Sudden Mortality Research Articles

Seizure-related autonomic changes in children.

Although sudden unexpected death in epilepsy is encountered less frequently in children versus adults, it is still an important direct epilepsy-related cause of death in this population. Just as in adults, the pathophysiology of sudden unexpected death in epilepsy in children is believed to involve seizure-related autonomic dysfunction. Seizures that develop during the pediatric period can be marked by some of the most dramatic alterations in autonomic functions seen at any age. This article reviews such seizure-related autonomic changes, including ictal nausea/emesis, hypersalivation, hypoxemia, apnea, tachycardia, bradycardia, cardiac repolarization anomalies, reduced heart rate variability, and postictal generalized EEG suppression. Understanding age-related changes in the autonomic effects of seizures and how they relate to risk of sudden death may help us to one day better elucidate the pathophysiology of sudden unexpected death in epilepsy. Given the high rate of sudden unexpected death in epilepsy in certain pediatric populations (such as those with Dravet syndrome), this knowledge is desperately needed.

Sudden cardiac death rates in an Australian population: a data linkage study.

The aim of the present study was to develop criteria to identify sudden cardiac death (SCD) and estimate population rates of SCD using administrative mortality and hospital morbidity records in Western Australia. Four criteria were developed using place, death within 24 h, principal and secondary diagnoses, underlying and associated cause of death, and/or occurrence of a post mortem to identify SCD. Average crude, age-standardised and age-specific rates of SCD were estimated using population person-linked administrative data. In all, 9567 probable SCDs were identified between 1997 and 2010, with one-third aged ≥ 35 years having no prior admission for cardiovascular disease. SCD was more frequent in men (62.1%). The estimated average annual crude SCD rate for the period was 34.6 per 100 000 person-years with an average annual age-standardised rate of 37.8 per 100 000 person-years. Age-specific standardised rates were 1.1 per 100 000 person-years and 70.7 per 100 000 person-years in people aged 1-34 and ≥ 35 years, respectively. Ischaemic heart disease (IHD) was recorded as the underlying cause of death in approximately 80% of patients aged ≥ 35 years, followed by valvular heart disease and heart failure. IHD was the most common cause of death in those aged 1-34 years, followed by unspecified cardiomyopathy and dysrhythmias. Administrative morbidity and mortality data can be used to estimate rates of SCD and therefore provide a suitable methodology for monitoring SCD over time. The findings highlight the magnitude of SCD and its potential for public health prevention.

Cell and Myofibril Contractile Properties of hiPSC-Derived Cardiomyocytes from a Patient with a MYH7 Mutation Associated with Familial Cardiomyopathy

Myosin heavy chain 7 (MYH7) mutations are associated with familial cardiomyopathies (FCM) and result in a high rate of sudden cardiac death. Human induced pluripotent stem cells derived cardiomyocytes (hiPSC-CMs) have recently shown promise as a model for studying FCM. We identified a cohort with familial cardiomyopathy (FCM) associated with a MYH7 mutation (E848G) and middle-age onset of systolic dysfunction and arrhythmias. hiPSC-CMs from patient affected (FCM-CMs) and non-affected (WT-CMs) individuals were generated from skin fibroblasts. Here we report, for the first time, contractile properties of isolated myofibrils from these cultured hiPSC-CMs for comparison using cultured cells and 3D engineered cardiac tissue (3D-ECT) constructs. Isolated myofibrils were obtained from differentiation day 20 hiPSC-CMs that were replated onto fibronectin-coated nanopatterned cover slides and matured in culture for an additional 60 days to obtain elongated and aligned myofibrils. This procedure produced hiPSC-CMs that were usually > 100+ µm in length. hiPSC- FCM-CMs and WT-CMs were harvested and skinned in a rigor solution containing 1% Triton and contractile properties of single or small bundles of myofibrils were measured in a custom built apparatus with rapid solution switching capabilities. During maximal calcium activation FCM-CM myofibrils produced approximately half the amount of force of WT-CM myofibrils, but preliminary data suggests no differences in the kinetics of force development or relaxation. This compares well with 50 day cardiomyocytes plated on nano-patterned surfaces or seeded into 3D-ECT constructs, where shortening and force (respectively) of FCM-CMs was much less than for WT-CMs, with no difference in calcium transient amplitudes. We speculate this early stage contractile deficit may contribute to disease development and conclude hiPSC-FCM-CMs can be a viable model for mechanical studies of cardiomyopathies in vitro.

Sudden cardiac death

Sudden cardiac death is one of the most common cause of mortality worldwide. Despite significant advances in the medical science, there is little improvement in the sudden cardiac death related mortality. Coronary artery disease is the most common etiology behind sudden cardiac death, in the above 40 years population. Even in the apparently healthy population, there is a small percentage of patients dying from sudden cardiac death. Given the large denominator, this small percentage contributes to the largest burden of sudden cardiac death. Identification of this at risk group among the apparently healthy individual is a great challenge for the medical fraternity. This article looks into the causes and methods of preventing SCD and at some of the Indian data. Details of Brugada syndrome, Long QT syndrome, Genetics of SCD are discussed. Recent guidelines on many of these causes are summarised.

The effects of tirofiban infusion on clinical and angiographic outcomes of patients with STEMI undergoing primary PCI.

Objective:The present study was designed to determine the effects of tirofiban (Tiro) infusion on angiographic measures, ST-segment resolution, and clinical outcomes in patients with STEMI undergoing PCI. Glycoprotein (GP) IIb/IIIa inhibitors are beneficial in ST-segment elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention (PCI), while the most effective timing of administration is still under investigation.Methods:A total of 1242 patients (83.0% males, mean (standard deviation; SD) age: 54.7 (10.9) years) with STEMI who underwent primary PCI were included in this retrospective non-randomized study in four groups, composed of no tirofiban infusion [Tiro (-); n=248], tirofiban infusion before PCI (pre-Tiro; n=720), tirofiban infusion during PCI (peri-Tiro; n=50), and tirofiban infusion after PCI (post-Tiro; n=224). In all Tiro (+) patients, bolus administration of Tiro (10 pg/kg) was followed by infusion (0.15 pg/kg/min) for a mean (SD) duration of 22.4±6.8 hours.Results:The pre-PCI Tiro group was associated with the highest percentage of patients with TIMI 3 flow (99.4%; p<0.001), the lowest corrected TIMI frame count [21(18-23.4); p<0.001], the highest percentage of patients with >75% ST-segment resolution (78.1%; p<0.001), and the lowest rate of in-hospital sudden cardiac death and in-hospital all-cause mortality (3.2%, p<0.05, 3.3%, p=0.01). Major bleeding was reported in 18 (1.8%) patients who received tirofiban.Conclusion:Use of standard-dose bolus tirofiban in addition to aspirin, high-dose clopidogrel, and unfractionated heparin prior to primary PCI significantly improves myocardial reperfusion, ST-segment resolution, in-hospital mortality rate, and in-hospital sudden cardiac death in patients with STEMI with no increased risk of major bleeding.

Effects of vitamin D and yeast extract supplementation on turkey mortality and clostridial dermatitis incidence in a dexamethasone immunosuppression model.

Clostridial dermatitis (CD) is a production disease of commercial turkeys that is characterized by sudden mortality in market-aged male birds and by lesions that include fluid and air bubbles under the skin of the thigh, breast, and tail area. We have developed a model for CD using dexamethasone (Dex) injection that suggests this disease may be related to stressors during the last stages of turkey production. Male turkeys were provided with control feed and water or with feed supplemented with a commercial yeast extract (YE) product, water supplemented with vitamin D (VD), or the combination. At 6, 11, and 15 wk of age birds were treated with three intramuscular injections of Dex over a 5-day period. Both YE and VD, but not the combination, decreased early mortality. At week 7 mortality was increased by VD, and cellulitis lesions were seen in 7/8 mortalities. Mortality at week 12 was decreased by both YE and the combination of YE and VD, and cellulitis lesions were seen in 8/17 mortalities. There were no significant differences in mortality at week 16. Total mortality was 66 birds, and 23 of these had cellulitis lesions (38%). There were no YE-treated birds with CD lesions; however, 67% of VD-treated birds had CD lesions. This study suggests that feed supplementation with YE may improve the ability of turkeys to withstand the stressors during late production and provide protection against the development of CD; however, high levels of VD supplementation may be detrimental.

Abstract 15915: Gender Matters in the Risk for Sudden Death in Young Competitive Athletes

Background: Sudden deaths in young competitive athletes are highly visible and tragic events, which receive much public visibility. However, little is known regarding the specific impact of gender on these events. Methods and Results: The U.S. National Registry of Sudden Death in Athletes was accessed to identify the causes, frequency and epidemiology of sudden deaths in U.S. competitive athletes by gender. A total of 2,408 deaths (2155 male; 253 female) were identified in athletes engaged in 41 diverse organized sports from 1980 to 2011. Most sudden deaths occurred with physical exertion during competition/training (66%), and were predominantly due to cardiovascular disease (54%). In high school and college athletes, accounting for participation rates, the ratio of male to female deaths was 5.4:1. Males were somewhat older than females (19±6 vs. 17.8±6; P=0.003), and were more commonly black (30% vs. 17%; P&lt;0.001). Of the male athletes, the highest rate of cardiovascular sudden death was in blacks (65% vs. 49% in whites; P&lt;0.001). The most frequent sports were football (n=725) and basketball (n=437) in males, and basketball (n=47) and cross country/track (n=41) in females. Most common cardiovascular cause of death was hypertrophic cardiomyopathy (HCM), which accounted for a greater proportion of confirmed cardiovascular deaths in males (47%) vs. females (14%; P&lt;0.001); a 19:1 male:female ratio in high school and college athletes. In contrast, females experienced greater frequency of death due to congenital coronary artery anomalies (30% vs. 14%; P&lt;0.001), arrhythmogenic right ventricular dysplasia (12% vs. 4%; P=0.018), and long-QT syndrome (7% vs. 1%; P&lt;0.001). Blunt trauma, including commotio cordis, occurred more frequently in males (24% vs. 15% in females; P=0.001). Conclusions: Female athletes have a 5-fold lower risk for sudden death, compared to males, and were almost 20-times less likely to die of HCM. Black males had the highest rate of sudden death due to cardiovascular disease, with HCM most common.

Abstract 16492: A Common Gene Network Governs the Cellular Phenotypes in Acute Aortic Dissection

Acute aortic dissection (AAD) is a common disease with sudden onset and high mortality, for which pathogenesis is largely unknown. To better understand AAD pathogenesis, we examined three mouse models of AAD; knockout mice for tenascin C, an extracellular glycoprotein that is secreted by vascular smooth muscle cells (VSMCs), macrophage-specific knockout of SOCS3 (mSOCS3-KO), a negative regulator of JAK/STAT signaling, and infusion of beta-aminopropionitrile, that blocks crosslinking of elastin and collagens. All of three models develop AAD upon the continuous infusion of angiotensin II (AngII). We performed transcriptome analyses at the early time point of AngII infusion when the aortic structure showed no obvious abnormality. Interestingly, the gene expression patterns showed common changes; induction of proinflammatory molecules and cell cycle machinery, and suppression of the structural extracellular matrix (ECM) and cytoskeletal molecules of VSMCs. Such a pattern is consistent with that in human AAD as previously reported. We performed detailed analysis in mSOCS3-KO. Bayesian network model revealed that upregulation of cell cycle machinery precedes other changes in the gene expression. Cell cycle analyses using Ki67 staining and BrdU uptake assay showed that AngII caused proliferative response before AAD development both in macrophages and in VSMCs, indicating the macrophage-VSMC interaction. In addition, the proliferative response of macrophages was associated with the preferential differentiation into the proinflammatory M1 phenotype as determined by the high expression of Ly6C. Our findings showed a gene expression network of AAD that is common to human and mouse models. The findings in mouse models suggest that cell cycle activation precedes both the proinflammatory response in macrophages and the functional deterioration of VSMCs, which in turn would weaken the aortic wall strength. In addition, tissue-specific knockout studies revealed that interactions between macrophages and VSMCs underlie the gene expression network in AAD. Deciphering such cellular interactions and gene expressions would lead to better understanding of this fatal disease.

Effects of cinacalcet on atherosclerotic and nonatherosclerotic cardiovascular events in patients receiving hemodialysis: the EValuation Of Cinacalcet HCl Therapy to Lower CardioVascular Events (EVOLVE) trial.

BackgroundPremature cardiovascular disease limits the duration and quality of life on long‐term hemodialysis. The objective of this study was to define the frequency of fatal and nonfatal cardiovascular events attributable to atherosclerotic and nonatherosclerotic mechanisms, risk factors for these events, and the effects of cinacalcet, using adjudicated data collected during the EValuation of Cinacalcet HCl Therapy to Lower CardioVascular Events (EVOLVE) Trial.Methods and ResultsEVOLVE was a randomized, double‐blind, placebo‐controlled clinical trial that randomized 3883 hemodialysis patients with moderate to severe secondary hyperparathyroidism to cinacalcet or matched placebo for up to 64 months. For this post hoc analysis, the outcome measure was fatal and nonfatal cardiovascular events reflecting atherosclerotic and nonatherosclerotic cardiovascular diseases. During the trial, 1518 patients experienced an adjudicated cardiovascular event, including 958 attributable to nonatherosclerotic disease. Of 1421 deaths during the trial, 768 (54%) were due to cardiovascular disease. Sudden death was the most frequent fatal cardiovascular event, accounting for 24.5% of overall mortality. Combining fatal and nonfatal cardiovascular events, randomization to cinacalcet reduced the rates of sudden death and heart failure. Patients randomized to cinacalcet experienced fewer nonatherosclerotic cardiovascular events (adjusted relative hazard 0.84, 95% CI 0.74 to 0.96), while the effect of cinacalcet on atherosclerotic events did not reach statistical significance.ConclusionsAccepting the limitations of post hoc analysis, any benefits of cinacalcet on cardiovascular disease in the context of hemodialysis may result from attenuation of nonatherosclerotic processes.Clinical Trials RegistrationUnique identifier: NCT00345839. URL: ClinicalTrials.gov.

The impact of triathlon training and racing on athletes' general health.

Although the sport of triathlon provides an opportunity to research the effect of multi-disciplinary exercise on health across the lifespan, much remains to be done. The literature has failed to consistently or adequately report subject age group, sex, ability level, and/or event-distance specialization. The demands of training and racing are relatively unquantified. Multiple definitions and reporting methods for injury and illness have been implemented. In general, risk factors for maladaptation have not been well-described. The data thus far collected indicate that the sport of triathlon is relatively safe for the well-prepared, well-supplied athlete. Most injuries ‘causing cessation or reduction of training or seeking of medical aid’ are not serious. However, as the extent to which they recur may be high and is undocumented, injury outcome is unclear. The sudden death rate for competition is 1.5 (0.9–2.5) [mostly swim-related] occurrences for every 100,000 participations. The sudden death rate is unknown for training, although stroke risk may be increased, in the long-term, in genetically susceptible athletes. During heavy training and up to 5 days post-competition, host protection against pathogens may also be compromised. The incidence of illness seems low, but its outcome is unclear. More prospective investigation of the immunological, oxidative stress-related and cardiovascular effects of triathlon training and competition is warranted. Training diaries may prove to be a promising method of monitoring negative adaptation and its potential risk factors. More longitudinal, medical-tent-based studies of the aetiology and treatment demands of race-related injury and illness are needed.Electronic supplementary materialThe online version of this article (doi:10.1007/s40279-014-0244-0) contains supplementary material, which is available to authorized users.

Sudden cardiac death in the young (5-39 years) in the canton of Vaud, Switzerland.

BackgroundSudden cardiac death (SCD) among the young is a rare and devastating event, but its exact incidence in many countries remains unknown. An autopsy is recommended in every case because some of the cardiac pathologies may have a genetic origin, which can have an impact on the living family members. The aims of this retrospective study completed in the canton of Vaud, Switzerland were to determine both the incidence of SCD and the autopsy rate for individuals from 5 to 39 years of age.MethodsThe study was conducted from 2000 to 2007 on the basis of official statistics and analysis of the International Classification of Diseases codes for potential SCDs and other deaths that might have been due to cardiac disease.ResultsDuring the 8 year study period there was an average of 292′546 persons aged 5-39 and there were a total of 1122 deaths, certified as potential SCDs in 3.6% of cases. The calculated incidence is 1.71/100′000 person-years (2.73 for men and 0.69 for women). If all possible cases of SCD (unexplained deaths, drowning, traffic accidents, etc.) are included, the incidence increases to 13.67/100′000 person-years. However, the quality of the officially available data was insufficient to provide an accurate incidence of SCD as well as autopsy rates. The presumed autopsy rate of sudden deaths classified as diseases of the circulatory system is 47.5%. For deaths of unknown cause (11.1% of the deaths), the autopsy was conducted in 13.7% of the cases according to codified data.ConclusionsThe incidence of presumed SCD in the canton of Vaud, Switzerland, is comparable to the data published in the literature for other geographic regions but may be underestimated as it does not take into account other potential SCDs, as unexplained deaths. Increasing the autopsy rate of SCD in the young, better management of information obtained from autopsies as well developing of structured registry could improve the reliability of the statistical data, optimize the diagnostic procedures, and the preventive measures for the family members.

Rationale and design of the Pan-African Sudden Cardiac Death survey: the Pan-African SCD study.

SummaryBackgroundThe estimated rate of sudden cardiac death (SCD) in Western countries ranges from 300 000 to 400 000 annually, which represents 0.36 to 1.28 per 1 000 inhabitants in Europe and the United States. The burden of SCD in Africa is unknown. Our aim is to assess the epidemiology of SCD in Africa.MethodsThe Pan-Africa SCD study is a prospective, multicentre, community-based registry monitoring all cases of cardiac arrest occurring in victims over 15 years old. We will use the definition of SCD as ‘witnessed natural death occurring within one hour of the onset of symptoms’ or ‘unwitnessed natural death within 24 hours of the onset of symptoms’. After appro val from institutional boards, we will record demographic, clinical, electrocardiographic and biological variables of SCD victims (including survivors of cardiac arrest) in several African cities. All deaths occurring in residents of districts of interest will be checked for past medical history, circumstances of death, and autopsy report (if possible). We will also analyse the employment of resuscitation attempts during the time frame of sudden cardiac arrest (SCA) in various patient populations throughout African countries.ConclusionThis study will provide comprehensive, contemporary data on the epidemiology of SCD in Africa and will help in the development of strategies to prevent and manage cardiac arrest in this region of the world.

Genetic and forensic implications in epilepsy and cardiac arrhythmias: a case series.

Epilepsy affects approximately 3% of the world's population, and sudden death is a significant cause of death in this population. Sudden unexpected death in epilepsy (SUDEP) accounts for up to 17% of all these cases, which increases the rate of sudden death by 24-fold as compared to the general population. The underlying mechanisms are still not elucidated, but recent studies suggest the possibility that a common genetic channelopathy might contribute to both epilepsy and cardiac disease to increase the incidence of death via a lethal cardiac arrhythmia. We performed genetic testing in a large cohort of individuals with epilepsy and cardiac conduction disorders in order to identify genetic mutations that could play a role in the mechanism of sudden death. Putative pathogenic disease-causing mutations in genes encoding cardiac ion channel were detected in 24% of unrelated individuals with epilepsy. Segregation analysis through genetic screening of the available family members and functional studies are crucial tasks to understand and to prove the possible pathogenicity of the variant, but in our cohort, only two families were available. Despite further research should be performed to clarify the mechanism of coexistence of both clinical conditions, genetic analysis, applied also in post-mortem setting, could be very useful to identify genetic factors that predispose epileptic patients to sudden death, helping to prevent sudden death in patients with epilepsy.

The consequences of contracting early and often

Frequent premature ventricular contractions (PVCs) are associated with structural heart disease and an increase in sudden and overall mortality. PVCs themselves, if in sufficient numbers, may be associated with the development of a reversible form of cardiomyopathy (CM). A number of small series have suggested that PVC density and features, such as QRS duration, location of origin, and coupling, may increase the predilection to cause CM in structurally normal and diseased hearts. Moreover, elimination of PVCs by catheter ablation has improved ventricular function. Thus, frequent PVCs are a previously underappreciated target for therapeutic intervention in CM. However, the fundamental triggers for the development of myopathy and the details of structural and electrical remodeling have been impeded by the development of a suitable model system. Pacing has been exploited to generate reversible forms of tachycardia-induced CM. Huizar et al have used a premature pacing algorithm to create a model of PVC-induced CM in structurally normal hearts. The algorithm generates a high PVC burden, in this case in a bigeminal pattern pacing from the right ventricular apex. PVC pacing increased the heart rate, on average, from 80 bpm to approximately 130 bpm over 4 months of pacing. Previous characterization of this model demonstrated reversible cardiac dilation and reduced ejection fraction with a compromise in repolarizing reserve evidenced by an increase in ventricular refractory periods. This occurred in the absence of inflammation, fibrosis, increased programmed cell death, or compromised oxidative phosphorylation. In a study reported in this issue of HeartRhythm, Wang et al describe heterogeneously prolonged action potential durations (APD) in myocytes isolated from the left ventricular free wall, associated with reductions in the transient outward (Ito) and inward rectifier (IK1) potassium currents without significant changes in the delayed rectifier (IKr, IKs) currents. The decrease in repolarizing reserve is associated

HEVEA BRASILIENSIS POISONING IN MALNAD GIDDA CATTLE, KARNATAKA, INDIA

Hevea brasiliensis , the rubber tree , is a tropical tree belonging to the family Euphorbiaceae , native to Amazon basin in Brazil and most economically important member of the genus Hevea , because of the milky latex extracted from the tree is the primary source of natural rubber . The young leaves of this tree are poisonous to most animals. In India it is fo und in areas where plantation is done for the commercial purpose. Hence poisoning in ruminants due to rubber tree is a rare phenomenon unless they have access to it. In the present investigation there were deaths of six adult Malnad G idda cattle in Hal e Ik keri village of Shimoga , Karnataka , India in a span of two days. An attempt has been made to know the cause of sudden mortality in Malnad Gidda Cattle. Post - mortem examination was conducted on carcasses and samples were collected for the detection of toxic principle, Hydrocyanic acid (HCN) by Picric acid paper spot test . The young rubber tree leaves showed positive for the presence of toxic principle HCN. HCN is one of the most potent, rapid - acting poisons known. When a lethal dose is consumed, animals die from asphyxiation in a few minutes. Deaths in animals due to HCN poisoning, can be reduced by administering with a mixture of sodium thiosulfate and methylene blue.

Eosinophilic coronary monoarteritis.

Eosinophilic coronary monoarteritis is an unfamiliar cause of acute myocardial ischemia. Most commonly, it presents as a left-sided chest pain or sudden death in middle-aged women with no traditional risk factors for coronary artery disease. Because the abrupt onset leaves almost no time for intervention, the symptoms readily lead to death, and most cases are diagnosed at necropsy. Dissection of the coronary artery wall with resultant occlusion of the lumen, which commonly affects the left anterior descending artery, is a consistent gross finding. An inflammatory infiltrate, which is predominantly composed of eosinophils in the tunica adventitia and tunica media and is often accompanied by a hematoma in between these 2 layers, is observed histologically. The etiology remains unclear, but an increase in the activity of eosinophils because of hormonal interactions during pregnancy has been suggested. Interplay of hormones is thought to culminate in the release of histolytic agents by the eosinophils, which initiate the dissection process. Currently, there is no specific treatment for eosinophilic coronary monoarteritis, but cyclophosphamide and prednisone have shown positive results in the treatment of spontaneous coronary artery dissection with unspecified periadventitial inflammation. Percutaneous coronary procedures have also resulted in favorable outcomes in a subset of patients. Because of the high, sudden death rate in eosinophilic coronary monoarteritis, deciphering the underlying pathophysiology of this almost invariably fatal disease remains both a challenge and a key to developing screening methods that will allow timely detection and thus treatment.

Need for a working classification system for sudden and unexpected infant deaths.

* Abbreviations: ICD-10 — : International Classification of Disease, Tenth Revision SIDS — : sudden infant death syndrome SUID — : sudden and unexpected infant death Since the 1980s, the rate of sudden infant death syndrome (SIDS) has declined worldwide1; this is largely attributed to “Back to Sleep” campaigns. However, concurrently, there have been increases in the rates of other sudden and unexpected infant deaths (SUIDs),2,3 and the overall SUID rate has not improved in the past decade.4 This “diagnostic shift” is partly due to standardization of, and improvement in, death scene investigations; many cases that would have been classified 20 years ago as SIDS ( International Classification of Disease, Tenth Revision [ICD-10] R95) are now being classified as accidental suffocation (ICD-10 W75) and, when there is uncertainty about the cause of death, ill defined (ICD-10 R99). While this diagnostic shift has been helpful in some respects, there is now a great deal of variability in, and confusion about, how these deaths are categorized. When an infant dies after rolling prone onto a pillow, when is the case an accidental suffocation death, and when is it SIDS? Depending on the jurisdiction in which the … Address correspondence to Rachel Moon, MD, Goldberg Center for Community Pediatric Health, Children’s National Medical Center, 111 Michigan Ave, NW, Washington, DC 20010. E-mail: rmoon{at}cnmc.org

84 Safety of Selective Early Discharge Following Transcatheter Aortic Valve Implantation

IntroductionTranscatheter Aortic Valve Implantation (TAVI) is being used increasingly in patients with severe symptomatic Aortic Stenosis (AS). There are few data on length of stay (LOS) in this elderly and...

Prediction of heart rate variability on cardiac sudden death in heart failure patients: A systematic review

Prediction of heart rate variability on cardiac sudden death in heart failure patients: A systematic review

Double‐edged effect of early reperfusion on arrhythmias and death after transient coronary artery occlusion in the rat (652.16)

Reperfusion of blood supply following a sustained period of ischemia can be injurious to the heart. Here, we monitored cardiac reperfusion in rats subjected to 10 min of wide‐area coronary artery occlusion (CAO) by injecting them with the Evans blue dye, a visible inert tracer. The rats were then divided into three groups depending on their rate of reperfusion. Group 1 consisted of rats that showed no signs of early reperfusion within the 10 min period of ischemia, and these rats demonstrated a moderate rate of sudden cardiac death within the ischemic period. Group 2 included rats that showed early signs of reperfusion, and these rats demonstrated a higher rate of cardiac death than those in Group 1. Rats in Group 3 had poor ligation such that they sustained partial reperfusion almost immediately post‐CAO, yet surprisingly, this group demonstrated highest rate of cardiac death during the ischemic period. In contrast to mortality during the ischemic period, rats that survived the first 10 min of ischemia then received ligation‐removal and thus full‐blown reperfusion. Interestingly, surviving rats from Group 3 now has best chance of continued survival post‐reperfusion, whereas rats from Group 2 had poor survival rate and no rats from Group 1 survived reperfusion. To better understand the pre‐conditioning effect of early reperfusion on full‐reperfusion‐mediated sudden cardiac death, we challenged rats to 5 min of small‐area CAO. This model produced 100% survival rate during the ischemic period, and therefore all rats survived to receive full‐reperfusion. In this model, rats from Group 1 demonstrated highest rate of sudden cardiac death after full‐reperfusion, whereas rats from Group 2 demonstrated higher rate of survival and all rats from Group 3 survived reperfusion. Taken together, early reperfusion of blood supply may induce sudden death of the ischemic heart, but if the heart survived this earlier attack, it becomes more resistant to full‐reperfusion‐mediated sudden cardiac death.Grant Funding Source: Supported by the National Science Council of Taiwan