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Relevant bibliographies by topics / Cardiac death

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Academic literature on the topic 'Cardiac death'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "Cardiac death"

1

Basanets, A. V., T. A. Ostapenko, V. V. Cherkesov, and O. Y. Fartushna. "Sudden cardiac death at workplace." Ukrainian Journal of Occupational Health 2014, no. 2 (June 30, 2014): 13–20. http://dx.doi.org/10.33573/ujoh2014.02.013.

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Miller, Nichole. "Cardiac death vs. brain death." Nursing Made Incredibly Easy! 13, no. 2 (2015): 44–50. http://dx.doi.org/10.1097/01.nme.0000460361.65798.bc.

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&NA;. "Cardiac death vs. brain death." Nursing Made Incredibly Easy! 13, no. 2 (2015): 50–51. http://dx.doi.org/10.1097/01.nme.0000461306.30989.28.

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Das, Saikat, Soumeek Chowdhuri, and Ritwik Ghosh. "Biomarkers in Forensic Diagnosis of Sudden Cardiac Death (SCD)." Arab Journal of Forensic Sciences & Forensic Medicine 1, no. 9 (June 15, 2019): 1248–55. http://dx.doi.org/10.26735/16586794.2019.011.

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Arandjelovic, Aleksandra, Sinisa Pavlovic, Sanja Mazic, and Branimir Aleksandric. "Sudden cardiac death." Srpski arhiv za celokupno lekarstvo 132, no. 5-6 (2004): 194–97. http://dx.doi.org/10.2298/sarh0406194a.

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Sudden cardiac death in an athlete is rare and tragic event. An athlete's death draws high public attention given that athletes are considered the healthiest category of society. The vast majority of sudden cardiac death in young athletes is due to congenital cardiac malformations such as hypertrophie cardiomyopathy and various coronary artery anomalies. In athletes over age 35, the usual cause of sudden cardiac death is coronary artery disease. With each tragic death of a young athlete, there is a question why this tragedy has not been prevented. The American College of Sports Medicine and the American Heart Association recommend that a pre-participation exam should include a complete cardiovascular history and physical examination.

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Ro, Young Moo. "Sudden Cardiac Death." Journal of the Korean Medical Association 41, no. 3 (1998): 312. http://dx.doi.org/10.5124/jkma.1998.41.3.312.

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Kim, Nam-Ho, Kyeong Ho Yun, and Seok Kyu Oh. "Sudden Cardiac Death." Journal of the Korean Medical Association 53, no. 3 (2010): 214. http://dx.doi.org/10.5124/jkma.2010.53.3.214.

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Piantanida, Nicholas A., Ralph G. Oriscello, Frank A. Pettrone, and Francis G. OʼConnor. "Sudden Cardiac Death." Current Sports Medicine Reports 3, no. 2 (April 2004): 89–92. http://dx.doi.org/10.1249/00149619-200404000-00007.

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Lowbeer, Leo. "Sudden Cardiac Death." Southern Medical Journal 80, no. 11 (November 1987): 1467. http://dx.doi.org/10.1097/00007611-198711000-00040.

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Sheppard, MaryN. "Sudden cardiac death." Journal of the Practice of Cardiovascular Sciences 1, no. 2 (2015): 103. http://dx.doi.org/10.4103/2395-5414.166319.

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Dissertations / Theses on the topic "Cardiac death"

1

Murray, Anne-Marie. "Investigations into cardiac sudden death." Thesis, St George's, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252099.

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Wesslén, Lars. "Sudden Cardiac death in Swedish orienteers." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-632.

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An accumulation of sudden unexpected cardiac deaths (SUCD) occurred in young Swedish orienteers, most of whom were elite athletes. From 1979 to 1992 the incidence in 18 to 34 year old male elite orienteers ranked on the national level the same year as death was calculated to 30 (per 100,000), which represents a 20 to 40 fold increase from the expected rate. From 1989 to 1992, the incidence was 50. There were, however, no indications on any similar clusters of SUCD in other sports. A special program to alter behaviour in orienteers was implemented in 1992-1993, after which there have been no more cases of SUCD in orienteers below 35 years of age. A histopathological re-evaluation of 16 cases of SUCD revealed myocarditis in 75% of these cases. In parallel, four of those cases also had changes mimicing arrhythmogenic right ventricular cardiomyopathy (ARVC). The combination of an increased incidence and myocarditis suggested that infection may be a pathogenetic factor. A broad search for different microorganisms in archival sera from five cases and tissues from the autopsies in two of those cases revealed the only common finding that all had antibodies to Chlamydia pneumoniae. DNA from C. pneumoniae was detected in the lung and heart in one of two cases. The intimate contact with nature of orienteers suggested possible zoonotic/vectorborne pathogens. Bartonella is such a pathogen and known to cross-react with C. pneumoniae. The use of PCR to test for DNA from the gltA gene of Bartonella in the two formerly mentioned cases of SUCD, and in three additional cases, gave positive bands from the hearts in four cases and the lung in a fifth case. The PCR products were sequenced and found to be identical to B. henselae in three cases and almost identical to B. quintana in the remaining two cases. Four of the five cases had antibodies to Bartonella when using micro immunofluorescence test with the antigens B. henselae, B. quintana, and B. elizabethae. The total prevalence of antibodies to Bartonella was 31% in 1,136 elite orienteers vs. 6.8% in 322 healthy blood donors (p<0.001), suggesting widespread exposure in the elite. It is hypothesized that subacute or reactivated Bartonella infection has a pathogenetic role in SUCD in orienteers, and may be involved in the development of ARVC-like disease.

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Wesslén, Lars. "Sudden cardiac death in Swedish orienteers /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4986-7/.

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Roberts, Timothy Lloyd. "Linoleic acid and sudden cardiac death." Thesis, University College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281772.

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O'Mahony, C. "Sudden cardiac death in hypertrophic cardiomyopathy." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1408332/.

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Introduction: Hypertrophic cardiomyopathy (HCM) is an inherited myocardial disease associated with sustained ventricular arrhythmias and sudden cardiac death (SCD). Patients at high risk of SCD are currently identified by specific clinical characteristics, as outlined in an algorithm proposed by the American College of Cardiology and European Society of Cardiology in 2003. Patients at high risk of SCD are treated with Implantable Cardioverter Defibrillators (ICD), but the accuracy of the risk stratification algorithm, the long term outcome of ICD recipients and the nature of ventricular arrhythmias are unclear. Objectives: The aims of the thesis were to: a) characterise the electrophysiological nature of ventricular arrhythmias; b) determine long term outcomes post ICD implantation; c) validate the current risk stratification strategy; d) develop a novel clinical risk prediction model for SCD. Methods: Retrospective, observational cohort studies. Results: Monomorphic ventricular tachycardia is the most common ICD-treated ventricular arrhythmia (86%), and premature ventricular complexes are the most common electrical triggers (72%). ICD recipients had an appropriate shock rate of 2.3%/year (none suffered SCD), but experienced inappropriate shocks (4.6%/year), implant complications (5.1%/year) and heart failure death/transplantation (1.7%/year). Cox proportional hazards analysis showed that the risk of SCD increases with the aggregation of risk factors, but the current risk stratification strategy has poor discrimination (time dependent receiver operating characteristic curve c=0.64 at 5 years). An alternative clinical risk prediction model providing more individualised SCD risk estimates is proposed. The risk prediction model was externally validated in an Italian cohort (Harrell’s c=0.78; calibration slope: 0.82). Conclusions: The mode of initiation and morphology of ventricular arrhythmias suggest that underlying mechanism is re-entry. The current risk stratification strategy has limited predictive capabilities, and as a consequence the majority of ICD recipients do not receive appropriate shocks and are exposed to ICD related complications. The novel SCD risk prediction model offers an alternative approach by providing validated SCD risk estimates.

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Thomas, Nia Lowri. "Molecular mechanisms underlying cardiac ryanodine receptor dysfunction in sudden cardiac death." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/54084/.

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Ca²⁺ release via the cardiac ryanodine receptor (RyR2) is a fundamental event in excitation-contraction coupling. Point mutations in the gene encoding RyR2 are associated with arrhythmogenic right ventricular dysplasia type 2 (ARVD2), a disease likely characterised by abnormal release of Ca²⁺ that may result in sudden death. GFP-tagged RyR2 mutants (R¹⁷⁶Q/T²⁵⁰⁴M, L⁴³³P and N²³⁸⁶I) were generated and expressed in a human embryonic kidney (HEK) cell model, enabling profiling of the amplitude and temporal characteristics of caffeine-evoked Ca²⁺release through homotetrameric channels using confocal microscopy. Mutants were functionally heterogeneous and demonstrated profound differences in Ca²⁺ release when compared with WT channels, including the novel observation that one of the mutants (L⁴³³P) exhibited reduced sensitivity to caffeine activation. The molecular basis of this heterogeneity was investigated by determining the sensitivity of the mutant channels to cytoplasmic Ca²⁺. This was achieved by evaluation of caffeine-induced Ca²⁺ release from WT or mutants channels in streptolysin-O permeabilised HEK cells, where the cytoplasmic Ca²⁺ concentration was clamped. Although resting ER Ca²⁺store and cytoplasmic Ca²⁺ levels were comparable in all cells, RyR2 mutants were characterised by a profound loss of Ca²⁺-dependent inactivation. We also investigated whether these mutations disrupted the interaction between RyR2 and accessory proteins involved in normal channel function. cDNA encoding mutation susceptible regions were constructed and screened against a human cardiac cDNA library using a yeast two hybrid system. The N²³⁸⁶I mutation abolished association of the RyR2 domain with two cardiac proteins, which robustly occurred with the corresponding WT domain. These findings demonstrate that ARVD2-linked RyR2 mutations critically affect channel activation and suggest that differential sensitivity to cytoplasmic Ca²⁺ may be a causative mechanism in the pathogenesis of this disease.

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Yamada, Tetsu. "Impact of the cardiac arrest mode on cardiac death donor lungs." Kyoto University, 2015. http://hdl.handle.net/2433/200492.

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Dougherty, Cynthia Marie. "Recovery following sudden cardiac death during hospitalization /." Thesis, Connect to this title online; UW restricted, 1990. http://hdl.handle.net/1773/7284.

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Hookana, E. (Eeva). "Characteristics of victims of non-ischemic sudden cardiac death." Doctoral thesis, Oulun yliopisto, 2012. http://urn.fi/urn:isbn:9789526200224.

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Abstract A non-ischemic etiology of sudden cardiac death (SCD), mostly due to various cardiomyopathies (CMP), accounts for about 20% of all SCDs. Most of the major studies of risk factors for SCD have focused on coronary artery disease (CAD). The aim of the present study was to clarify the characteristics of non-ischemic SCD in Northern Finland. In this study, consecutive victims of SCD (n=2661) were prospectively collected, and among whom post-mortem examinations were performed between 1998 and 2007. Information about the SCD victims was obtained from a combination of available medical records, postmortem examination reports, medication used at the time of SCD, and standardized questionnaire filled out by the closest family members of the victims of SCD. We also screened the candidate genes from a Finnish family in which fatal arrhythmias was first manifestation of a cardiac disease. The collagen content of the myocardium from histological samples in victims of SCD due to idiopathic myocardial fibrosis (IMF) was also evaluated. CAD was the most common cause of death (2082 victims, 78.2%). The prevalence of non-ischemic SCDs was 21.8% of all the SCDs. After sub-grouping the non-ischemic SCDs into various categories, the most common cause of death was CMP related to obesity (23.7%), followed by alcoholic CMP (19.0%), hypertensive CMP (15.5%) and IMF (13.6%). The association of SCD with IMF is notably frequent among victims <40 years old (28.3%). The prevalence of family history of SCD was significantly higher in the victims of ischemic (34.2%) than non-ischemic SCD (13.4%, P<0.001) or controls (17.6%, P<0.001). Lamin A/C gene mutation R541C was found from Finnish SCD family, in which the IMF was predominant pathologic-anatomic finding. Myocardial type I collagen synthesis was increased in victims of SCD due to IMF. In conclusion, the characteristics of non-ischemic SCD in Finland differ from those reported previously. Higher prevalences of CMP-associated SCDs related to obesity, IMF and alcoholic CMP were observed as clinical and/or pathologic bases for non-ischemic SCD. The family history of SCD is not significantly increased in victims of non-ischemic SCD, suggesting a larger role of sporadic occurrence than inherited traits as the cause of non-ischemic SCD. Replacement of cardiac myocytes by fibrosis can be responsible for fatal cardiac arrhythmias in subjects with the lamin A/C gene mutation. The victims of SCD due to IMF have increased myocardial type I collagen synthesis
Tiivistelmä Ei-iskeeminen sydänperäinen äkkikuolema aiheuttaa noin 20 % kaikista sydänperäisistä äkkikuolemista. Suurin osa ei-iskeemisistä sydänperäisistä äkkikuolemista johtuu erilaisista sydänlihassairauksista, kardiomyopatioista. Useimmat sydänperäisen äkkikuoleman riskitekijöitä kartoittavista tutkimuksista ovat keskittyneet sepelvaltimotautiin. Tämän tutkimuksen tarkoituksena oli selvittää ei-iskeemisen sydänperäisen äkkikuoleman tunnuspiirteitä pohjoissuomalaisessa väestössä. Tutkimuksessa käytettiin potilasaineistona sydänperäiseen äkkikuolemaan menehtyneitä vainajia (n=2661), joille on tehty oikeuslääketieteellinen ruumiinavaus. Tiedot vainajista saatiin saatavilla olevista potilaskertomuksista, ruumiinavauspöytäkirjoista, äkkikuoleman aikaisesta lääkityksestä ja lähiomaisille lähetetystä standardisoidusta kyselylomakkeesta. Kandidaattigeenit tutkittiin pohjoissuomalaisesta perheestä, jossa ensimmäinen oire sydänsairaudesta oli hengenvaarallinen rytmihäiriö. Lisäksi sydänlihaksen kollageenikoostumus analysoitiin histologisista näytteistä potilailta, joiden sydänperäinen äkillinen kuolema johtui idiopaattisesta sydänlihaksen sidekudoskasvusta. Sepelvaltimotauti oli yleisin sydänperäisen äkkikuoleman aiheuttaja (n=2082, 78,2 %). Ei-iskeemisten sydänperäisten äkkikuolemien osuus oli 21,8 % (n=579) kaikista sydänperäisistä äkkikuolemista. Ei-iskeemiset sydänperäiset äkkikuolemat jaettiin alaryhmiin, joista yleisimmät olivat lihavuuteen assosioituva kardiomyopatia (23,7 %), alkoholikardiomyopatia (19,0 %), korkeaan verenpaineeseen assosioituva kardiomyopatia (15,5 %) sekä idiopaattinen sydänlihaksen sidekudoskasvu (13,6 %), joka myös oli yleisin ei-iskeemiseen sydänperäiseen äkkikuolemaan johtava syy alle 40-vuotiailla (28,3 %). Positiivinen sydänperäisen äkkikuoleman sukuhistoria oli tilastollisesti merkitsevästi yleisempää iskeemisillä (34,2 %) kuin ei-iskeemisillä (13,4 %) sydänperäisen äkkikuoleman uhreilla. Lamin A/C – geenin mutaatio löydettiin pohjoissuomalaisesta äkkikuolemaperheestä, jossa idiopaattinen sydänlihaksen sidekudoskasvu todettiin pääasialliseksi patologiseksi löydökseksi. Tyypin I kollageenin synteesi todettiin kohonneeksi idiopaattiseen sydänlihaksen sidekudoskasvuun menehtyneillä vainajilla. Yhteenvetona voidaan todeta, pohjoissuomalaisen väestön ei-iskeemisen sydänperäisen äkkikuoleman tunnuspiirteet eroavat aiemmin raportoiduista; lihavuuteen assosioituva kardiomyopatia, alkoholikardiomyopatia, sekä idiopaattinen sydänlihaksen sidekudoskasvu olivat aiempaa yleisempiä ei-iskeemisen äkkikuoleman aiheuttajia. Positiivinen sydänperäisen äkkikuoleman sukuhistoria ei ollut tilastollisesti merkitsevästi kohonnut ei-iskeemisen sydänperäiseen äkkikuolemaan menehtyneillä. Tämä tarkoittaa, että perinnöllinen syy ei-iskeemisen sydänperäisen äkkikuoleman aiheuttajana on luultua harvinaisempi. Lamin A/C – geenimutaation kantajilla sydänlihassolujen korvautuminen sidekudoksella todettiin hengenvaarallisen rytmihäiriön aiheuttajaksi. Lisäksi, tyypin I kollageenin synteesi todettiin kohonneeksi idiopaattiseen sydänlihaksen sidekudoskasvuun menehtyneillä vainajilla

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Jenkins, Micaela Maria. "The role of MAP4K4 in cardiac muscle cell death." Thesis, Imperial College London, 2018. http://hdl.handle.net/10044/1/62638.

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Mitogen-activated protein kinase kinase-kinase-kinase-4 (MAP4K4) is activated in failing human hearts and by apoptotic triggers in cultured cardiomyocytes and mouse hearts. Potent, highly selective inhibitors of human MAP4K4 were previously identified that protect against hydrogen peroxide (H2O2)-induced cell death in rat cardiomyocytes and human iPSC-derived cardiomyocytes (hiPSC-CMs), a newly emerging platform for improved target validation and cardiac drug development. Here, we investigate whether MAP4K4 activity influences mitochondrial function, contractility and calcium cycling in hiPSC-CMs using H2O2, menadione or doxorubicin as three inducers of reactive oxygen species (ROS). Human iPSC-CM metabolism was assessed using a Seahorse XF24 analyser to monitor oxygen consumption rate (OCR). Both exogenous (H2O2) and endogenous ROS (menadione) reduced mitochondrial respiration levels as measured by OCR. Pharmacological inhibition of MAP4K4 using three complementary inhibitors did not by itself affect mitochondrial function, demonstrating the lack of any potential adverse effect, and was at least partially protective against decreased mitochondrial function induced by H2O2 or menadione. Likewise, MAP4K4 inhibition protected against calcium cycling impairment by menadione, as measured by the % of wells with detectable calcium transients. To circumvent the limitations of using 2D cultures alone, human engineered heart tissue (hEHT) was also used, providing greater biochemical and functional maturity. None of the 3 MAP4K4 inhibitors altered spontaneous contraction frequency (beats per min, BPM) or force in hEHT. MAP4K4 inhibition was protective against menadione-induced cell death 24 after treatment, as measured by adenylate kinase (AK) release. Force, beating rate, time to peak contraction and time from peak to 80% relaxation were preserved for 24 hrs. These results identify MAP4K4 as a mediator of oxidative stress-induced cell death whose pharmacological inhibition preserves cell death, mitochondrial function and contractility in a human setting.

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Books on the topic "Cardiac death"

1

E, Josephson Mark, ed. Sudden cardiac death. Boston: Blackwell Scientific Publications, 1994.

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E, Josephson Mark, ed. Sudden cardiac death. Philadelphia: F.A. Davis Co., 1985.

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de Luna, A. Bayés, P. Brugada, J. Cosin Aguilar, and F. Navarro-Lopez, eds. Sudden Cardiac Death. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-009-0573-3.

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Priori, Silvia G., and Douglas P. Zipes, eds. Sudden Cardiac Death. Oxford, UK: Blackwell Publishing Ltd., 2005. http://dx.doi.org/10.1002/9781444312881.

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Antonio, Bayés de Luna, ed. Sudden cardiac death. Dordrecht: Kluwer Academic Publishers, 1991.

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Antonio, Bayés de Luna, and Guindo Soldevila J, eds. Sudden cardiac death. Armonk, N.Y: Futura Pub. Co., 1994.

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Delise, Pietro, and Paolo Zeppilli, eds. Sport-related sudden cardiac death. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-80447-3.

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Edwards, Brooks S., and Jesse E. Edwards, eds. Pathology of Sudden Cardiac Death. Malden, Massachusetts, USA: Blackwell Publishing, 2006. http://dx.doi.org/10.1002/9780470988480.

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Hackel, Donald B. Sudden death: Cardiac and other causes. Durham, N.C: Carolina Academic Press, 1993.

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J, Wang Paul, ed. Ventricular arrhythmias and sudden cardiac death. Malden, Mass: Blackwell Futura, 2008.

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Book chapters on the topic "Cardiac death"

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Soto, Ana Victoria, and William Whang. "Cardiac Death." In Encyclopedia of Behavioral Medicine, 370–71. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1249.

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Soto, Ana Victoria, and William Whang. "Cardiac Death." In Encyclopedia of Behavioral Medicine, 331. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1249.

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Soto, Ana Victoria, and William Whang. "Cardiac Death." In Encyclopedia of Behavioral Medicine, 1. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-6439-6_1249-2.

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Suvarna, S. Kim. "Sudden Cardiac Death." In Cardiac Pathology, 245–70. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2407-8_14.

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Suvarna, S. Kim. "Sudden Cardiac Death." In Cardiac Pathology, 277–311. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24560-3_14.

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Gomes, J. Anthony. "Sudden Cardiac Death." In Heart Rhythm Disorders, 241–53. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45066-3_17.

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Akhtar, Masood, Mohammad R. Jazayeri, Jasbir S. Sra, Zalmen Blanck, Sanjay Deshpande, Anwer Dhala, and Kathi Axtell. "Sudden Cardiac Death." In Implantable Cardioverter Defibrillator Therapy: The Engineering-Clinical Interface, 1–15. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-6345-7_1.

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Zipes, Douglas P., and Hein J. J. Wellens. "Sudden cardiac death." In Professor Hein J.J. Wellens: 33 Years of Cardiology and Arrhythmology, 621–45. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4110-9_60.

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Cipolletta, Laura. "Sudden Cardiac Death." In Clinical Cases in Cardiology, 311–24. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19926-9_27.

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Rasekh, Abdi, Mehdi Razavi, and Ali Massumi. "Sudden Cardiac Death." In Cardiovascular Medicine, 2039–83. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_101.

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Conference papers on the topic "Cardiac death"

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Canizares-Otero, M. C., R. Cabrera, M. A. Silberstein, D. P. High, M. Danckers, and S. Kathuria. "Double Defibrillation for Sudden Cardiac Death." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2837.

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Rodríguez, Eduardo, Claudia Lerma, Juan C. Echeverría, Jose Alvarez-Ramirez, Leonardo Dagdug, and Leopoldo Gracía-Colin S. "Intra-beat Scaling Properties of Cardiac Arrhythmias and Sudden Cardiac Death." In COMPLIFE 2007: The Third International Symposium on Computational Life Science. AIP, 2008. http://dx.doi.org/10.1063/1.2891416.

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Devi, Reeta, Hitender Kumar Tyagi, and Dinesh Kumar. "Early stage prediction of sudden cardiac death." In 2017 International Conference on Wireless Communications, Signal Processing and Networking (WiSPNET). IEEE, 2017. http://dx.doi.org/10.1109/wispnet.2017.8300112.

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Duval, A. J., and A. Berman. "Obstructive Sleep Apnea and Sudden Cardiac Death." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4601.

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Dagres, Nikolaos, and Robert van den Heuvel. "Cardiac magnetic resonance imaging improves prediction of post-MI sudden cardiac death." In The Annual Congress of the European Heart Rhythm Association 2022, edited by Michiel Rienstra. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/d4d68d85.

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Wu, Hui-Ching, Hua Ting, Ming-Hseng Tseng, Yu-Feng Shen, and Che-Chia Chang. "Mobile healthcare monitoring system for sudden cardiac death." In International Conference on Industrial Electronics and Engineering. Southampton, UK: WIT Press, 2014. http://dx.doi.org/10.2495/iciee140591.

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Glass, Leon. "“Understanding and preventing sudden cardiac death”." In 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4649064.

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Vanitha, L., G. R. Suresh, and C. JenefarSheela. "Sudden Cardiac Death prediction system using Hybrid classifier." In 2014 International Conference on Electronics and Communication Systems (ICECS). IEEE, 2014. http://dx.doi.org/10.1109/ecs.2014.6892677.

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Lopez-Caracheo, Francisco, Antonio Bazaldua Camacho, Carlos A. Perez-Ramirez, Martin Valtierra-Rodriguez, Aurelio Dominguez-Gonzalez, and Juan P. Amezquita-Sanchez. "Fractal Dimension-based Methodology for Sudden Cardiac Death Prediction." In 2018 IEEE International Autumn Meeting on Power, Electronics and Computing (ROPEC). IEEE, 2018. http://dx.doi.org/10.1109/ropec.2018.8661371.

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Zuxiang Fang, Dakun Lai, Xin Ge, and Xiaomei Wu. "Successive ECG telemetry monitoring for preventing sudden cardiac death." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5333088.

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Reports on the topic "Cardiac death"

1

Sergeant suffers sudden cardiac death during training - Kentucky. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, January 2006. http://dx.doi.org/10.26616/nioshfffacef200532.

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Fire fighter has sudden cardiac death during training - Texas. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, December 2001. http://dx.doi.org/10.26616/nioshfffacef200120.

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Lieutenant suffers sudden cardiac death after SCBA training - Florida. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, August 2006. http://dx.doi.org/10.26616/nioshfffacef200602.

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4

Corporal suffers sudden cardiac death at structure fire - Oklahoma. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, April 2010. http://dx.doi.org/10.26616/nioshfffacef201003.

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Lieutenant suffers sudden cardiac death after structure fire - Florida. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, September 2010. http://dx.doi.org/10.26616/nioshfffacef201020.

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6

Fire fighter suffers on-duty sudden cardiac death - Missouri. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, September 2011. http://dx.doi.org/10.26616/nioshfffacef201111.

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7

Captain suffers sudden cardiac death while on-duty - Tennessee. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, June 2013. http://dx.doi.org/10.26616/nioshfffacef201301.

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Senior captain suffers sudden cardiac death during training - Alaska. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, August 2014. http://dx.doi.org/10.26616/nioshfffacef201410.

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Sergeant suffers sudden cardiac death while on duty - Michigan. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, August 2016. http://dx.doi.org/10.26616/nioshfffacef201602.

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Fire fighter suffers sudden cardiac death after emergency recall - Massachusetts. U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, July 2004. http://dx.doi.org/10.26616/nioshfffacef200408.

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