Sudden Death Research Articles

Clinical and genetic yield of familial screening after a sudden unexplained death at a young age.

In a population under 45 years of age, the predominant causes of sudden cardiac death (SCD) are inherited cardiac diseases. Determining the underlying cause may help identify relatives at risk and prevent further events but is more difficult if an autopsy has not been performed. We aimed to assess the diagnostic value of clinical and genetic screening in relatives of young non-autopsied sudden unexplained death (SUD) victims. Eighty-seven relatives of 65 young non-autopsied SUD victims from 39 families were evaluated from 2016 to 2019. The relatives underwent extensive noninvasive cardiac workup. Genetic examinations were performed in 39 families. The definite diagnoses were made in 17 of 39 (44%) families. Cardiomyopathies were identified in 10 families (5 hypertrophic, 4 dilated, and 1 arrhythmogenic), followed by long QT syndrome (5 families). In 3 families, probable diagnoses were made, whereas in 20 families no diagnosis was achieved. In total, definite and probable diagnoses were made in 18 and 5 patients, respectively. All affected relatives were offered medical management, one of them died of heart failure and one underwent transplantation during the median follow-up of 3 years. Disease-causing variants were found in 7 of 39 (18%) probands; all in families with a definite diagnosis. Variants of unknown significance were found in 2 probands. Screening of relatives of SUD victims is warranted and may save lives, even if it is not guided by autopsy results. Genetic testing in families without the disease phenotype has little effectiveness.

Extracellular vesicles characterization in patients with hypertrophic cardiomyopathy

Background: Hypertrophic cardiomyopathy (HCM) is diagnosed according to the presence of morphological and functional traits of the heart, often in the presence of genetic mutations. A specific biomarker assessing the aetiopathology of this condition is lacking. Extracellular vesicles (EVs), small particles released by all cells into biological fluids, hold promise as diagnostic and prognostic tools for cardiac diseases. We aim at characterising plasma-derived EVs isolated from 18 consecutive HCM patients and 13 healthy volunteers (CTR). Methods: HCM underwent echocardiographic assessment and genetic testing evaluating 200 genes (NGS). EVs were isolated via ultracentrifugation from platelet-free plasma. Quantitative and qualitative assessments of EVs were performed by nanoparticle tracking analysis and transmission electron microscopy. FACS analysis was used to characterize EV subpopulations. Data are expressed as median and interquartile ranges. Results: Most patients were male (70.8% HCM and 54% CTR) with a median age of 61 (52.5-71) years (HCM) and 47 (44-52) (CTR). Missense mutations in the MYH7 gene were the most found in HCM. The median maximum wall thickness in HCM was 16 mm (15-19) vs 8 mm (7-9) in CTR. No differences were found in EV concentrations between HCM and CTR, respectively, 3.6*109 EV/ml/cell count (2*109-5*109) and 5*10⁹ EV/ml/cell count (4*109-6*109). However, EV concentration was positively associated with the sudden cardiac death risk score in HCM (r= 0.63). Among the EVs positive for CFSE (a specific dye for EVs), those released from platelets, progenitor endothelial cells and neutrophils were increased in HCM patients vs CTR, respectively, by 1.7-, 1.5- and 1.1-fold. A strong negative association (r= -0.74) was found between progenitor endothelial cell-derived EVs and the E/E’ ratio of diastolic function, a strong predictor of first cardiac events. Conclusions: HCM patients present a peculiar phenotypic pattern of EVs that associates which diastolic function and sudden cardiac death.

How to support patients and families after a sudden death in the emergency department

How to support patients and families after a sudden death in the emergency department

Kounis Syndrome: A Comprehensive Review of Pathophysiology, Clinical Manifestations, Diagnostic Challenges, and Therapeutic Strategies

Kounis syndrome, also known as allergic angina or allergic myocardial infarction, is a rare but potentially life-threatening condition characterized by the acute onset of chest pain, myocardial infarction, or sudden cardiac death in the setting of allergic or hypersensitivity reactions. The syndrome encompasses a spectrum of acute coronary syndromes triggered by various allergic insults, including medications, insect stings, food allergens, and environmental exposures. The pathophysiology involves the activation of mast cells and platelets, leading to coronary artery spasm, atheromatous plaque erosion or rupture, and subsequent myocardial ischemia or infarction. Diagnosis can be challenging due to the diverse clinical presentations and the need for a high index of suspicion. Management includes the identification and avoidance of triggers, along with the use of standard therapies for acute coronary syndromes. This review aims to provide a comprehensive overview of Kounis syndrome, focusing on its pathophysiology, clinical manifestations, diagnostic considerations, and therapeutic strategies.

Sudden unexplained death in young people: A family matter.

Sudden unexplained death in young people: A family matter.

An Evaluation of Platelet Indices in Newly Diagnosed Cases of Acute Myocardial Infarction

Acute myocardial infarction (AMI) is characterized by prothrombotic phenotype associated with endothelial dysfunction, an increase in platelet activation and systemic inflammation. Platelet aggregation and activation are crucial in the formation of thrombi and acceleration of atherosclerosis, associated with unstable angina, sudden cardiac death is brought on by an acute myocardial infarction. Objective: To evaluate the platelet-indices in newly diagnosed cases of acute myocardial infarction. Methods: This cross-sectional study was conducted during November 2022 to December 2023 in Pathology Department of Sheikh Zayed Medical College/Hospital Rahim Yar Khan. Samples were collected from the patients of AMI admitted to Emergency Ward and from healthy controls as well. Complete Blood Count (CBC) with platelet indices, platelet count, Mean Platelet Volume (MPV), Platelet Crit (PCT) and Platelet Distribution Width (PDW) were investigated on five-part automated hematology analyzer BT-PRO 2300. Analysis of the data was done by using SPSS version 20.0. Results: Total 140 patients were divided into a healthy control group (70) and newly diagnosed cases of acute myocardial infarction (70). Among diagnosed cases of AMI 46 (65.7%) had ST-elevation myocardial infarction (STEMI) and 24 cases (34.2%) got non-ST-elevation myocardial infarction (NSTEMI). It was found that AMI patients had lower platelet counts and PCT with higher MPV and PDW. Conclusions: It was concluded that the platelet indices (PDW, and PCT, MPV) are significant predictors of myocardial infarction. They might be applied as an easy, reliable, and economical way to anticipate an impending acute coronary event.

Reduced Ejection Fraction in Elite Endurance Athletes: Clinical and Genetic Overlap With Dilated Cardiomyopathy.

Exercise-induced cardiac remodeling can be profound, resulting in clinical overlap with dilated cardiomyopathy, yet the significance of reduced ejection fraction (EF) in athletes is unclear. The aim is to assess the prevalence, clinical consequences, and genetic predisposition of reduced EF in athletes. Young endurance athletes were recruited from elite training programs and underwent comprehensive cardiac phenotyping and genetic testing. Those with reduced EF using cardiac magnetic resonance imaging (defined as left ventricular EF <50%, or right ventricular EF <45%, or both) were compared with athletes with normal EF. A validated polygenic risk score for indexed left ventricular end-systolic volume (LVESVi-PRS), previously associated with dilated cardiomyopathy, was assessed. Clinical events were recorded over a mean of 4.4 years. Of the 281 elite endurance athletes (22±8 years, 79.7% male) undergoing comprehensive assessment, 44 of 281 (15.7%) had reduced left ventricular EF (N=12; 4.3%), right ventricular EF (N=14; 5.0%), or both (N=18; 6.4%). Reduced EF was associated with a higher burden of ventricular premature beats (13.6% versus 3.8% with >100 ventricular premature beats/24 h; P=0.008) and lower left ventricular global longitudinal strain (-17%±2% versus -19%±2%; P<0.001). Athletes with reduced EF had a higher mean LVESVi-PRS (0.57±0.13 versus 0.51±0.14; P=0.009) with athletes in the top decile of LVESVi-PRS having an 11-fold increase in the likelihood of reduced EF compared with those in the bottom decile (P=0.034). Male sex and higher LVESVi-PRS were the only significant predictors of reduced EF in a multivariate analysis that included age and fitness. During follow-up, no athletes developed symptomatic heart failure or arrhythmias. Two athletes died, 1 from trauma and 1 from sudden cardiac death, the latter having a reduced right ventricular EF and a LVESVi-PRS >95%. Reduced EF occurs in approximately 1 in 6 elite endurance athletes and is related to genetic predisposition in addition to exercise training. Genetic and imaging markers may help identify endurance athletes in whom scrutiny about long-term clinical outcomes may be appropriate. URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=374976&isReview=true; Unique identifier: ACTRN12618000716268.

Prescription and Dispensation of QT-Prolonging Medications in Individuals Receiving Hemodialysis

Individuals with dialysis-dependent kidney failure have numerous risk factors for medication-related adverse events, including receipt of care by multiple clinicians and initiation of some QT-prolonging medications with known risk of torsades de pointes (TdP), which is associated with higher risk of sudden cardiac death. Little is known about the prescription and dispensation patterns of QT-prolonging medications among people receiving dialysis, hindering efforts to reduce drug-related harm from these and other medications in this high-risk population. To examine prescription and dispensation patterns of QT-prolonging medications with known TdP risk and selected interacting medications prescribed to individuals receiving hemodialysis. This cross-sectional study included patients 60 years or older who were enrolled in Medicare Parts A, B, and D receiving in-center hemodialysis from January 1 to December 31, 2019. Analyses were conducted from October 20, 2022, to June 16, 2023. New-user prescriptions for the 7 most frequently filled QT-prolonging medications characterized by the timing of the new prescription relative to acute care encounters, the type of prescribing clinician and pharmacy that dispensed the medication, and concomitant use of selected medications known to interact with the 7 most frequently filled QT-prolonging medications with known TdP risk. The main outcomes were the frequencies of the most commonly filled and new-use episodes of QT-prolonging medications; the timing of medication fills relative to acute care events; prescribers and dispensing pharmacy characteristics for new use of medications; and the frequency and types of new-use episodes with concurrent use of potentially interacting medications. Of 20 761 individuals receiving hemodialysis in 2019 (mean [SD] age, 74 [7] years; 51.1% male), 10 992 (52.9%) filled a study drug prescription. Approximately 80% (from 78.6% for odansetron to 93.9% for escitalopram) of study drug new-use prescriptions occurred outside of an acute care event. Between 36.8% and 61.0% of individual prescriptions originated from general medicine clinicians. Between 16.4% and 26.2% of these prescriptions occurred with the use of another QT-prolonging medication. Most potentially interacting drugs were prescribed by different clinicians (46.3%-65.5%). In this cross-sectional study, QT-prolonging medications for individuals with dialysis-dependent kidney failure were commonly prescribed by nonnephrology clinicians and from nonacute settings. Prescriptions for potentially interacting medications often originated from different prescribers. Strategies aimed at minimizing high-risk medication-prescribing practices in the population undergoing dialysis are needed.

АССОЦИАТИВНАЯ РОЛЬ ПОЛИМОРФИЗМА RS121908987 ГЕНА PRKAG2 В РАЗВИТИИ СИНДРОМА WPW

The study of cardiac arrhythmias and conduction is one of the most urgent and important tasks, since these diseases are often the cause of sudden cardiac death. We assumed that the study of the contribution of "predictor genes" of heart rhythm and conduction disorders would expand knowledge about the etiology and pathogenesis of these diseases. Thus, the purpose of our research was to study the contribution of the rs121908987 polymorphism of the PRKAG2 gene to the development of WPW syndrome. Material and methods: 200 patients with VPU syndrome were examined, among them men n=97 [18:32.66;81]; women n=103 [18;47,92;83]. All patients underwent clinical, laboratory, somatometric, instrumental studies, as well as molecular genetic studies DNA isolation was performed by the standard phenol-chloroform method. Genotyping of the PRKAG2 gene was performed by PCR-PDRF analysis (polymerase chain reaction-polymorphism of restriction fragment lengths). Statistical data processing was carried out using the Excel application software package, Statistica for Windows 10.0, IBM SPSS 20.Differences in the frequency distribution of alleles and genotypes of the PRKAG2 gene between the groups were assessed using the χ2 criterion. The relative risk of disease for a specific allele or genotype was calculated as the odds ratio (OR). Results: a statistically significant predominance of the heterozygous GA genotype in patients with VPU syndrome, compared with those in the control group (8 and 2%, respectively; Table 1). There was also a statistically significant predominance of allele A carriers in the group of patients with VPU syndrome by 4%, compared with those in the control group (2%). The risk of developing PRKAG2 genotype GA syndrome, estimated by OSH, was 2.09 times higher (95% CI 1.88–2.32; p &lt;0.001 compared with genotypes GG and AA, and in carriers of the A allele – 2.04 times higher (95% CI 1.90–2.19; p &lt;0.001) compared with allele A (see Table 2). Conclusions: The results of the study confirmed the contribution of polymorphism rs121908987 of the PRKAG2 gene to the development of VPU syndrome.

Electrocardiographic and Echocardiographic changes in Non-Hemodialysis Chronic Kidney Disease Patients: A Cross-Sectional Study

Abstract Chronic Kidney Disease (CKD) patients have a higher risk of cardiovascular manifestations such as coronary artery disease, heart failure, arrhythmias, and sudden cardiac death. Cardiovascular diseases are the main cause of death in patients with advanced CKD, rather than end-stage kidney disease itself. Essentially, CKD speeds up the ageing process in the cardiovascular system. Objectives: To determine the prevalence of cardiovascular abnormalities in non-hemodialysis CKD patients. Methods: A descriptive cross-sectional study, was conducted in the Department of Medicine, between October 2020 to September 2022. A total of 50 CKD patients were included. The patients were evaluated &amp; enrolled in the study, based on history, general physical examination, systemic examination, Blood Urea, Serum Creatinine, Urine Routine, Electrocardiograph (ECG) and Echocardiography. Results: In the present study Electrocardiograph &amp; echocardiography determined cardiovascular abnormalities in 68% of patients. Among these 50% of patients had Left Ventricular Hypertrophy (LVH) &amp; Left Ventricular Diastolic Dysfunction (LVDD), 8% of patients had Arrhythmias and 6% patients had conduction abnormality, 2% patients had LVH and 2% patients had LVDD. Conclusion: LVH &amp; LVDD are the most common morphological abnormalities observed in our study. We can diagnose Arrhythmias and conduction abnormality by electrocardiogram &amp; echocardiography and refer them for appropriate interventions promptly.

Prenatal and postnatal factors associated with sudden infant death syndrome: an umbrella review of meta-analyses.

Comprehensive quantitative evidence on the risk and protective factors for sudden infant death syndrome (SIDS) effects is lacking. We investigated the risk and protective factors related to SIDS. We conducted an umbrella review of meta-analyses of observational and interventional studies assessing SIDS-related factors. PubMed/MEDLINE, Embase, EBSCO, and Google Scholar were searched from inception until January 18, 2023. Data extraction, quality assessment, and certainty of evidence were assessed by using A Measurement Tool Assessment Systematic Reviews 2 following PRISMA guidelines. According to observational evidence, credibility was graded and classified by class and quality of evidence (CE; convincing, highly suggestive, suggestive, weak, or not significant). Our study protocol was registered with PROSPERO (CRD42023458696). The risk and protective factors related to SIDS are presented as equivalent odds ratios (eORs). We identified eight original meta-analyses, including 152 original articles, covering 12 unique risk and protective factors for SIDS across 21 countries/regions and five continents. Several risk factors, including prenatal drug exposure [eOR = 7.84 (95% CI = 4.81-12.79), CE = highly suggestive], prenatal opioid exposure [9.55 (95% CI = 4.87-18.72), CE = suggestive], prenatal methadone exposure [9.52 (95% CI = 3.34-27.10), CE = weak], prenatal cocaine exposure [4.38 (95% CI = 1.95-9.86), CE = weak], prenatal maternal smoking [2.25 (95% CI = 1.95-2.60), CE = highly suggestive], postnatal maternal smoking [1.97 (95% CI = 1.75-2.22), CE = weak], bed sharing [2.89 (95% CI = 1.81-4.60), CE = weak], and infants found with heads covered by bedclothes after last sleep [11.01 (95% CI = 5.40-22.45), CE = suggestive], were identified. On the other hand, three protective factors, namely, breastfeeding [0.57 (95% CI = 0.39-0.83), CE = non-significant], supine sleeping position [0.48 (95% CI = 0.37-0.63), CE = suggestive], and pacifier use [0.44 (95% CI = 0.30-0.65), CE = weak], were also identified. Based on the evidence, we propose several risk and protective factors for SIDS. This study suggests the need for further studies on SIDS-related factors supported by weak credibility, no association, or a lack of adequate research.

The Reduction of Blood Pressure in Elderly People with Hypertension Through Morning Walk Therapy

Background: Hypertension in the elderly is a very dangerous disease because without early indications it can cause sudden death. The prevalence of people with hypertension in the Burneh Health Center in 2021 is 15.935 people (11.29%). The proportion of elderly with hypertension is 1,820 elderly men (0.10%) and 1,670 elderly women (0.09%). Purpose: This study aims to analyze the effect of morning walking physical activity on reducing systolic blood pressure in elderly people with hypertension. Method: This study was conducted in the village of Burneh, Bangkalan, East Java, Indonesia from May to June 2022. The research design used a Quasy Experiment with a Pre-test and Post-test approach, the independent variable in this study was physical activity therapy for morning walks and the dependent variable systolic blood pressure in elderly with hypertension. The sample size is 14 elderly with purposive sampling technique. Data analysis used the Paired t-test. Results: The results of the statistical test obtained p-value = 0.041 &lt;0.05 indicating that there was a difference in systolic blood pressure before and after being given physical activity therapy for the morning walk. Most of the respondents (57.14%) experienced a decrease in systolic blood pressure with an average decrease of 8.72 mmHg. Conclusion: Therapeutic physical activity walking in the morning has a significant effect on systolic blood pressure in elderly people with hypertension. Health workers need to provide correct information about the benefits of morning walks for elderly people with hypertension and monitor the consistency of sufferers.

Sudden Cardiac Death in Young Age, What Should We Know?

While young sudden cardiac death (SCD) is statistically uncommon, its dramatic presentation and impact on families and communities make it a newsworthy issue. Nonetheless, it is important to view SCD in children and adolescents as a public health concern and devise strategies based on research and consensus to address it. Both individuals with and without a history of cardiovascular illness are susceptible to sudden cardiac death. Employing cardiovascular disease risk screening for healthy individuals and those with a family history of sudden cardiac death can serve as a preventive approach against sudden cardiac death. Assessing the severity of cardiovascular disease in people becomes essential to prevent disease progression and minimize the risk of mortality from cardiovascular conditions. Keyword: Young, Sudden Cardiac Death, Preventive.

Atorvastatin, etanercept and the nephrogenic cardiac sympathetic remodeling in chronic renal failure rats.

Chronic renal failure (CRF) patients are predisposed to arrhythmias, while the detailed mechanisms are unclear. We hypothesized the chronic inflammatory state of CRF patients may lead to cardiac sympathetic remodeling, increasing the incidence of ventricular arrhythmia (VA) and sudden cardiac death. And explored the role of atorvastatin and etanercept in this process. A total of 48 rats were randomly divided into sham operation group (Sham group), CRF group, CRF + atorvastatin group (CRF + statin group), and CRF + etanercept group (CRF + rhTNFR-Fc group). Sympathetic nerve remodeling was assessed by immunofluorescence of growth-associated protein 43 (GAP-43) and tyrosine hydroxylase positive area fraction. Electrophysiological testing was performed to assess the incidence of VA by assessing the ventricular effective refractory period and ventricular fibrillation threshold. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta were determined by Western blotting and enzyme-linked immunosorbent assay. Echocardiogram showed that compared with the Sham group, left ventricular end-systolic diameter and ventricular weight/body weight ratio were significantly higher in the CRF group. Hematoxylin-eosin and Masson staining indicated that myocardial fibers were broken, disordered, and fibrotic in the CRF group. Western blotting, enzyme-linked immunosorbent assay, immunofluorescence and electrophysiological examination suggested that compared with the Sham group, GAP-43 and TNF-α proteins were significantly upregulated, GAP-43 and tyrosine hydroxylase positive nerve fiber area was increased, and ventricular fibrillation threshold was significantly decreased in the CRF group. The above effects were inhibited in the CRF + statin group and the CRF + rhTNFR-Fc group. In CRF rats, TNF-α was upregulated, cardiac sympathetic remodeling was more severe, and the nephrogenic cardiac sympathetic remodeling existed. Atorvastatin and etanercept could downregulate the expression of TNF-α or inhibit its activity, thus inhibited the above effects, and reduced the occurrence of VA and sudden cardiac death.

Exploring biomarkers for identifying acute myocardial infarction based on lipidomics

ABSTRACT Acute myocardial infarction(AMI) is one of the most common causes of sudden cardiac death, but the accurate AMI identification biomarkers are still lacking. Recently, lipidomics shed new light on the exploration of AMI biomarkers. In this study, lipid molecules were examined in rat myocardial tissue based on Liquid chromatography-tandem mass spectrometry (LC-MS/MS) lipidomics to screen for metabolic markers for the identification of AMI. Results showed that 70 lipid molecules with different expressions identified by distinguishing between the sham group and the AMI 5 min group, 275 differentially expressed lipid molecules identified by distinguishing between the sham group and the AMI 4 hour group. And 257 differentially expressed lipid molecules identified by distinguishing between the AMI 5 min group and the AMI 4 hour group. Comprehensive analysis shows that PC (18:0_18:1)+HCOO and PC (16:0_18:2)+HCOO exhibited more significant changes. Two lipid molecules were applied to build AMI-identification models, the accuracy rate reached 77.8% and R2 = 0.539.

The surge of bromazolam-related fatalities replacing other novel designer benzodiazepines-related fatalities in San Francisco.

Bromazolam, a novel designer benzodiazepine (NBD), exhibits potent sedative, hypnotic and anxiolytic effects, raising concerns regarding its potential for misuse and fatal outcomes, particularly when combined with opioids such as fentanyl. Despite limited documented fatalities globally, its use poses a significant threat, exacerbated by under-reporting and a lack of routine testing. This study analysed NBD-related deaths in a major US city over a 4-year period. Analysis of accidental overdose deaths involving NBDs in San Francisco, CA, USA from 2020 to 2023, was performed utilizing medico-legal death investigations including comprehensive forensic toxicology, pathology and demographic information. San Francisco conducts thorough investigations into all non-natural and sudden unexpected deaths, including routine alcohol and drug testing of decedents under its jurisdiction, including etizolam, flualprazolam, flubromazolam and bromazolam analysis. There was a sudden surge in bromazolam-related deaths, with 44 fatalities documented in 2023, contrasting with relatively fewer deaths related to other NBDs. Bromazolam fatalities frequently involved co-ingestion with opioids, primarily fentanyl, and stimulants such as methamphetamine and cocaine. Demographic characteristics indicated a predominance of males, with a significant proportion lacking fixed addresses. Blood concentrations of bromazolam increased during the study period, suggesting heightened availability and/or purity in the community. There was a surge in bromazolam-related deaths during 2023 in San Francisco, CA, USA, contrasting with relatively stable numbers of deaths associated with other NBDs over the preceding years. The findings underscore the urgency for enhanced death investigation, testing and reporting to facilitate targeted harm reduction strategies for individuals at risk of bromazolam-related morbidity and mortality.

Association between opioid use disorder and palliative care: a cohort study using linked health administrative data in Ontario, Canada.

People with opioid use disorder (OUD) are at risk of premature death and can benefit from palliative care. We sought to compare palliative care provision for decedents with and without OUD. We conducted a cohort study using health administrative databases in Ontario, Canada, to identify people who died between July 1, 2015, and Dec. 31, 2021. The exposure was OUD, defined as having emergency department visits, hospital admissions, or pharmacologic treatments suggestive of OUD within 3 years of death. Our primary outcome was receipt of 1 or more palliative care services during the last 90 days before death. Secondary outcomes included setting, initiation, and intensity of palliative care. We conducted a secondary analysis excluding sudden deaths (e.g., opioid toxicity, injury). Of 679 840 decedents, 11 200 (1.6%) had OUD. Compared with people without OUD, those with OUD died at a younger age and were more likely to live in neighbourhoods with high marginalization indices. We found people with OUD were less likely to receive palliative care at the end of their lives (adjusted relative risk [RR] 0.84, 95% confidence interval [CI] 0.82-0.86), but this difference did not exist after excluding people who died suddenly (adjusted RR 0.99, 95% CI 0.96-1.01). People with OUD were less likely to receive palliative care in clinics and their homes regardless of cause of death. Opioid use disorder can be a chronic, life-limiting illness, and people with OUD are less likely to receive palliative care in communities during the 90 days before death. Health care providers should receive training in palliative care and addiction medicine to support people with OUD.

Target Cell Extraction and Spectrum-Effect Relationship Coupled with BP Neural Network Classification for Screening Potential Bioactive Components in Ginseng Extract with a Protective Effect against Myocardial Damage.

Cardiovascular disease has become a common ailment that endangers human health, having garnered widespread attention due to its high prevalence, recurrence rate, and sudden death risk. Ginseng possesses functions such as invigorating vital energy, enhancing vein recovery, promoting body fluid and blood nourishment, calming the nerves, and improving cognitive function. It is widely utilized in the treatment of various heart conditions, including palpitations, chest pain, heart failure, and other ailments. Although numerous research reports have investigated the cardiovascular activity of single ginsenoside, there remains a lack of systematic research on the specific components group that predominantly contribute to cardiovascular efficacy in ginseng medicinal materials. In this research, the spectrum-effect relationship, target cell extraction, and BP neural network classification were used to establish a rapid screening system for potential active substances. The results show that red ginseng extract (RGE) can improve the decrease in cell viability and ATP content and inhibit the increase in ROS production and LDH release in OGD-induced H9c2 cells. A total of 70 ginsenosides were identified in RGE using HPLC-Q-TOF-MS/MS analysis. Chromatographic fingerprints were established for 12 batches of RGE by high-performance liquid chromatography (HPLC). A total of 36 common ingredients were found in 12 batches of RGE. The cell viability, ATP, ROS, and LDH of 12 batches RGE were tested to establish gray relationship analysis (GRA) and partial least squares discrimination analysis (PLS-DA). BP neural network classification and target cell extraction were used to narrow down the scope of Spectral efficiency analysis and screen the potential active components. According to the cell experiments, RGE can improve the cell viability and ATP content and reduce the oxidative damage. Then, seven active ingredients, namely, Ginsenoside Rg1, Rg2, Rg3, Rb1, Rd, Re, and Ro, were screened out, and their cardiovascular activity was confirmed in the OGD model. The seven ginsenosides were the main active substances of red ginseng in treating myocardial injury. This study offers a reference for quality control in red ginseng and preparations containing red ginseng for the management of cardiovascular diseases. It also provides ideas for screening active ingredients of the same type of multi-pharmacologically active traditional Chinese medicines.

Study of Postmortem Pericardial Fluid Concentrations of Troponin T (cTnT) in Sudden Natural Death

Background: Cardiovascular diseases are the most common cause of sudden natural deaths. Cardiac troponin T is a specific biochemical marker of myocardial injury. It may help in diagnosis of early myocardial ischemia when macroscopic or microscopic evidence of necrosis is not available after autopsy. Aim of this study was to assess the effectiveness of pericardial fluid troponin T in predicting the cause of death in sudden natural death and in estimating the post mortem interval. Materials and methods: It was a pilot study. Sudden natural deaths brought to Forensic Medicine department of GMCH Nagpur for autopsy were included in this observational cross sectional study. Deaths were grouped into cardiac and non cardiac deaths. Pericardial fluid samples were collected by opening pericardial sac with sterile syringe and processed on Roche Cobas e411 autoanalyzer for estimation of levels of Troponin T. Results: There was a statistically significant difference seen for the values between the groups (p&lt;0.05) for Trop-T (ng/ml) with higher values in Cardiac cause. There was a statistically non significant correlation between postmortem interval vs Trop T (p&gt;0.05). Conclusion: Estimation of pericardial fluid Troponin-T may be used to predict the cause of death in sudden natural death.

Massive Myocardial Calcification: A Rare Autopsy Finding

Introduction: Myocardial calcification is rare and occur by two mechanisms- dystrophic and metastatic. It can present with variable clinical manifestations like congestive heart failure, cardiomyopathy, arrhythmia and sudden cardiac death. Case Report: Post mortem viscera of a 50 year old male was received in the department of pathology with alleged history of burns, who died after two weeks of hospital treatment. There was no past history or investigation available in the post mortem papers. Whole heart, pieces of brain, both lungs, liver, spleen and both kidneys were received. On gross examination no abnormality was observed in any of these viscera. Microscopic examination revealed extensive calcification in anterior, lateral &amp; posterior walls of left ventricle of the heart. Sections from kidney showed features of chronic tubulointerstitial nephritis. Conclusion: Myocardial calcification is rare and mostly diagnosed incidentally or on autopsy. Extensive sampling of heart and other viscera might help in finding the etiology in such rare cases of massive calcification in myocardium . Antemortem diagnosis can be made with computed tomography (CT) scan and endomyocardial biopsy.