophy. The presence of protein CD3 in the inflammatory infiltrate revealed a moderate inverse correlation between the CD3 values and the severity of inflammation and necrosis, and a strong inverse correlation with neutrophil levels. CD3 levels were higher in sudden death cases and lower in cases with numerous inflammatory foci, highlighting the discreet nature of lymphocytic myocarditis. Macrophage presence, assessed using CD163, showed a moderate inverse correlation with neutrophil levels and significant differences between sudden death and non-sudden death cases. Macrophage-rich inflammation was observed in cases with pneumonia/bronchopneumonia-associated lesions. IL-6 expression showed a moderate direct correlation with inflammation severity (p = 0.028), severity of necrosis (p = 0.005), and the number of inflammatory foci per section (p = 0.047). A moderate inverse correlation was found between CD3 and IL-6 expression (p = 0.005). Conclusions: These findings highlight the need for a unique immunohistochemical approach in forensic cases of myocarditis, differing from guidelines for endomyocardial biopsies due to diverse inflammatory cells. The study suggests exploring inflammatory chemokines within myocarditis foci for their significance in clinical scenarios. Specifically, IL-6, a crucial pro-inflammatory interleukin, correlated significantly with the severity of inflammation and necrosis (p < 0.05). This study provides novel and valuable insights into the histopathological and immunological markers of myocarditis in autopsy cases.

Cardiac sympathetic neurons are additional cells affected in genetically determined arrhythmogenic cardiomyopathy.

Arrhythmogenic cardiomyopathy (AC) is a familial cardiac disease, mainly caused by mutations in desmosomal genes, which accounts for most cases of stress-related arrhythmic sudden death, in young and athletes. AC hearts display fibro-fatty lesions that generate the arrhythmic substrate and cause contractile dysfunction. A correlation between physical/emotional stresses and arrhythmias supports the involvement of sympathetic neurons (SNs) in the disease, but this has not been confirmed previously. Here, we combined molecular, in vitro and ex vivo analyses to determine the role of AC-linked DSG2 downregulation on SN biology and assess cardiac sympathetic innervation in desmoglein-2mutant (Dsg2mut/mut) mice. Molecular assays showed that SNs express DSG2, implying that DSG2-mutation carriers would harbour the mutant protein in SNs. Confocal immunofluorescence of heart sections and 3-D reconstruction of SN network in clarified heart blocks revealed significant changes in the physiologialc SN topology, with massive hyperinnervation of the intact subepicardial layers and heterogeneous distribution of neurons in fibrotic areas. Cardiac SNs isolated from Dsg2mut/mut neonatal mice, prior to the establishment of cardiac innervation, show alterations in axonal sprouting, process development and distribution of varicosities. Consistently, virus-assisted DSG2 downregulation replicated, in PC12-derived SNs, the phenotypic alterations displayed by Dsg2mut/mut primary neurons, corroborating that AC-linked Dsg2 variants may affect SNs. Our results reveal that altered sympathetic innervation is an unrecognized feature of AC hearts, which may result from the combination of cell-autonomous and context-dependent factors implicated in myocardial remodelling. Our results favour the concept that AC is a disease of multiple cell types also hitting cardiac SNs. KEY POINTS: Arrhythmogenic cardiomyopathy is a genetically determined cardiac disease, which accounts for most cases of stress-related arrhythmic sudden death. Arrhythmogenic cardiomyopathy linked to mutations in desmoglein-2 (DSG2) is frequent and leads to a left-dominant form of the disease. Arrhythmogenic cardiomyopathy has been approached thus far as a disease of cardiomyocytes, but we here unveil that DSG2 is expressed, in addition to cardiomyocytes, by cardiac and extracardiac sympathetic neurons, although not organized into desmosomes. AC-linked DSG2 downregulation primarily affect sympathetic neurons, resulting in the significant increase in cardiac innervation density, accompanied by alterations in sympathetic neuron distribution. Our data supports the notion that AC develops with the contribution of several 'desmosomal protein-carrying' cell types and systems.

Characterization of a novel SCN5A mutation associated with long QT syndrome and arrhythmogenic right ventricular cardiomyopathy in a family.

Sudden cardiac death represents a significant diagnostic challenge for forensic pathologists, particularly in inherited arrhythmia syndromes or cardiomyopathies resulting from genetic defects. Molecular autopsies can reveal the underlying molecular etiology in such cases. In this study, we investigated a family with a history of sudden cardiac death to elucidate the molecular basis responsible for sudden cardiac death. The proband underwent a comprehensive forensic examination. Family members received thorough clinical evaluations, including electrocardiogram, Holter monitoring, echocardiography, and cardiac magnetic imaging. Whole exome sequencing and genetic analysis were performed on the deceased and her parents. In addition, Western blotting and patch-clamp recordings were employed to evaluate the expression and function of the mutant protein in vitro. Forensic examination diagnosed arrhythmogenic right ventricular cardiomyopathy (ARVC) as the cause of sudden death. Genetic analysis identified a novel missense mutation in SCN5A (p.V1323L), which was assessed as likely pathogenic by the ACMG guideline. Another family member carrying the mutation manifested long QT syndrome and mild cardiac fibrosis. The cellular electrophysiological study demonstrated that the mutation resulted in an enhanced late sodium current, suggesting it was a gain-of-function mutation. This study characterizes a novel SCN5A mutation that putatively causes long QT syndrome and may contribute to the development of ARVC. Our work expands the pathogenic spectrum of SCN5A variants and underscores the importance of molecular autopsy in sudden death cases, especially in those with suspected genetic disorders.

Forensic medical characterization of sudden death in young people with connective tissue dysplasia according to the data of the Bureau of Medical Examinations of Moscow City

BACKGROUND: Sudden death is an urgent problem of modern public healthcare, with prevalence in the Russian Federation. The wide range of causes and data scarcity led to the complexity of diagnosis and interpretation of pathologic changes at autopsy. This study presents an epidemiologic analysis of the causes of sudden death in a young population. AIM: To provide a forensic medical description of cases of sudden death of young people with connective tissue dysplasia using data from forensic autopsies conducted at the Bureau of Medical Examinations of the Moscow City Health Department. MATERIALS AND METHODS: A sample study of 48 corpses of young people aged 18–44 years who died suddenly, was performed based on data from the Forensic Medical Examination Bureau of the Moscow Department of Health. The protocols for examining the corpse at the scene of the incident, medical records were analyzed comprehensively. An extended description of the external and internal examinations of corpses was performed, and materials for histological, histochemical, and immunohistochemical studies were collected. RESULTS: Cardiovascular pathologies were the main cause of sudden death in young people. In some cases, an asthenic type was established with the following signs: high stature, elongated chest with an acute epigastric angle, poorly defined subcutaneous fatty tissue, weight less than the age norm, and narrow shoulders. Pathological changes were identified in the sternum, spine, limbs, dental status, and internal organs, which corresponded to connective tissue dysplasia. A correlation was noted between sudden death in young people and asthenic skeletopathy with exposure to extreme factors such as physical stress, psychoemotional stress, and previous infectious diseases. In most cases of sudden death, pathological changes in blood vessels were diagnosed in young people. CONCLUSION: The development of a modern comprehensive scientific and methodological approach is necessary to assess pathomorphological changes in young people who died suddenly.

Choking or Café Coronary Syndrome: A Series of Three Sudden Death Cases

Death by Café' coronary syndrome is very rarely seen and at the same time challenging to interpret at the autopsy. We highlight the importance of autopsy in such cases and solve Café coronary at autopsy. Café coronary syndrome was first reported as sudden collapse at restaurants while dining. Death was attributed to neurogenic cardiac arrest due to food in the upper airway and reflex vagal inhibition. Many of those individuals had consumed large amounts of alcohol before the incident. We present a series of three cases of sudden death by Café coronary in which food accidentally lodged in upper airways and collapsed suddenly without showing signs of asphyxia. Different risk factors were observed in all cases, including obesity as one of the associated risk factors for such incidence. This paper underlines the significance of detailed autopsy and reliable history given by the witnesses related to death occurring by Café coronary syndrome.

Cardiac rhabdomyoma: an uncommon culprit in sudden infant death

Sudden death in infants remains a common and poorly understood cause of childhood mortality in the USA. Pediatric cardiac tumors, although rare, may underlie some cases of unexplained sudden infant death. Autopsy is a crucial diagnostic step in these cases, as both gross and microscopic examination of the heart may uncover occult cardiac tumors. Rhabdomyomas are the most common cardiac tumors in childhood and may result in arrythmia and sudden death. We present a case of sudden death in a healthy 5-month-old infant which initially appeared “SIDS-like” until thorough histological analysis revealed an underlying cardiac rhabdomyoma. The case is of particular importance in that the gross examination of the heart was considered completely normal, and the tumor only involved certain portions of the heart microscopically. Had a single random section of myocardium been the only heart section examined microscopically, the diagnosis might have been missed. This case emphasizes the importance of thorough microscopic examination in infant cases, especially in cases where the heart appears grossly normal.

An atypical case of fatal ‘esophageal apoplexy’: post-mortem findings and differential diagnosis

Forensic pathologists need to have comprehensive knowledge of a large variety of causes of sudden natural death. We describe a case of sudden and unexpected death in woman in her sixties due to rupture of a large paraesophageal hematoma. The post-mortem examination and differential diagnosis are discussed. The combined findings of whole-body post-mortem CT imaging (PMCT), targeted PMCT angiography, autopsy, and histology are most in keeping with ‘esophageal apoplexy’; a rare cause of hemorrhage in the esophageal wall. A review of the literature indicates that most cases of esophageal apoplexy are self-limiting and that fatal complications are exceedingly rare. Our case demonstrates that esophageal apoplexy can present as sudden unexpected death.

Added value of postmortem mri in sudden unexpected infant death cases.

We aimed to investigate the potential added value of postmortem MRI (PMMRI) in sudden unexpected infant death (SUID) cases referred to our center between September 2020 and June 2023. Ultimately, 19 SUID cases underwent PMMRI alongside standard autopsy procedures, which included technical examinations such as postmortem CT (PMCT). Four radiologists, two with prior PMMRI experience, provided structured reports following consensus. For each case, the responsible forensic medicine specialist documented the cause of death before and after reviewing the PMMRI report. Additionally, they assessed the overall impact of the PMMRI report and had the opportunity to provide written comments. The results of our study indicate that none of the PMMRI reports altered the prior determined cause of death, which included cases of infection, asphyxia, and sudden infant death syndrome (SIDS). However, we observed a moderate impact in one case and a low impact in 10 cases. The moderate impact arose from the PMMRI report identifying hypoxic-ischemic changes, where histologic examination of the brain was perceived as normal. Conversely, in the 10 cases with a low impact, the PMMRI reports supported the autopsy findings, specifically indicating brain injury and intra-alveolar cellular infiltrates. In conclusion, our study suggests that while PMMRI may not be pivotal in determining the cause of death in SUID cases, it could aid in detecting hypoxic-ischemic changes and reinforcing brain and lung observations. However, distinguishing genuine lung pathology from postmortem changes using PMMRI remains challenging. Further research is warranted to clarify the role of PMMRI in forensic SUID investigations.

Ibogaine Induces Cardiotoxic Necrosis in Rats-The Role of Redox Processes.

Ibogaine is an organic indole alkaloid that is used in alternative medicine to combat addiction. Numerous cases of life-threatening complications and sudden deaths associated with ibogaine use have been reported, and it has been hypothesized that the adverse effects are related to ibogaine's tendency to induce cardiac arrhythmias. Considering that the bioavailability of ibogaine and its primary metabolite noribogaine is two to three times higher in female rats than in male rats, we here investigated the effect of a single oral dose (1 or 20 mg/kg) of ibogaine on cardiac histopathology and oxidative/antioxidant balance. Our results show that ibogaine induced dose-dependent cardiotoxic necrosis 6 and 24 h after treatment and that this necrosis was not a consequence of inflammation. In addition, no consistent dose- and time-dependent changes in antioxidant defense or indicators of oxidative damage were observed. The results of this study may contribute to a better understanding of ibogaine-induced cardiotoxicity, which is one of the main side effects of ibogaine use in humans and is often fatal. Nevertheless, based on this experiment, it is not possible to draw a definitive conclusion regarding the role of redox processes or oxidative stress in the occurrence of cardiotoxic necrosis after ibogaine administration.