Cause Of Sudden Death Research Articles

Sudden death in the southern region of Saudi Arabia: A retrospective study.

Sudden death is unanticipated, non-violent death taking place within the first 24 h after the onset of symptoms. It is a major public health problem worldwide. Moreover, the effects of living at moderate altitude on mortality are poorly understood. To retrospectively report the frequency and the main causes of sudden deaths in relation to total deaths at Asir Central Hospital, 2255 m above sea level, in the southern region of Saudi Arabia over a period of 4 years from 2013 to 2016. The medical records of 1821 deaths were examined and showed 353 cases (19.4%) of sudden death. The highest incidence of sudden death was among the elderly (51%), whereas, the lowest was among children and adolescents (6.5%). With regard to gender, the incidence of sudden death was higher in males (54.4%) compared to 45.6% in females. In this study, we found that the most common direct causes of sudden death were cardiovascular diseases (29.2%), respiratory disease (22.7%), infectious disease (12.2%), cancer (9.4%) and hematological diseases (6.2%). With respect to seasonal variation, the highest incidence was during winter (31.32%) followed by summer (25.8%). The results of this study will help emergency physicians and health care providers to exercise due care to reduce the incidence of sudden death and raise public awareness about the impact of sudden death.

Commotio cordis – a review of a rare cause of sudden death in young athletes

Commotio cordis, from Latin “agitation of the heart” is a potentially fatal sudden disruption and alteration of heart electric activity. It is usually caused by relatively mild blunt non-penetrating trauma to the specific point on anterior part of the chest wall during beginning of the heart muscle repolarization phase. It leads to ventricular fibrillation presenting as a collapse few seconds after the blow. It can be lethal without taking proper steps of management in a short ammount of time.

LV and LA mechanics in pediatric HCM : a CMR study of phenotype-genotype correlation

Abstract Funding Acknowledgements Type of funding sources: None. Background Paediatric hypertrophic cardiomyopathy (HCM) is a leading cause of sudden death. The relationship between the genotype variation and phenotype expression has not been fully elucidated, with some studies showing association with an increased hypertrophy and MYH7 or multiple genetic variations. In HCM fibrosis and hypertrophy contribute to left ventricular (LV) mechanics’ alteration resulting in subendocardial dysfunction. The latter is associated with a decreased global longitudinal and radial strains (GLS, GRS), whereas epicardial thickening leads to preserved global circumferential strain (GCS) and LV twist. Children with HCM have reduced LA function, measurable by both volumetric and strain analysis and reduced LA mechanics are associated with poor exercise capacity. Feature tracking –cardiac magnetic resonance (FT-CMR) has enhanced the non-invasive assessment of myocardial deformation in HCM. The main aim of our study was to assess differences of LV and LA mechanics features on CMR between patients harbouring multiple pathogenic or likely pathogenic variants (MGv, n=16) or single genetic variations (SGv, n=35). Methods Our retrospective CMR study included 51 patients (1.7–18.8 years ago). CMR data were: LV and LA’s morphological values, late gadolinium enhancement (LGE) of LA and LV walls, LV feature tracking (FT) derived strain and LV twist (LVT). LV twist was calculated as the difference between basal and apical rotation. The LA feature FT derived strain, LA conduit function, reservoir function and pump function were computed. Results In MGv group, the indexed LV mass 108.8 +/-53.0 vs 74.3+/- 22.2 in SGv (p = 0.03). LGE was present in 51% patients of the whole cohort, with LGE in 64 % of MGv group. LV FT derived strain values and LA function were not statistically significant different between groups (MGv vs SGv: GLS −15.8+/−5.3 vs −18.7+/−4.8, GCS −27.8+/8 vs −31.1+/−8.6, GRS 44.7+/−24.6 vs 62.3+/−32). LVT was reduced in MGv group (0.04+/−7.6) vs (7.4+/−7.4) in SGv (p = 0.003). LA contractile function did not differ between the groups (MGv vs SGv: GLS LA 25.1+/−14.2 vs 27.6+/−13.5). LA reservoir, conduction and pump function did not differ between the groups. LVT was significantly correlated with the LA contractile function. An increased of LVT was associated with an increased LA GLS and EF (p = 0.011; p = 0.004). Conclusions Patients with multiple genetic variants have a greater LV mass and altered LV mechanics with reduced LV twist. This study gives insights in phenotype- genotype correlation in paediatric HCM and warrants larger longitudinal studies to assess its clinical significance.

Integrating Bioinformatics and Network Pharmacology to Explore the Therapeutic Target and Molecular Mechanisms of Schisandrin on Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease and is currently the leading cause of sudden death in adolescent athletes. Schisandrin is a quality marker of the traditional Chinese medicine Schisandra chinensis, which has an excellent therapeutic effect on HCM, but its pharmacological mechanism remains unclear. This study aimed to explore the potential and provide scientific evidence for schisandrin as a lead compound against hypertrophic cardiomyopathy. The drug-like properties of schisandrin were predicted using the SwissADME website. Then, the PharmMapper database was used to predict potential drug targets and match gene names in the Uniprot database. HCM targets were collected from NCBI, OMIM, and Genecards databases and intersected with drug targets. The intersection targets were imported into the STRING database for PPI analysis, and core targets were identified. KEGG and GO enrichment analysis was performed on the core targets through the DAVID database, and all network maps were imported into Cytoscape software for visualization optimization. HCM-related datasets were downloaded from the GEO database to analyze core targets and screen differentially expressed target genes for molecular docking. After the PPI network analysis of the intersection targets of drugs and diseases, 12 core targets were screened out. The KEGG analysis results showed that they were mainly involved in Rap1, TNF, FoxO, PI3K-Akt, and other signaling pathways. After differential analysis, PPARG, EGFR, and MMP3 targets were also screened. The molecular docking results showed that schisandrin was well bound to the protein backbone of each target. This study used network pharmacology combined with differential expression and molecular docking to predict that schisandrin may treat HCM by acting on PPARG, EGFR, and MMP3 targets, and the regulatory process may involve signaling pathways, such as Rap1, TNF, FoxO, and PI3K-Akt, which may provide a valuable reference for subsequent studies.

Pre-excited atrial fibrillation revealed at a very delayed age: case report

BackgroundWolff-Parkinson-White (WPW) syndrome is a condition characterized by the persistence of an accessory pathway responsible for ventricular pre-excitation that can lead to symptomatic and potentially severe arrhythmias. Coexistence with atrial fibrillation is well known and not uncommon, exposing to potential degenerescence into ventricular fibrillation when atrial impulses are transmitted along the accessory pathway. WPW syndrome is most prevalent in younger patients and cases revealed after an advanced age have rarely been described in the literature.Case presentationHere, we report a case of atrial pre-excitation first diagnosed at the age of 72 years that required external electrical cardioversion with a favorable outcome. The diagnosis was based on clinical and electrographic findings.ConclusionsWPW syndrome is a relatively rare cardiac disorder that can be a cause of sudden death, especially when combined with atrial fibrillation. Therefore, cardiologists have to consider this diagnosis in patients presenting clinical signs of arrhythmia with an electrical pattern of WPW.

Computational Study on Effect of KCNQ1 P535T Mutation in a Cardiac Ventricular Tissue.

Heart diseases such as arrhythmia are the main causes of sudden death. Arrhythmias are typically caused by mutations in specific genes, damage in the cardiac tissue, or due to some chemical exposure. Arrhythmias caused due to mutation is called inherited arrhythmia. Induced arrhythmias are caused due to tissue damage or chemical exposure. Mutations in genes that encode ion channels of the cardiac cells usually result in (dysfunction) improper functioning of the channel. Improper functioning of the ion channel may lead to major changes in the action potential (AP) of the cardiac cells. This further leads to distorted electrical activity of the heart. Distorted electrical activity will affect the ECG that results in arrhythmia. KCNQ1 P535T mutation is one such gene mutation that encodes the potassium ion channel (KV7.1) of the cardiac ventricular tissue. Its clinical significance is not known. This study aims to perform a simulation study on P535T mutation in the KCNQ1 gene that encodes the potassium ion channel KV7.1 in the ventricular tissue grid. The effect of P535T mutation on transmural tissue grids for three genotypes (wild type, heterozygous, and homozygous) of cells are studied and the generated pseudo-ECGs are compared. Results show the delayed repolarization in the cells of ventricular tissue grid. Slower propagation of action potential in the transmural tissue grid is observed in the mutated (heterozygous and homozygous) genotypes. Longer QT interval is also observed in the pseudo-ECG of heterozygous and homozygous genotype tissue grids. From the pseudo-ECGs, it is observed that KCNQ1 P535T mutation leads to Long QT Syndrome (LQTS) which may result in life-threatening arrhythmias, such as Torsade de Pointes (TdP), Jervell and Lange-Nielsen syndrome (JLNS), and Romano-Ward syndrome (RWS).

Automated classification of pediatric age from 12-lead ECG using deep residual convolutional neural networks

With increased interest in screening of young people for potential causes of sudden death, accurate automated detection of ventricular pre-excitation (VPE) or Wolff–Parkinson–White syndrome (WPW) in the pediatric resting ECG is important. Several recent studies have shown interobserver variability when reading screening ECGs and thus an accurate automated reading for this potential cause of sudden death is critical. We designed and tested an automated algorithm to detect pediatric VPE optimized for low prevalence.Digital ECGs with 12 leads or 15 leads (12-lead plus V3R, V4R and V7) were selected from multiple hospitals and separated into a testing and training database. Inclusion criterion was age less than 16 years. The reference for algorithm detection of VPE was cardiologist annotation of VPE for each ECG. The training database (n = 772) consisted of VPE ECGs (n = 37), normal ECGs (n = 492) and a high concentration of conduction defects, RBBB (n = 232) and LBBB (n = 11). The testing database was a random sample (n = 763). All ECGs were analyzed with the Philips DXL ECG Analysis algorithm for basic waveform measurements. Additional ECG features specific to VPE, mainly delta wave scoring, were calculated from the basic measurements and the average beat. A classifier based on decision tree bootstrap aggregation (tree bagger) was trained in multiple steps to select the number of decision trees and the 10 best features. The classifier accuracy was measured on the test database.The new algorithm detected pediatric VPE with a sensitivity of 78%, a specificity of 99.9%, a positive predictive value of 88% and negative predictive value of 99.7%.This new algorithm for detection of pediatric VPE performs well with a reasonable positive and negative predictive value despite the low prevalence in the general population.

Modulation of cytoskeleton in cardiomyopathy caused by mutation in LMNA gene.

Dilated cardiomyopathy caused by mutations in LMNA, encoding A-type lamins (i.e., LMNA cardiomyopathy), is characterized by a left ventricle enlargement and ultimately results in poor cardiac contractility associated with conduction disease. Despite current strategies to aggressively manage the symptoms, the disorder remains a common cause of sudden death and heart failure with decreased ejection fraction. Patients care includes cardioverter defibrillator implantation but the last therapeutic option remains cardiac transplantation. A-type lamins are intermediate filaments and are the main components of the nuclear lamina, a meshwork underlying the inner nuclear membrane, which plays an essential role in both maintaining the nuclear structure and organizing the cytoskeletal structures within the cell. Cytoskeletal proteins function as scaffold to resist external mechanical stress. An increasing amount of evidence demonstrates that LMNA mutations can lead to disturbances in several structural and cytoskeletal components of the cell such as microtubules, actin cytoskeleton and intermediate filaments. Collectively, this review focuses on the significance of these cytoskeletal modulators and emphasizes their potential therapeutic role in LMNA cardiomyopathy.

Changes in cardiac troponin I (cTnI), T (cTnT), and some biochemical parameters in Arabian racehorses after training

The aim of this study was to compare the changes in the content of cTnI, cTnT and some biochemical parameters (CK–MB, LDH, AST, ALT) in Arabian racehorses before and after training. Diagnosis of myocardial disease in horses is very difficult due to the lack of specific cardiac signs. Cardiac diseases are seen as a cause of sudden death or decreased performance in horses. It has also been reported that excessive exercise may cause transient myocardial damage. In our study, 20 healthy stallion Arabian racehorses aged 4–10 y (6.00 ± 0.52 y) were used. Five millilitres of blood was collected from the V. jugularis of clinically healthy horses into serum tubes before and after training. Training time was determined as 30 min for each horse. Pre-training cTnI, cTnT, CK–MB, LDH, AST, and ALT contents were determined to be 0.130 ± 0.01 ng/mL, 0.007 ± 0.00 ng/mL, 231.15 ± 8.96 U/L, 692.45 ± 34.12 U/L, 309.92 ± 18.48 U/L, and 11.83 ± 0.92 U/L, respectively. After training, cTnI, cTnT, CK–MB, LDH, AST, and ALT contents were determined to be 0.169 ± 0.01 ng/mL, 0.008 ± 0.00 ng/mL, 289.80 ± 10.96 U/L, 704.25 ± 22.03 U/L, 328.47 ± 19.58 U/L, and 15.24 ± 1.03 U/L, respectively. As a result, it was determined that exercise triggered myocardial damage to some extent in Arabian horses. Exercise stimulates troponin release and the differences that may occur in troponin tests in horses after exercise should be taken into consideration.

Variation circadienne et hebdomadaire de la mort subite d'origine cardiaque : registre autopsique du nord de la Tunisie

IntroductionSeveral studies have suggested a circadian and septadian pattern of incidence of sudden cardiac death with a morning peak and a Monday peak. ObjectiveTo analyze the circadian and septadian pattern of occurrence of sudden cardiac death in the eight northern Tunisian governorates. MethodsWe prospectively collected epidemiological and autopsy data of sudden cardiac death victims occurring in the northern region of Tunisia between January 2013 and December 2019. ResultsThe population included 1834 men (79.6%) and 468 women (20.4%) with a mean age of 56.5 ± 14 years. Smoking (53.9%) was the most prevalent cardiovascular risk factor. One-fifth (20.9%) of victims had known heart disease, and 3% had a family history of sudden death.ischemic heart disease was the leading cause of sudden death (46.8% of cases). One- fourth (25.7%) of autopsies were negative.Analysis of the circadian pattern of occurrence of sudden cardiac death identified a peak (36.1%, p < 0.001) between midnight and 6 am. This nocturnal excess mortality was significant (p < 0.001) and independent of sex (34.1 % in men and 43.8 % in women) and cause of death (39.3 % of cases of sudden ischemic death and 33.3 % of cases of nonischemic death).Moreover, there was a significant septadian variability in the occurrence of sudden death (p: 0.0015), with a peak on Friday (15.8 %, p: 0.042). ConclusionThis study showed a peak of sudden death between midnight and 6 am, and on Fridays, confirming the modification of the classic circadian and septadian pattern of sudden death occurrence. These results may help optimize the deployment of emergency mobile teams and structures during the most vulnerable periods.

DeepArr: An investigative tool for arrhythmia detection using a contextual deep neural network from electrocardiograms (ECG) signals

In the context of Cardiovascular Diseases, arrhythmia is one of the causes of sudden death, which is related to abnormal electrical activities of the heart that can be reflected by the electrocardiogram (ECG) which plays the main role in heart disease analysis. However, it is still a challenge to detect arrhythmia based on ECG basic characteristics because of the non-stationary nature of ECG signal even cardiologists faced challenges in arrhythmia diagnosis. Therefore, automatic arrhythmia detection-based ECG signals with height accuracy is a serious and indispensable task. Hence In this paper, we propose a new deep learning-based approach called “DeepArr” that uses a sequential fusion method to combine feed-forward and recurrent deep neural networks to exploit relevant features representation of arrhythmia from electrocardiograms (ECG) signals. A comprehensive experimental study has been made in this research, which shows that the proposed approach offers the most efficient tool for accurate classification and ranks top of the list of recently published algorithms on the MIT-BIH arrhythmia dataset. 10-fold cross-validation is carried out. The proposed DeepArr model achieved an accuracy, specificity, sensitivity, precision, and F1-score of 99.46%, 99.57%, 97.01%, 98.26%, and 97.63%, respectively. The proposed model provides a robust tool for the early detection of Arrhythmia.

Plasma Advanced Glycation End Products and Dicarbonyl Compounds Are Not Associated with Coronary Atherosclerosis in Athletes.

Coronary atherosclerosis is the leading cause of sudden death among athletes >35 yr old, but current cardiovascular risk prediction algorithms have not been validated for athletes. Advanced glycation end products (AGE) and dicarbonyl compounds have been associated with atherosclerosis and rupture-prone plaques in patients and ex vivo studies. The detection of AGE and dicarbonyl compounds might be a novel screening tool for high-risk coronary atherosclerosis in older athletes. Concentrations of three different AGE and the dicarbonyl compounds methylglyoxal, glyoxal, and 3-deoxyglucosone were measured in plasma with ultraperformance liquid chromatography tandem mass spectrometry in athletes from the Measuring Athletes' Risk of Cardiovascular Events 2 study cohort. Coronary plaques, plaque characteristics (calcified, noncalcified or mixed), and coronary artery calcium (CAC) scores were assessed with coronary computed tomography, and potential associations with AGE and dicarbonyl compounds were analyzed using linear and logistic regression. A total of 289 men were included (60 [quartiles 1-3 = 56-66] yr old, body mass index = 24.5 [22.9-26.6] kg·m -2 ), with a weekly exercise volume of 41 (25-57) MET-hours. Coronary plaques were detected in 241 participants (83%), with a dominant plaque type of calcified plaques in 42%, noncalcified plaques in 12% and mixed plaques in 21%. No AGE or dicarbonyl compounds were associated with total number of plaques or any of the plaque characteristics in adjusted analyses. Similarly, AGE and dicarbonyl compounds were not associated with CAC score. Concentrations of plasma AGE and dicarbonyl compounds do not predict the presence of coronary plaques, plaque characteristics or CAC scores, in middle-age and older athletes.

Thromboembolic complications of infectious endocarditis

Pulmonary embolism is understood as occlusion of the pulmonary arterial bed by blood clots. This is a common pathology, but it is difficult to judge the true frequency of this disease. This is primarily due to the asymptomatic course of the disease when the segmental pulmonary arteries are affected, the second reason is undiagnosed cases of pulmonary embolism even with its massive nature (in 40-70% of patients) or an erroneous interpretation of clinical manifestations and the resulting diagnosis of another pathology. In terms of mortality, pulmonary embolism ranks 3rd among the causes of sudden death after myocardial infarction and stroke.

Traumatic Brain Injury Induces Microglial and Caspase3 Activation in the Retina

Traumatic brain injury (TBI) is among the main causes of sudden death after head trauma. These injuries can result in severe degeneration and neuronal cell death in the CNS, including the retina, which is a crucial part of the brain responsible for perceiving and transmitting visual information. The long-term effects of mild-repetitive TBI (rmTBI) are far less studied thus far, even though damage induced by repetitive injuries occurring in the brain is more common, especially amongst athletes. rmTBI can also have a detrimental effect on the retina and the pathophysiology of these injuries is likely to differ from severe TBI (sTBI) retinal injury. Here, we show how rmTBI and sTBI can differentially affect the retina. Our results indicate an increase in the number of activated microglial cells and Caspase3-positive cells in the retina in both traumatic models, suggesting a rise in the level of inflammation and cell death after TBI. The pattern of microglial activation appears distributed and widespread but differs amongst the various retinal layers. sTBI induced microglial activation in both the superficial and deep retinal layers. In contrast to sTBI, no significant change occurred following the repetitive mild injury in the superficial layer, only the deep layer (spanning from the inner nuclear layer to the outer plexiform layer) shows microglial activation. This difference suggests that alternate response mechanisms play a role in the case of the different TBI incidents. The Caspase3 activation pattern showed a uniform increase in both the superficial and deep layers of the retina. This suggests a different action in the course of the disease in sTBI and rmTBI models and points to the need for new diagnostic procedures. Our present results suggest that the retina might serve as such a model of head injuries since the retinal tissue reacts to both forms of TBI and is the most accessible part of the human brain.

Scoping review of echocardiographic parameters associated with diagnosis and prognosis after resuscitated sudden cardiac arrest

AimCurrent international guidelines recommend early echocardiography after resuscitated sudden death despite limited data. Our aim was to analyze published data on early post-resuscitation echocardiography to identify cardiac causes of sudden death and prognostic implications. MethodsWe reviewed MEDLINE, EMBASE, and CENTRAL databases to December 2021 for echocardiographic studies of adult patients after resuscitation from non-traumatic sudden death. Studies were included if echocardiography was performed <48 hours after resuscitation and reported (1) diagnostic accuracy to detect cardiac etiologies of sudden death or (2) prognostic outcomes. Diagnostic endpoints were associations of regional wall motion abnormalities (RWMA), ventricular function, and structural abnormalities with cardiac etiologies of arrest. Prognostic endpoints were associations of echocardiographic findings with survival to hospital discharge and favorable neurological outcome. ResultsOf 2877 articles screened, 16 (0.6%) studies met inclusion criteria, comprising 2035 patients. Two of six studies formally reported diagnostic accuracy for echocardiography identifying cardiac etiology of arrest; RWMA (in 5 of 6 studies) were associated with presumed cardiac ischemia in 17–89% of cases. Among 12 prognostic studies, there was no association of reduced left ventricular ejection fraction with hospital survival (v10) or favorable neurologic status (n = 5). Echocardiographic high mitral E/e′ ratio (n = 1) and right ventricular systolic dysfunction (n = 2) were associated with poor survival. ConclusionThis scoping review highlights the limited data on early echocardiography in providing etiology of arrest and prognostic information after resuscitated sudden death. Further research is needed to refine the clinical application of early echocardiographic findings in post arrest care.

Assessment of Sudden Natural Deaths in Medico-Legal Autopsies at Tertiary Care Teaching Hospital

Background and Aim: Sudden natural death that occurred apparently to a healthy individual sometimescreates suspicions of foul play, thus subjected to medicolegal (ML) examinations. The study aims to assess thesociodemographic profile of the sudden natural death cases brought for medicolegal autopsy and identify thecommonest accountable cause of sudden natural death.Material and Methods: The study was conducted in the Department of Forensic Medicine, at tertiary care teachinghospital, India for the duration of 1 year. During the study period total of 784 cases were brought for medicolegalautopsies to mortuary, out of which 50 cases were found to be sudden natural death constituting an overall burdenof 6.37%. All the cases of autopsy having the opinion of natural death as a cause of death and cases brought deadin casualty without evidence of unnatural cause were included. The distribution of the cases concerning varioussociodemographic variables was presented as frequencies and percentages.Results: Male predominance was observed among the sudden death cases as out of 50 cases, 40 cases (80%) weremale, and 10 cases were female with a sex ratio of 4:1. Most of the cases were reported from the adult age groupand the commonly involved age group was 31 to 40 years. Among the causes of sudden death, the most involvedorgan system was the cardiovascular system (44%), followed by the gastrointestinal system (22%), respiratorysystem (18%), central nervous system (14%) and genitourinary system (2%).Conclusion: Cardiac causes are the most common cause of sudden natural death among the adult population inthe study site. Increased frequency of sudden deaths among urban, married and adult male populations might bedue to sedentary lifestyles in urban areas and increased stress among married individuals due to workload andfamily responsibilities, indicating a physical and mental disequilibrium in modern times resulting in this type ofunexpected deaths.

Zaživotno neprepoznat miokarditis kao uzrok iznenadne srčane smrti radnika službe dostave hrane

Introduction/Objective The COVID-19 pandemic enabled an increase in the use of food delivery apps and provided more work for delivery services, especially while the lockdown measures were in place. Many scientific papers have been written about epidemiological measures and the safety of delivered food in the prevention of COVID-19, but there is little research dedicated to the pressures suffered by delivery service workers and the health consequences that may have arisen due to their unregulated work status. We present the rare combination of difficult work conditions and myocarditis, which led to the sudden cardiac death of a food delivery worker. Case report The Emergency Medical Team (EMT) was dispatched to help a person lying in a corridor of a building showing no signs of life. Upon arrival at the scene, they found an approximately 30-40-year-old man lying on the ground near the entrance of the building next to his bicycle with a delivery bag still on his back. He was unconscious, with no breathing or pulse, and with no visible signs of injury. Information was obtained from bystanders about a delivery to the fifth floor of the building with no elevator, but there was no reliable information about the time of cardiac arrest. The initial rhythm was asystole, so the non-shockable rhythm cardiopulmonary resuscitation (CPR) protocol was immediately initiated. During CPR, two IV lines were opened, seven adrenaline injections were administered intravenously (IV), a 0.9% NaCl solution was initiated, and the airway was secured by placing an endotracheal tube. Despite all the efforts, the resuscitation measures were unsuccessful, and the patient was pronounced dead. Because the patient had died in a public place of an unknown cause, the police was notified, and the body was transferred to forensic pathology. The autopsy revealed no macroscopic changes in the myocardium, but pathohistology did reveal myocarditis. Since all this occurred during the COVID-19 pandemic, a PCR test was performed, which was negative. Toxicology findings revealed the presence of amphetamine and THC in traces, which were not thought to have affected the fatal outcome. Conclusion Myocarditis is an important but underrecognized cause of sudden death in young people, including delivery workers. Future research should be focused on adopting more precise criteria for myocarditis detection in such high-risk occupations.

PS-B02-5: NICORANDIL SUPPRESSES ISCHEMIA-INDUCED CARDIAC NOREPINEPHRINE ENHANCEMENT AND VENTRICULAR ARRHYTHMIAS IN PRESSURE OVERLOAD-INDUCED HYPERTROPHIC HEARTS.

Objective: Ventricular arrhythmias are a common cause of sudden death in acute myocardial infarction (MI) and hypertension is a major risk factor of MI. Nicorandil, an ATP sensitive potassium channel (KATP) opener, is usually used in the treatment of acute MI. KATP expresses in nerve terminals as well as cardiomyocytes and KATP in nerve terminals regulates norepinephrine release. The effects of nicorandil on ischemic myocyte are fully defined. On the other hand, the roles of nicorandil on ischemic norepinephrine release in hypertrophic cardiac tissue has remained unexplored. We examined whether nicorandil suppressed interstitial norepinephrine level and ventricular arrhythmia during acute ischemia in chronic pressure overload-induced hypertrophic hearts. Design and Methods: Rats were divided into two groups: abdominal aortic constriction (AAC) group and sham-operated (Sham) group. Four weeks after constriction, cardiac geometry and function were examined using echocardiography and hemodynamic measurements, and cardiac tissues were stained with hematoxylin and eosin and Sirius Red for histological examinations. In other rats, 4 weeks after constriction myocardial ischemia was induced by the left anterior descending artery occlusion for 100 minutes in the presence or absence of intravenous infusion of nicorandil. Cardiac interstitial norepinephrine concentration in ischemic region was measured using the microdialysis method. Ventricular arrhythmias were monitered by ECG during whole ischemic period. Results: Four weeks after constriction, remarkable left ventricular wall thickening and diastolic dysfunction were observed in AAC group. In histological examination, remarkable myocyte hypertrophy and interstitial fibrosis were observed in AAC group. Before ischemia, ventricular arrhythmia was not found in both groups. Number of ventricular arrhythmias, including ventricular tachycardia and ventricular fibrillation, was increased in early ischemic period (−20 min) in both groups, and was grater in AAC group. Before ischemia, interstitial norepinephrine concentration in cardiac tissue was higher level in AAC group than in Sham group, and ischemia increased norepinephrine concentration in both groups. Nicorandil administration in ischemic period significantly suppressed the number of ventricular arrhythmias and abolished the ventricular tachycardia and fibrillation without hemodynamic alterations in hypertrophic hearts. Nicorandil also attenuated epinephrine enhancement in acute ischemic period in hypertrophic hearts. Conclusion: Ischemia-induced ventricular arrhythmias were more frequent and severe in hypertrophic hearts and associated with high interstitial norepinephrine concentration. Nicorandil suppressed ischemia-induced interstitial norepinephrine release by neuronal KATP opening, which attenuated ventricular arrhythmias in pressure overload-induced hypertrophic hearts.

Seizure Prediction Analysis of Infantile Spasms.

Infantile spasms (IS) is a typical childhood epileptic disorder with generalized seizures. The sudden, frequent and complex characteristics of infantile spasms are the main causes of sudden death, severe comorbidities and other adverse consequences. Effective prediction is highly critical to infantile spasms subjects, but few related studies have been done in the past. To address this, this study proposes a seizure prediction framework for infantile spasms by combining the statistical analysis and deep learning model. The analysis is conducted on dividing the continuous scalp electroencephalograms (sEEG) into 5 phases: Interictal, Preictal, Seizure Prediction Horizon (SPH), Seizure, and Postictal. The brain network of Phase-Locking Value (PLV) of 5 typical brain rhythms is constructed, and the mechanism of epileptic changes is analyzed by statistical methods. It is found that 1) the connections between the prefrontal, occipital, and central regions show a large variability at each stage of seizure transition, and 2) 4 sub-bands of brain rhythms (θ, α, β, γ) are predominant. Group and individual variabilities are validated by using the Resnet18 deep model on data from 25 patients with infantile spasms, where the consistent results to statistical analyses can be observed. The optimized model achieves an average of 79.78 %, 94.46%, 75.46% accuracy, specificity, and recall rate, respectively. The method accomplishes the analysis of the synergy between infantile spasms mechanism, model, data and algorithm, providing a guideline to build an intelligent and systematic model for comprehensive IS seizure prediction.

Autopsy Study of Sudden Death Cases With Special Reference to Histopathological Changes in Heart

Background: Sudden cardiac death and arrhythmia accounts for 15 – 20% of all deaths. Though Coronaryartery disease is the major cause of sudden deaths, diagnosis of other underlying causes is necessary. Hence weintended to analyze the various cardiac causes related to sudden deaths and the associated histopathologicalfindings of heart.Methods: Present study was an autopsy based cross sectional observational study conducted at MaduraiMedical College mortuary for a period of one year. 100 cases of sudden deaths were subjected to autopsy andhistopathological changes of heart were studied.Results: In the present study, majority of cases belonged to the age group of 40 - 60 years with male preponderance.In histopathological examination, atherosclerosis was the most common finding with involvement of left anteriordescending artery. Other findings include myocardial infarction, myocarditis, pericarditis and dysarrythmogenicventricular hypoplasia. Multiple cardiac lesions were noted in few cases.Conclusion: An accurate diagnosis of the underlying morbidity at risk of sudden death either at postmortemor in living patients and life threatening arrhythmias is the pre – requisite to adopt therapeutic and preventivestrategies.