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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 synthesisTiivistelmä 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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Leonard, Sam J. "Stress signalling to cardiac gene expression and cell death." Thesis, University of Reading, 2018. http://centaur.reading.ac.uk/78948/.
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Background: Cardiovascular diseases such as heart failure and myocardial infarction are associated with increased oxidative stress, the release of pro-inflammatory cytokines such as tumour necrosis factor-alpha (TNFα) and interleukin 1β (IL1β) and increased death of the contractile cardiomyocytes. Oxidative stress (exemplified by H2O2) is a pivotal modulator of the balance between the life and death of cardiomyocytes. H2O2 promotes cardiomyocyte apoptosis, induces substantial changes in gene expression and activates the three principal mitogen-activated protein kinase (MAPK) pathways (ERK1/2, JNKs and p38-MAPKs), which regulate gene expression in other cell types. However, the roles of the MAPK pathways in regulation of cardiomyocyte gene expression in response to H2O2 are yet to be reported. A further pathway that may play important roles cardiac survival vs death is regulated by the protein kinase, RIPK1. In non-cardiac cell types, TNFα signals via RIPK1 to cytoprotection or cell death, depending on the cellular environment. Polyubiquitinylated RIPK1 promotes cytoprotection through activation of NFκB, JNKs and p38-MAPKs while phosphorylation and activation of RIPK1 kinase activity is associated with induction of necroptosis, a novel regulated cell death modality. Hypotheses: The first hypothesis is that ERK1/2, JNKs and p38-MAPKs play substantial roles in regulation of cardiomyocyte RNA expression during cardiomyocyte apoptosis induced by H2O2. The second hypothesis is that RIPK1, which can signal to cytoprotection through NFκB and MAPKs, or to cell death by apoptosis or necroptosis, makes important contributions to mediating the balance between life and death of cardiomyocytes. Results: To dissect the roles of the MAPK pathways in the cardiomyocyte RNA expression response to H2O2, neonatal rat cardiomyocytes were untreated or exposed to H2O2 (0.2 mM, 2 h) with or without pre-treatment (15 min) with PD184352 (2 μM, inhibits ERK1/2 signalling), JNK-IN-8 (1 μM, inhibits JNKs) or SB203580 (0.7 μM, inhibits p38-MAPKα/β) or to the inhibitors alone (2 h 15 min). RNA expression profiles were determined using Affymetrix microarrays and GeneSpring software. PD184352 alone downregulated 92 and upregulated 32 RNAs, indicating that ERK1/2 influence basal gene expression. JNK-IN-8 and SB203580 affected expression of 14 and 6 RNAs, respectively. H2O2 upregulated 295, and downregulated 195 RNAs, of which 43% and 44%, respectively, were unaffected by any inhibitor. MAPK inhibitors affected the upregulation of 37% (PD184352), 25% (JNK-IN-8) or 28% (SB203580) RNAs, and affected the downregulation of 33% (PD184352), 28% (JNK-IN-8) or 35% (SB203580) RNAs. Microarray data for selected genes were validated using qPCR. To examine the roles of cardiac RIPK1, neonatal rat cardiomyocytes were exposed to various pathophysiological stimuli and extracts immunoblotted with antibodies to RIPK1. Proinflammatory cytokines (TNFα or IL1β) induced the appearance of reduced mobility RIPK1 bands within 5 – 15 min, consistent with phosphorylation but not ubiquitinylation. Further evidence of RIPK1 phosphorylation in response to IL1β was obtained using anion-exchange chromatography. Additionally, the p38-MAPKα/β inhibitor SB203580 attenuated the appearance of reduced mobility RIPK1 bands in response to IL1β, suggestive of a potential novel regulatory mechanism of RIPK1. Concentrations of H2O2 that promote apoptosis or necrosis (>0.2 mM) resulted in reduced mobility bands of RIPK1, maximal at 60 min. Reduced mobility bands of RIPK1 were also detected in adult male rat hearts perfused with H2O2 (0.2 mM, 60 min) or subjected to ischaemia-reperfusion. To explore the regulation of RIPK1 by phosphorylation and ubiquitinylation in cardiomyocytes, adenoviruses expressing exogenous FLAG-tagged wild type and mutant RIPK1 were produced. However, the exogenously expressed RIPK1 constructs appeared to undergo cleavage when expressed in cardiomyocytes. Conclusions: The three main MAPK pathways play substantial yet differential roles in the regulation of RNA expression in response to H2O2, with the greatest contribution by ERK1/2 and smaller roles for JNKs and p38-MAPKα/β. Furthermore, RIPK1 in neonatal cardiomyocytes or whole adult hearts exhibits reduced mobility in response to oxidative stress or pro-inflammatory cytokines, likely reflective of phosphorylation and potentially activation. Accordingly, RIPK1 may play important roles in modulating the balance of life vs death of cardiomyocytes. This response may, in part, be mediated by p38-MAPK signalling.
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Ellison, Georgina May. "Myocyte death and regeneration in cardiac and skeletal muscle." Thesis, Liverpool John Moores University, 2004. http://researchonline.ljmu.ac.uk/5638/.
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Roberts, Robert. "Discovery of a Gene Responsible for Sudden Cardiac Death ∗." ELSEVIER SCIENCE & TECHNOLOGY JOURNALS, 2017. http://hdl.handle.net/10150/623295.
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Shah, Lisa Lynn. "Family communication of genetic risk for sudden cardiac death." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/5629.
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Background: Hypertrophic Cardiomyopathy (HCM) and Long QT Syndrome (LQTS) are genetic cardiovascular diseases that cause sudden cardiac death. When an individual is diagnosed with an inherited disease such as HCM/LQTS it is critical that their biological relatives are notified of their increased risk. Newly diagnosed individuals in turn notify other at-risk family members through a successive process called cascade screening. This facilitates screening of at-risk biological relatives through genetic testing and/or clinical testing, and treatment for HCM/LQTS prior to development of life-threatening complications. However, for cascade screening to detect all potential cases the disease risk must be effectively communicated to all at-risk relatives. The responsibility for notifying family members of this risk largely falls to the first person diagnosed in the family (proband). Empiric evidence suggests that around half of at-risk relatives are not screened in accordance with cascade screening recommendations, potentially due to information about HCM/LQTS risk not being communicated effectively in their families. Factors have been identified that influence communication about genetic risk in families with non-cardiac disease; however, it is not known if or how these factors apply in families with genetic cardiac disease. These include network factors, which describe characteristics of relationships between family members and non-network factors, which describe characteristics of individuals including individual factors, disease factors, and sociocultural factors. There is a critical need to understand communication in families with HCM/LQTS in order to facilitate effective genetic risk communication in families, improve adherence to cascade screening recommendations, and prevent death and complications from cardiovascular diseases.
Objectives: The purpose of this study was to improve our understanding of the relationships among network and non-network factors and communication of genetic risk for HCM/LQTS between probands and their relatives. I proposed the following aims:
Aim 1: Describe family social network structures and communication paths about risk for HCM/LQTS from probands to their relatives.
Aim 2: Identify which network and non-network factors are associated with who is told about risk for HCM/LQTS.
Methods: The sample for this study included individuals with HCM or LQTS recruited through the University of Iowa Cardiology Clinics (UI) and the University of Wisconsin Inherited Arrhythmia Clinic (UW). Data were collected using a structured interview, family pedigree, and survey. Analysis included egocentric social network analysis, descriptive, bivariate, and multilevel logit regression modeling.
Results: Participants in this study had an average of 24 living at-risk relatives in their families. Overall, just over half (52%) of these at-risk relatives had been reported to have been told about their risk. However, within families, the percentage of relatives told about their risk ranged from 0%-100%. Ninety percent of first-degree relatives were told about their risk, 61% of second-degree relatives were told and 33% of third-degree relatives were told. Recruitment site affiliation was determined to be a confounder and so analyses were calculated separately for UI and UW. In both the UI and UW samples, network factors including closer geographic distance, increased emotional closeness, increased relationship quality, increased frequency of communication, higher betweenness centrality, and closer degree of biological relation were independently associated with increased odds of communication of risk.
In the UI sample, non-network factors that were independently associated with increased odds of communication of risk included younger age at diagnosis; having LQTS; having positive genetic test results; having an ICD; younger current age; being female; having increased role limitations due to physical functioning; feeling anxious about telling family members about risk; feeling communication was a burden; feeling that communication was a responsibility or duty; being happy to be able to share important information; and identifying financial issues, pregnancies, or upcoming marriages as playing a role in communication. In a multivariate model, increased frequency of communication, closer degree of biological relation, having an ICD, and identifying financial issues and pregnancies as contributors to communication were significantly associated with communication of genetic risk information.
In the UW sample, non-network factors that were independently associated with increased odds of communication of risk included younger age, decreased emotional wellbeing, increased role limitations due to emotional wellbeing, and decreased energy and fatigue. In a multivariate model, increased frequency of communication and closer degree of biological relation were significantly associated with communication.
Although over half of at-risk relatives were told about their risk, just over half of those (53.8%) were reported to have screened for disease, which represents 27% of all at-risk relatives. Of those tested, 35% were reported as diagnosed with HCM/LQTS.
Conclusion: Communication of genetic risk for HCM/LQTS in families is inadequate and contributes to the problem of relatives not being screened for disease. Insight on the factors that influence communication in families at risk of sudden cardiac death can guide development of interventions, policies, and future research aimed at improving genetic risk communication and cascade screening, and preventing death and complications from inherited cardiac diseases. This research is applicable for genetic conditions where population based screening methods are not effective and rely on families to communicate risk and need for screening.
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TAKAHASHI, AKIRA, YOSHIO HASHIZUME, and NOBUKO UJIHIRA. "A CLINICO-NEUROPATHOLOGICAL STUDY ON BRAIN DEATH." Nagoya University School of Medicine, 1993. http://hdl.handle.net/2237/15930.
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Wu, Ling. "Functional Characterization of SCN5A, The Cardiac Sodium Channel Gene Associated With Cardiac Arrhythmias and Sudden Death." Cleveland State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=csu1206732295.
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Femia, Giuseppe. "Cardiac Magnetic Resonance Imaging in the Diagnosis and Prognosis of Conditions Associated with Sudden Cardiac Death." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/25073.
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Cardiac magnetic resonance (CMR) provides advantages over other cardiac imaging modalities when evaluating conditions associated with sudden cardiac death. CMR provides high-quality, cross-sectional images that enable accurate anatomical delineation, precise and reproducible measurements of right ventricular volumes and robust identification of non-compacted myocardium. Despite this, the diagnosis and prognosis of some conditions associated with sudden cardiac death remain challenging or indeed uncertain. This has implications for not just the decedent but also surviving family members in whom imaging screening for cardiovascular conditions may be of benefit.
In this thesis, I assessed the ability of CMR to prognosticate patients with right ventricular abnormality and clinical suspicion of arrhythmogenic right ventricular cardiomyopathy (ARVC). Using our novel technique based on CMR signal intensity, I calculated left ventricular noncompacted mass and determined the correlation to long term outcomes. Finally, I evaluated the accuracy of post mortem CMR to identify causes of unexplained death, when compared to traditional autopsy, and its potential role in the coronial process.
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Stewart, Katy L. "Cardiac death in the young in Scotland : implications for screening." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5595/.
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Cardiovascular pre-participation screening in sport remains a controversial area. The general consensus is that it should be available given the increased risk of sudden cardiac death with exercise, but debate exists to the format of this screening. Part 1 of this thesis examines the incidence and epidemiology of death in young people to set the context; Part 2 evaluates the results of the Cardiac Assessment in Young Athletes (CAYA) programme in Scotland. Part 1 investigated a database of 41,049 deaths in those aged 0-35 years in Scotland from 1986-2008. Information such as location of death, whether a PM had taken place and cause of death was examined for all subjects with deaths categorised as those which occurred in-hospital or out-of-hospital and by age category and sex. Cardiac deaths (n=2084) were then investigated further. Analysis showed that the majority of deaths in young people in Scotland are due to accidents (27%), self-harm (16.2%) and cancers (11.8%). Coronary artery disease is the largest contributor of cardiac deaths in young people in Scotland (30%) with the greatest number occurring out-of-hospital (55.3%). Only a relatively small number of deaths (0.9% of total) were due to conditions that would be identified and potentially prevented by a cardiac screening programme. Part 2: The CAYA study was based on the Italian Model of screening by personal and family history, physical examination and resting 12-lead ECG, with the addition of an echocardiogram for all participants. Data was available for 1713 subjects from the CAYA study from October 2009-December 2012. Results showed a high incidence of hypertension in this young, athletic population, with a pilot study suggesting that this is likely to be 'white coat hypertension'. Screening with ECG identified 3 subjects with Wolff Parkinson-White syndrome and 1 with Long QT syndrome. Around 5% of subjects demonstrated left ventricular hypertrophy out with normal limits on echo (>13mm), but no structural abnormalities such as cardiomyopathy were diagnosed. Use of the ECG in cardiac screening remains controversial but these results suggest that, although the ECG is not a useful diagnostic tool for identifying those with left ventricular hypertrophy, it has a high negative predictive value meaning it can identify those without pathology. In conclusion, these results do not support the inclusion of echocardiography as a tool in cardiovascular screening in Scotland. The majority of cardiovascular deaths identified in this study were due to undiagnosed coronary heart disease which would not be identified by screening. Other causes of sudden cardiac death which may be identified by screening, such as familial arrhythmias and cardiomyopathies, are rare in Scotland. A screening service with ECG should be available to athletes and young people in Scotland but this should remain voluntary for those with symptoms or a positive family history. Improved first aid education and provision of defibrillators at sporting facilities would perhaps help to reduce the number of fatalities that occur in young athletes.
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Langen, Irene Marijke van. "Clinical genetic care in diseases predisposing to sudden cardiac death." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/88619.
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Martinez, Franco Ibeth Andrea. "Mechanism of cell death in cardiac myocytes exposed to doxorubicin." [Gainesville, Fla.] : University of Florida, 2006. http://purl.fcla.edu/fcla/etd/UFE0015730.
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Lee, Ming-tong Tony, and 李銘棠. "Detection of occult influenza infection in patients with sudden cardiac death." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738218.
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Lee, Ming-tong Tony. "Detection of occult influenza infection in patients with sudden cardiac death." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40738218.
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Aro, A. (Aapo). "Electrocardiographic risk markers of sudden cardiac death in middle-aged subjects." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526201795.
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Abstract Sudden cardiac death (SCD) is a major medical and public health concern responsible for 50% of cardiovascular deaths and as much as 15% to 20% of overall mortality. Coronary heart disease is the underlying cause of most of these deaths, and in 50% of such cases, SCD is the first manifestation of the disease. Researchers have investigated numerous noninvasive methods to more accurately identify individuals at high risk of SCD, but most such studies have focused on patients with specific heart disease. The standard 12-lead electrocardiogram (ECG) is a widely available tool to analyze the electrical activity of the heart, but few epidemiological studies have successfully identified specific electrocardiographic risk markers of SCD at the population level. This thesis aims to clarify the prognostic implications of several ECG patterns in the general population. We evaluated the 12-lead ECGs of 10899 middle-aged Finnish subjects (52% male) recorded between 1966 and 1972, and followed the subjects for 30 ± 11 years. The prevalence of a prolonged QRS duration ≥ 110 ms and nonspecific intraventricular conduction delay (IVCD; defined as QRS ≥ 110 ms with no partial or complete bundle branch block) in the population was 1.3% and 0.6%, respectively. Both were significantly associated with an elevated risk of all-cause mortality and cardiovascular mortality. QRS duration ≥ 110 ms doubled the risk of SCD, and IVCD was associated with a three-fold higher risk of SCD. Two percent of the subjects presented with wide frontal QRS-T angle ≥ 100° (the angle between the QRS axis and the T-wave axis in the frontal plane). A wide QRS-T angle was associated with higher overall mortality and more than doubled the risk of SCD, which was mainly due to an abnormal T-wave axis. Inverted T-waves in the right precordial leads (V1–V3) or beyond were present in 0.5% of the population. No increase in mortality or SCD was associated with right precordial T-wave inversions. In contrast, inverted T-waves in other leads than V1–V3 were associated with higher risk of cardiovascular mortality and SCD. Altogether 2.1% of the study participants presented with a prolonged PR interval > 200 ms. No rise in overall mortality, SCD, or hospitalizations due to heart failure, atrial fibrillation, or stroke was observed among these subjects during the follow-up period. In conclusion, of the electrocardiographic parameters studied, prolonged QRS duration, IVCD, and wide QRS-T angle are associated with SCD in the general population, and such changes in an ECG should therefore alert the physician to more closely evaluate and follow the patient. On the other hand, a prolonged PR interval and right precordial T-wave inversions seem to have no prognostic implications in the absence of other features suggestive of underlying heart diseaseTiivistelmä Sydänperäinen äkkikuolema on yleisin kuolinsyy länsimaissa, missä puolet sydänkuolemista ja 15–20 % kokonaiskuolleisuudesta johtuu äkillisestä sydänpysähdyksestä. Sepelvaltimotauti on yleisin taustalla oleva syy, ja jopa puolessa sepelvaltimotautikuolemista äkkikuolema on taudin ensimmäinen oire. Jo pitkään on yritetty kehittää menetelmiä, joilla voitaisiin tunnistaa suurimmassa äkkikuoleman vaarassa olevat. 12-kanavainen EKG on laajalti käytössä oleva tutkimus, jolla tutkitaan sydämen sähköistä toimintaa, mutta sydänperäistä äkkikuolemaa spesifisti väestössä ennustavia EKG-poikkeavuuksia ei ole juuri pystytty osoittamaan. Tämän väitöskirjatyön tarkoituksena oli tutkia, miten EKG:ssä nähtävät ilmiöt kuten QRS kompleksin kesto, QRS-kompleksin ja T-aallon välinen kulma, kääntyneet T-aallot sekä PR-aika korreloivat ennusteeseen väestötasolla. Tutkimme 10899 suomalaisen keski-ikäisen henkilön (52 % miehiä) EKG:t, jotka oli rekisteröity 1966–1972, ja seurasimme tutkittavia keskimäärin 30 (± 11) vuotta. Leventynyt QRS kompleksi ≥ 110 ms löytyi 1.3 %:lta ja epäspesifi kammionsisäinen johtumishäiriö eli IVCD (QRS ≥ 110 ms ilman osittaista tai täydellistä haarakatkosta) 0.6 %:lta tutkituista. Molemmat muutokset liittyivät lisääntyneeseen kokonaiskuolleisuuteen sekä sydänkuoleman riskiin. QRS kompleksin kesto ≥ 110 ms assosioitui lisäksi kaksinkertaiseen ja IVCD kolminkertaiseen äkkikuolemariskiin. 2 %:lla tutkituista sydänlihaksen depolarisaation suuntaa kuvaavan QRS-kompleksin akselin ja repolarisaatiota kuvaavan T-aallon akselin välinen frontaalitason QRS-T kulma oli leveä ≥ 100°. Näillä henkilöillä kokonaiskuolleisuus oli lisääntynyt, ja sydänperäisen äkkikuoleman riski oli yli kaksinkertainen verrattuna henkilöihin jolla QRS-T kulma oli < 100°. Oikeanpuoleisissa rintakytkennöissä V1–V3 todettiin negatiiviset T-aallot 0.5 %:lla tutkituista, mutta näillä ei ollut vaikutusta kuolleisuuteen. Sen sijaan henkilöillä, joilla todettiin negatiiviset T-aallot muissa kytkennöissä, oli yli kaksinkertainen sydänkuoleman ja äkillisen sydänpysähdyksen vaara muihin tutkittuihin verrattuna. Osallistujista 2.1 %:lla todettiin pidentynyt PR-aika > 200 ms. Tämä ei kuitenkaan vaikuttanut henkilöiden kuolleisuuteen eikä sydämen vajaatoiminnasta, eteisvärinästä tai aivoverenkiertohäiriöistä johtuvien sairaalahoitojen määrään. Tutkituista EKG:n poikkeavuuksista siis pidentynyt QRS-kompleksin kesto, IVCD ja leveä QRS-T kulma liittyvät selvästi lisääntyneeseen äkillisen sydänpysähdyksen riskiin. Sen sijaan pidentynyt PR-aika tai T-inversiot oikeanpuoleisissa rintakytkennöissä ilman muuta viitettä sydänsairaudesta eivät vaikuta ennusteeseen keski-ikäisessä väestössä
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Kalynych, Sergei. "Exploring the non-death function of caspase activity during cardiac hypertrophy." Thesis, University of Ottawa (Canada), 2009. http://hdl.handle.net/10393/28061.
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Various pathological conditions that exert stress on cardiac muscle severely compromise the supply of oxygenated blood to peripheral tissues. To maintain steady cardiac output during adverse times, the myocardium is forced to undergo tissue remodeling in a process known as cardiac hypertrophy. The loss of cardiac myocytes during the transition to heart failure has been a subject of intense investigation, and this loss is hypothesized to originate from apoptosis/programmed cell death. In particular, caspase proteases have been implicated as primary components in this process. However, caspase activity has been linked to many cellular remodeling events independent of inducing cell death. Therefore, the possibility that alterations in caspase activity precipitate the cellular alterations that give rise to pathological cardiac hypertrophy was investigated in the current study:
Using cultures of primary neonatal cardiomyocytes and a combination of pharmacological and biological inhibitors it is demonstrated that: (a) Physical growth of a myocyte is not dependant on activity of the apoptotic caspases; (b) Caspase activity is not necessary for the transcriptional control of natriuretic peptide production (ANF and BNP); (c) Transcriptional activity of a general stress-responsive transcription factor Nf-kB is dependent on caspase enzymatic activity in the neonatal cardiomyocyte.
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Day, Christopher Paul. "The QT interval revisited : implications for arrhythmias and sudden cardiac death." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308764.
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Robey, Thomas Edwin. "Reducing fibrosis and cell death in cardiomyoplasty /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8031.
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Levin, Noah Michael. "The Role of Death in The Moral Permissibility of Solid Organ Procurement After Cardiac Death and Its Implications." Bowling Green State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1383308740.
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Major, Jennifer Lynn. "E2F6: A Unique Regulator of Post-natal Cardiac Growth, Death, and Function." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36014.
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Rationale/Background: The adult mammalian heart has a very limited potential for regeneration due to cardiomyocyte cell cycle withdrawal which occurs shortly after birth. One potential avenue to repair the heart following stress/injury is to reprogram pre-existing cardiomyocytes to re-enter the cell cycle. The E2F family is a group of transcription factors which ubiquitously regulate the cell cycle, but it has previously been difficult to fully appreciate their role in the post-natal myocardium due to either redundancy or embryonic lethality of genetic models. Thus we generated a dominant negative model of the E2F/Rb pathway via expression of the unique transcriptional repressor E2F6 in postnatal myocardium. E2F6 transgenic (Tg) mice developed dose dependent Dilated Cardiomyopathy (DCM) and sudden death without hypertrophy or apoptosis. This was accompanied by the partial loss of E2F3 (critical for cardiac development) and connexin-43 important for metabolic and electrical coupling.
Methods/Results: In this thesis E2F6-Tg mice were examined for markers of cardiac differentiation/ function and exposed to stressors to evaluate the capacity for the E2F pathway to regulate cardiomyocyte growth (isoproterenol) and death (doxorubicin and cobalt chloride). E2F6-Tg mice were twice as sensitive to isoproterenol as their Wt counterparts due to the observed activation of a β2-adrenergic survival pathway. Cardiac hypertrophy in E2F6-Tg mice was accompanied by the rescue of E2F3 expression. Treatment of neonatal cardiomyocytes isolated from Wt and E2F6-Tg pups with cobalt chloride revealed a protective effect for E2F6 against apoptosis. Doxorubicin exposure led to the loss of E2F6 protein and abolished its protective effect. Examination of neonatal hearts and cardiomyocytes isolated from them demonstrated a shift in the cell cycle and metabolic profiles of E2F6-Tg myocardium. Tg cardiomyocytes show decreased glycolysis and a dramatic increase in the regulator of ketolysis, β-hydroxybutyrate dehydrogenase (BDH1), prior to DCM. The substrate of BDH1 (β-hydroxybutyrate) was demonstrated to influence the levels of CX-43 in cardiomyocytes. E2F6 also deregulated expression of T-cap which has been linked to human DCM.
Conclusions: I provide evidence that the E2F pathway can regulate growth, death, and differentiation through a variety of mechanisms which link the cell cycle and metabolism to growth and survival to critically govern post-natal cardiac function. Furthermore, I reveal a new biomarker (BDH1) for early DCM which may be useful in diagnosis/ treatment of idiopathic cases of disease.
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Wilson, Mathew. "Athletes' heart and exercise related sudden cardiac death : across the age span." Thesis, University of Wolverhampton, 2010. http://hdl.handle.net/2436/122548.
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Background - Regular exercise reduces the risk of cardiovascular disease and subsequent sudden cardiac death (SCD). However, a small, but notable proportion of athletes die suddenly due to inherited or congenital disorders of the heart that predispose to malignant ventricular arrhythmias. Such tragedies are highly publicised, particularly when high-profile athletes are involved. To date, limited evidence for the efficacy of cardiovascular pre-participation screening exists outside of the Italian experience. Furthermore, limited data exists examining the impact of ethnicity on cardiac adaptations to physical training. Whilst the cardiovascular benefits of exercise are well known, the impact of life-long endurance exercise is less well understood. Long term high-intensity endurance exercise is associated with changes in cardiac morphology together with electrocardiographic alterations that are believed to be physiologic in nature. Recent data however, has suggested a number of deleterious adaptive changes in cardiac structure, function and electrical activity in response to life-long endurance activity. Aims and Objectives - The aims of this PhD were; 1) To find an effective preparticipation screening method that would successfully identify pre-existing cardiovascular abnormalities, 2) To identify the prevalence of hypertrophic cardiomyopathy and Long QT syndrome in elite UK athletes; 3) To examine the impact and significance of ethnicity upon left ventricular remodelling in elite athletes, and 4) To examine the acute and chronic impact of ultra-endurance exercise across the life-span in male endurance athletes. Major Results and Conclusions – 1) Study 2 sought to confirm the efficacy of resting 12-Lead ECG ‘alongside’ personal/family history questionnaires and physical examinations as collective tools to identify diseases that have the potential of causing sudden death within a cohort of elite junior athletes (n=1074) and physically active school children (n=1646). Nine participants were identified with a positive diagnosis of a disease associated with SCD. None of those diagnosed with a disease associated with SCD were symptomatic or had a family history of note. Thus, personal symptoms and family history questionnaires alone are inadequate in the identification of individuals with diseases associated with SCD. In conclusion, resting 12-Lead ECG is paramount when screening for diseases that have the potential of causing sudden death in the young. 2) Study 3 examined 3,500 asymptomatic elite athletes (75% male) with a mean age of 20.5 ± 5.8 years with 12-lead ECG and 2-dimensional echocardiography. None had a known family history of HCM. Of the 3,500 athletes, 53 (1.5%) had LVH (mean 13.6 ± 0.9mm, range 13 to 16mm), and of these 50 had a dilated LV cavity with normal diastolic function to indicate physiological left ventricular hypertrophy. Three (0.08%) athletes with LVH had a non-dilated LV cavity and associated deep T-wave inversion that could have been consistent with HCM. However, none of the 3 athletes had any other phenotypic features of HCM on further non-invasive testing and none had first-degree relatives with features of HCM. In conclusion, the prevalence of HCM in elite athletes is significantly less than in the general population; with the demands of strenuous exercise on the cardiovascular system selecting out most individuals with HCM. Study 4 examined 2000 elite athletes in order to identify the prevalence of Long QT syndrome. Three athletes had a QTc value of >500 ms and all exhibited one of: paradoxical prolongation of QTc during exercise, a confirmatory genetic mutation, or prolonged QTc in a first-degree relative. In contrast, none of the athletes with a QTc value of <500 ms had any other features to indicate LQTS. Accordingly, the prevalence of a prolonged QTc interval in elite British athletes is 0.4%. 3) Study 6 examined 300 nationally ranked UK black male athletes (mean age 20.5 years) in comparison to 150 black and white sedentary individuals and 300 highly-trained white male athletes. Black athletes exhibited greater LV wall thickness and cavity size compared with sedentary black and white individuals. Black athletes had greater LV wall thickness compared with white athletes. A minority of black athlete’s exhibit LVH ≥15 mm; proposing that in the absence of cardiac symptoms or a family history of HCM, an LV wall thickness ≥15 mm in black athletes may represent physiologic LVH when the LV cavity is enlarged and diastolic indexes are normal. 7 black athletes (12%) with LVH displaying deep T-wave inversions in leads V1 to V4. In conclusion, in the absence of obvious pathology, these electrical anomalies in black athletes likely represent a normal spectrum of ECG changes in response to physical training. 4) Study 8 examined 17 male participants (age 33.5 ± 6.5 years, 26–40 years) using cardiac magnetic resonance (CMR) and echocardiography before and after a marathon to investigate the relationship between systolic function and diastolic function against biomarkers of cardiac damage. Results demonstrates biomarkers of myocardial cell damage following an acute bout of prolonged exercise are not associated with either systolic or diastolic functional measures, and do not seem to be associated with any detectable myocardial inflammation, oedema, or scarring using either gold standard techniques of gadolinium enhanced CMR or echocardiography respectively. The impact of multiple episodes of prolonged exercise, as experienced by highly trained veteran endurance athlete is not fully understood. 5) Study 10 examined the cardiac structure and function of 12 life-long, competitive endurance veteran athletes (> 50 yrs, mean ± SD marathons 178 ± 209 (range 20 – 650)) against 17 young male endurance athletes (<40 yrs) using echocardiography and CMR with late gadolinium enhancement (LGE) to assess myocardial fibrosis. Lifelong veteran athletes had smaller LV and RV end-diastolic and end-systolic volumes (p<0.05) but maintained LV and RV systolic function compared with young athletes. In 6 (50%) of the veteran athletes LGE of CMR indicated the presence of myocardial fibrosis; no LGE in the young athletes. The prevalence of LGE in veteran athletes was not associated with the number of competitive marathons or ultra-endurance marathons (>50 miles) completed, age, LV and RV end-diastolic volumes or LV mass (p>0.05). In conclusion, there is limited evidence at present demonstrating that cardiovascular re-modelling following lifelong endurance exercise leads to long-term disease progression, cardiovascular disability or SCD.
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Rosengarten, James A. "Risk stratification in sudden cardiac death : engineering novel solutions in heart failure." Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/407449/.
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Sudden cardiac death (SCD) risk is reduced by implantable cardioverter defibrillator (ICD) use in appropriately selected patients. Established markers such as impairment of left ventricular function and QRS duration are non specific for arrhythmic death and therefore many patients receive ICD therapy from which they gain no benefit, either due to survival without arrhythmia or death from pump failure. Both myocardial scar and serum protein biomarkers have potential as SCD risk stratifiers, but novel solutions are needed to deliver non invasive tests that are suitable for point of care testing. The aims of this thesis were to explore novel assessment methods for the risk stratification of SCD, with particular focus on heart failure. Several approaches were chosen to explore these concepts: (i) meta-analysis to assess the utility of fragmented QRS, (ii) retrospective evaluation of ECG and CMR to assess ECG markers of repolarisation and (iii) QRS scoring, (iv) prospective evaluation of an automated QRS scoring algorithm to predict myocardial scar, (v) artificial intelligence machine learning techniques to develop and validate an algorithm capable to classifying ECG scar, and (vi) a novel high resolution proteomic technique to propose biomarkers of SCD risk, validated using ELISA (vii). The hypothesis is that novel clinical tools, encompassing technologies and techniques which could stretch across the clinical landscape from primary to specialised care services, can be identified as indicators of ICD benefit in patients at risk of SCD. My results indicate that simpler ECG markers such as T-peak-end, fQRS and QRS scoring have a significant association with myocardial scar, although the strength of association varies according to scar characteristics, and is not specific. The specificity of these markers for mode of death is also weak. Computerised algorithms can serve to speed up manual ECG scoring, whilst maintaining overall accuracy, but greatest potential is seen in using a novel marker, custom developed using artificial intelligence techniques. I also found that candidate serum biomarkers, predictive of death or ventricular arrhythmia, could be identified through high resolution proteomic techniques. Clinical and technical validation with ELISA is possible. Novel non invasive markers, such as serum proteins and computer ECG analysis may be valuable tools to improve risk prediction. The incremental benefit of these tools to determine prognosis, and select those who will most benefit from ICD therapy, can now be addressed by future prospective studies.
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Poulikakos, Dimitrios. "Electrocardiography for risk stratification of sudden cardiac death in chronic kidney disease." Thesis, St George's, University of London, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.703279.
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Sudden cardiac death accounts for one fourth of deaths in prevalent dialysis patients yet risk stratification for targeted preventive treatment remains an unmet clinical need. This thesis belongs to the field of non-invasive electrophysiology and its goal is to investigate if electrocardiographic monitoring during dialysis can provide subject specific profiles of selected indices of repolarisation and cardiac autonomic modulation derived with computerised analysis of the surface electrocardiogram that would be suitable for risk stratification purposes for sudden cardiac death in dialysis patients. To this end the following objectives were set: a) test the intrasubject reproducibility of selected repolarisation descriptors and of spectral parameters of heart rate variability (HRV) during 5 dialysis sessions, b) investigate their relationship with clinical and laboratory parameters associated with increased cardiovascular risk, c) examine the interrelationship between cardiac autonomic regulation and repolarisation indices, and d) follow up the study population for major arrhythmic events. The thesis is organised in a manner that allows selected chapters based on published articles to be read in their own right. A literature review on the epidemiology and possible underlying mechanisms of ventricular arrhythmias in chronic kidney disease is presented in Chapter 2. Chapter 3 deals with aspects of the study design and methodology. Chapter 4 includes the results on intrasubject stability of selected repolarisation descriptors. Chapter 5 reports on repolarisation descriptors in patients that suffered major arrhythmic events after a follow up period of 18 months. Chapter 6 reports on sex dependent association between HRV and pulse pressure and Chapter 7 reports an association between HRV and bone mineral abnormalities. T.he interrelationship between HRV and the studied repolarisation indices is investigated in Chapter 8. In Chapter 9 the future research plan is briefly outlined and Chapter 10 summarises and concludes the thesis.
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Nakajima, Daisuke. "Reconditioning Lungs Donated After Cardiac Death Using Short-Term Hypothermic Machine Perfusion." Kyoto University, 2016. http://hdl.handle.net/2433/216177.
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Chow, Elaine Yee Kwan. "Mechanisms of hypoglycaemia related sudden cardiac death in type 2 diabetes mellitus." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9317/.
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Kizhakkepatt, Jipin Das. "Clinico-pathological & genetic analysis of sudden cardiac death in the young." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/12707.
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Sudden cardiac death (SCD) is defined as sudden unexpected death occurring within one hour of onset of symptoms in an individual with or without pre-existing heart disease. The main hypothesis underlying this PhD thesis was that inherited heart diseases are responsible for a significant number of SCD in the young, including those in which the heart appears completely “normal” at postmortem (i.e. “sudden unexplained death or SUD”). Postmortem genetic studies, specifically an exome sequencing based molecular autopsy, will offer a comprehensive analysis of cardiac disease-related genes in SUD cases and families. Exome sequencing in a subgroup of 28 SUD cases (aged 1 to 40 years) revealed 3 rare variations in the common LQTS genes and 6 rare variations in an additional 25 common genes of cardiac arrhythmias and cardiomyopathies. Further, whole exome sequencing performed in a multigenerational family with two SUD cases, subtle post-mortem abnormalities and 12-lead ECG abnormalities identified two rare missense variants in non-cardiac genes and a novel missense variant in a cardiomyopathy-associated mitochondrial gene. These variants needs to be further evaluated by screening additional family members, tissue expression and functional studies. Probands seen at a multidisciplinary cardiac genetic clinic with a reported pathogenic mutation or variants of uncertain significance were further reviewed for any single nucleotide variant (SNV) reclassification by a blinded analysis. Five variants in six hypertrophic cardiomyopathy probands and four variants in probands with other inherited heart conditions were reclassified. In summary, exome based molecular autopsy ensures a comprehensive review of cardiac genes, has an increased likelihood of identifying pathogenic gene mutations including novel genes that may be associated with cardiac disease and sudden death. Periodic reassessment of SNV data is vital in all inherited cardiac disorders.
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Wong, Kenneth. "Towards reducing cardiovascular deaths in cerebrovascular disease : using QT interval analysis to identify the spectrum of cardiac abnormalities leading to cardiac death in cerebrovascular disease and to guide proper targeting of cardiac investigations." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432576.
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Ghassemi, Mohammad Mahdi. "Life after death : techniques for the prognostication of coma outcomes after cardiac arrest." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/118092.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2018.Cataloged from PDF version of thesis.
Includes bibliographical references (pages 120-134).
Electroencephalography (EEG) features are known to predict neurological outcomes of patients in coma after cardiac arrest, but the association between EEG features and outcomes is time-dependent. Recent advances in machine learning allow temporally-dependent features to be learned from the EEG waveforms in a fully-automated way, allowing for faster, better-calibrated and more reliable prognostic predictions. In this thesis, we discuss three major contributions to the problem of coma prognostication after cardiac arrest: (1) the collection of the world's largest multi-center EEG database for patients in coma after cardiac arrest, (2) the development of time-dependent, interpretable, feature-based EEG models that may be used for both risk-scoring and decision support at the bedside, and (3) a careful comparison of the performance and utility of feature-based techniques to that of representation learning models that fully-automate the extraction of time-dependent features for outcome prognostication.
by Mohammad Mahdi Ghassemi.
Ph. D.
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Benton, Eleanor. "The role of the mitochondrial permeability transition pore in cardiac myocyte cell death." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446529/.
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Ischaemia-reperfusion injury, sustained when the blood and oxygen supply is removed and then reinstated, is a common cause of cardiac tissue damage and therefore a popular area of scientific research. It is commonly thought that the mitochondria play an important role in mediating ischaemia-reperfusion injury. Particular attention has been focused on the mitochondrial permeability transition pore. This has many times been shown to open only during the reperfusion phase disrupting the mitochondrial transmembrane potential and therefore the synthesis of ATP. This study endeavours to examine the activity of the pore in rat neonatal primary cardiomyocytes during cell death. Models of apoptotic and necrotic cell death are established, as both have been implicated in ischaemia-reperfusion injury. An in vitro model of ischaemia- reperfusion injury is set up and an in vivo model of ischaemia-reperfusion injury is also examined. Many studies have shown that inhibition of cyclophilin D can successfully block the opening of the mitochondrial pore. In this study, the cyclophilin inhibitor cyclosporin A is applied to determine the importance of cyclophilin D as an attenuator of ischaemia-reperfusion injury. The resulting effect on cell viability is analysed by various assays. Changes in the activity of the mitochondrial permeability transition pore are also monitored using a fluorescent mitochondrial transmembrane potential-sensitive dye. A kinetic assay is established to measure the peptidyl prolyl cis-trans-isomerase activity of cyclophilin D, which is believed to have a role in regulation of the pore. Additionally ATP synthesis is measured by a luciferase-based assay and free radical production is monitored using a radical-sensitive dye during cell death. The effect of cyclosporin A on all measured parameters is examined. The results presented in this study show that the importance of the mitochondrial permeability transition pore can vary widely according to the prevailing conditions. However, the data obtained in both isolated cardiomyocytes and cardiac tissue broadly uphold the concept of the major impact of mitochondrial permeability transition pore induction during ischaemia-reperfusion injury and strongly support the hypothesis of a significant role for cyclophilin D in the molecular mechanism of the pore.
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Chandra, Navin. "General population screening for sudden cardiac death in young individuals : the UK experience." Thesis, St George's, University of London, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.676896.
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BACKGROUND: Sudden cardiac death (SCD) in any young person is a tragic event with a significant number of life-years lost. Previous data from Italy suggest that pre-participation screening using an electrocardiogram (ECG) reduces the incidence of SCD in competitive athletes. However, the majority of SCD occurs in non-athletes within the general population. In the United Kingdom, state sponsored screening for cardiac disorders is confined to symptomatic individuals or those with a family history of inherited cardiac conditions or premature cardiac death. AIMS: To assess the feasibility and efficacy of screening, incorporating an ECG and point-ofcare echocardiography, in young individuals from the general population for cardiovascular conditions associated with SCD. METHODS: Between 2008-2012, 10,359 young individuals aged 14-35 years underwent screening by an attending cardiologist comprising a health questionnaire, physical examination and ECG. ECGs were analysed in accordance with the European Society of Cardiology (ESC} recommendations for ECG interpretation in athletes for Group-1 (trainingrelated) and Group-2 (potentially pathological) patterns. Group-2 ECG patterns warrant further cardiac evaluation. Individuals with findings raising suspicion of cardiomyopathy underwent on-site echocardiography. Individuals with abnormalities from the screening episode were referred for further evaluation for conditions associated with SCD and followed up annually to assess outcomes. Based on these data comparisons of the efficacy of different screening strategies were made and costs and cost effectiveness were calculated. RESULTS: Symptoms of a cardiovascular nature were reported in 44.2% of individuals, a family history of SCD or condition associated with SCD was reported in 3.8% and an abnormal physical examination occurred in 0.3% of individuals. ECG patterns suggestive of cardiac pathology were identified in 22.4% of individuals, predominantly due to abnormalities of QTc measurement. Male gender and black ethnicity demonstrated the strongest association with ESC Group-2 ECG patterns. Point-of-care echocardiography for individuals with suspicion of cardiomyopathy significantly reduced the number of patients requiring further evaluation as only 14.8% of these individuals demonstrated abnormal echocardiographic findings. Positive diagnosis of a cardiovascular condition associated with SCD was identified in 0.3% of individual;; (cardiomyopathy, n=6; primary electrical disease, n=17; Marfan syndrome, n=4). This screening strategy demonstrated a sensitivity of 100%, specificity of 93.2% and false-positive rate of 6.8% with an estimated cost of £106,141 per diagnosis made. CONCLUSIONS: Screening for conditions associated with SCD in the general population is feasible. A screening strategy incorporating the ECG and point-of-care echocardiography is associated with a high sensitivity and specificity and low false-positive rate as well as favourable cost analyses.
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Abbas, Hesham Magdi. "Estrogenic Compounds Protect Rat Cardiac Myoblasts (H9c2 Cells) Against Doxorubicin-Induced Cell Death." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd_retro/131.
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The antineoplastic drug doxorubicin is widely used in the treatment of various types of cancers including breast, colon and lung cancer. However, doxorubicin has adverse effects on the heart and prolonged doxorubicin administration results in cardiomyopathy and congestive heart failure. In the present study we have established that treatment of rat cardiac myoblasts (H9c2 cells) for 24 hours with doxorubicin resulted in concentration and time dependent cell death as determined by proliferation assay. Almost 50-55% cell death was attained at 24 hours treatment of H9c2 cells with 5 μM doxorubicin. We have selected about 50% cell injury as an optimum doxorubicin-induced cell injury because once this threshold is reached, cells became irreversibly injured and are unable to respond to protective treatment. We have observed that another potent antineoplastic drug, cyclophosphamide, had no cardiotoxic effects even with exposure at 35 μM concentrations for a treatment time of up to 72 hours. Pretreatment of H9c2 cells for 24 hours with 100 nM 17β-estradiol protects about 30% cell death against subsequent treatment for 24 hours with 5 μM doxorubicin. Interestingly 500 nM quecertin and 20 μM resveratrol pretreatment provide about 30% and 40% protection, respectively, to the H9c2 cells against subsequent doxorubicin treatment. However, diethylstilbestrol (DES), bisphenol A, and estrone exhibit no protective effects. It is concluded that 17β-estradiol, resveratrol and quercetin considerably protect H9c2 cells against doxorubicin-induced cell death.
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Wang, Yan. "p53 mediates autophagy and cell death by a mechanism contingent upon Bnip3." Hypertension, 2013. http://hdl.handle.net/1993/21702.
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Autophagy is a process by which cells re-cycle organelles and macromolecular proteins during cellular stress. Defects in the regulation of autophagy have been associated with various human pathologies including heart failure. In the heart tumor suppressor p53 protein is known to promote apoptotic and autophagic cell death. We found p53 over-expression increased endogenous protein level of the hypoxia-inducible Bcl-2 death gene Bnip3 which leads to loss of mitochondrial membrane potential (ΔΨm). This was accompanied by autophagic flux and cell death. Conversely, loss of function of Bnip3 in cardiac myocytes or Bnip3-/- mouse embryonic fibroblasts prevented mitochondrial targeting of p53 and autophagic cell death. These data provide the first evidence for the dual regulation of autophagic cell death of cardiac myocytes by p53 that is mutually dependent on Bnip3 activation. Hence, our findings may explain how autophagy and cell death are dually regulated during cardiac stress conditions where p53 is activated.
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Bashir, Yaver. "Management of ventricular arrhythmias in the failing heart : a clinical study." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318809.
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Terho, H. (Henri). "Electrocardiographic risk markers for cardiac events in middle-aged population." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526223841.
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Abstract Cardiovascular diseases are the leading cause of death in developed countries. Approximately 50% of these events are due to sudden cardiac death (SCD) and often without preceding diagnosis of cardiac disease. Many risk factors for cardiac events have been identified and prevention strategies have improved markedly. The aim of this thesis was to evaluate the usability of the 12-lead electrocardiogram (ECG) to predict cardiac events. The study population consisted of 10,904 middle-aged general population subjects with ECG recordings between the years 1966–1972 with a long follow-up (30±11 years). The first part of the thesis (I) focused on the prevalence and prognostic significance of fragmented QRS complex (fQRS). The prevalence of fQRS was 19.7%. Fragmented QRS complex did not predict mortality in subjects with no history of cardiac disease. Among subjects with underlying cardiac disease and lateral fQRS, the risk of cardiac death was 2.5-fold (P=0.001) and the risk of SCD was almost 3-fold (P=0.004). Other major electrocardiographic abnormalities were assessed in subjects without known cardiac disease for the risk of cardiac death, SCD and hospitalization due to coronary artery disease (II, III). Abnormal ECG was moderately associated with cardiac death after 10 and 30 years of follow-up (hazard ratio 1.7, P=0.009; hazard ratio 1.3, P>0.001, respectively) (II). The risk of hospitalization was not associated with abnormal ECG findings. Abnormal ECG moderately predicted SCD during 10 and 30 years of follow-up (hazard ratio 1.6, P=0.052; hazard ratio 1.3, P=0.007) (III). The risk of SCD was 3-fold when ≥2 ECG abnormalities were present. In conclusion, lateral fQRS in middle-aged subjects with underlying cardiac disease was associated with increased risk of death. Certain abnormal ECG findings associated with the risk of non-arrhythmic cardiac mortality and arrhythmic death. The risk of arrhythmic mortality was substantially elevated when multiple ECG abnormalities were present in middle-aged populationTiivistelmä Sydänsairaudet ovat yleisin kuolinsyy kehittyneissä maissa. Noin 50 % näistä kuolemista aiheutuu äkillisestä sydänpysähdyksestä, suuri osa ilman aiempaa tietoa sairaudesta. Useita sydänsairauksien riskitekijöitä on tunnistettu ja ennaltaehkäisy on kehittynyt merkittävästi. Väitöstutkimuksen tavoitteena on tutkia 12-kytkentäisen sydänsähkökäyrän (EKG) käyttökelpoisuutta sydänsairauksien ilmenemisen ennustamisessa. Tutkimusväestöön kuului 10,904 keski-ikäistä suomalaista henkilöä. Aineisto kerättiin vuosina 1966-1972 ja seuranta-aika oli 30 (±11) vuotta. Ensimmäisessä osajulkaisussa (I) tutkimme QRS-kompleksin fragmentaation vallitsevuutta ja sen vaikutusta ennusteeseen väestössä. Fragmentoituneen QRS-kompleksin esiintyvyys oli 19.7 %. Fragmentoitunut QRS-kompleksi ei lisännyt kuolemanriskiä henkilöillä, joilla ei ollut sydänsairautta. Henkilöillä, joilla oli todettu sydänsairaus, lateraalinen fQRS lisäsi sydänperäistä kuolleisuutta 2.5-kertaiseksi (P=0.001) ja rytmihäiriöperäistä kuolleisuutta 3-kertaiseksi (P=0.004). Tutkimme muiden poikkeavien EKG-löydösten ennustearvoa kuolleisuuteen ja sairaalahoidon tarpeeseen sepelvaltimokohtauksen vuoksi (II, III). Poikkeavien EKG-muutosten esiintymiseen liittyi lisääntyneen sydänperäisen kuoleman riski sekä 10 vuoden (riskitiheyssuhde 1.7, P=0.009) että 30 vuoden seurannassa (riskitiheyssuhde 1.3, P>0.001) (II). Poikkeavat EKG-muutokset eivät ennustaneet sairaalahoitojaksoja. Poikkeava EKG ennusti rytmihäiriöperäisen kuoleman riskiä sekä 10 vuoden (riskitiheyssuhde 1.6, P=0.052) että 30 vuoden seurannassa (riskitiheyssuhde 1.3, P=0.007) (III). Äkkikuoleman riski oli 3-kertainen henkilöillä, joilla todettiin ≥ 2 EKG-poikkeavuutta. Tutkimuksen yhteenvetona voidaan todeta, että fQRS lateraalisissa kytkennöissä lisäsi sydänperäisen kuoleman riskiä henkilöillä, joilla on todettu sydänsairaus. Tiettyihin poikkeaviin EKG-muutoksiin liittyi lisääntynyt ei-rytmihäiriöperäisen ja rytmihäiriöperäisen kuoleman riski. Useiden tutkittujen EKG-muutosten ilmentyminen samanaikaisesti lisäsi merkittävästi rytmihäiriöperäisen kuoleman riskiä keski-ikäisessä väestössä
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Rashevskaya, V., A. Ros, Оксана Костянтинівна Романюк, Оксана Константиновна Романюк, and Oksana Kostiantynivna Romaniuk. "Sudden infant death syndrom (sids). Spesial featyres of a pathomorphological study." Thesis, Видавництво СумДУ, 2008. http://essuir.sumdu.edu.ua/handle/123456789/6170.
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Ryti, N. R. (Niilo R. I. ). "On health effects of cold spells with a special reference to sudden cardiac death." Doctoral thesis, Center for Environmental and Respiratory Health Research (CERH), 2017. http://urn.fi/urn:isbn:9789526217574.
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Abstract There is substantial evidence on the associations between cold ambient temperature and adverse health effects. Less is known about the role of prolonged episodes of cold weather denoted as cold spells. This study assessed relations between cold spells and adverse health effects globally, and quantified and elaborated the associations between cold spells and sudden cardiac death (SCD) in northern Finland. Based on random-effects models in the meta-analyses of evidence from 9 studies around the world, cold spells were associated with increased mortality rates from all or all non-accidental causes (RR 1.10; 95% CI: 1.04–1.17), cardiovascular diseases (RR 1.11; 95% CI: 1.03–1.19), and respiratory diseases (RR 1.21; 95% CI: 0.97–1.51). Suggestive evidence of other health effects was identified. Investigating 51-years of coordinate-specific weather data at the home coordinates of autopsy-verified cases of SCD, conditional logistic regression in a case-crossover setting produced an estimate for the association between cold spells and the risk of SCD (OR 1.33; 95% CI: 1.00–1.78). A greater number of cold days preceding death increased the risk of SCD approximately 19% per day (OR 1.19; 95% CI: 1.07–1.32). The association between season-specific cold spells and SCD was strongest during autumn and winter, and lowest during spring and summer. The association was stronger for ischemic (OR 1.55; 95% CI: 1.12–2.13) than for non-ischemic SCD (OR 0.68; 95% CI: 0.32–1.45) (Q-statistic 3.85, p 0.05), confirmed by the autopsy finding. Among cases suffering ischemic SCD, the association seemed stronger in those without a prior diagnosis of ischemic heart disease than in those diagnosed during lifetime. The association seemed stronger with severe coronary stenosis (OR 1.60; 95% CI: 1.11–2.30), and weaker with moderate stenosis (OR 0.97; 95% CI: 0.37–2.55). The use of aspirin, β-blockers, and nitrates seemed to decrease the risk of ischemic SCD during cold spells. In conclusion, cold spells increased the risk of ischemic SCD, and patients without appropriate diagnosis and medications for ischemic heart disease seemed most susceptible. The results indicate that coronary stenosis plays a central role in the cold-related pathogenesis of SCD. Timely diagnosis and treatment of ischemic heart disease might reduce weather-related SCDs in a communityTiivistelmä Kylmän lämpötilan ja terveyshaittojen välisistä yhteyksistä on vahva tutkimusnäyttö. Vähemmän tiedetään pitkittyneiden kylmäjaksojen ja terveyshaittojen välisistä yhteyksistä. Tutkimuksessa arvioitiin kylmäjaksojen ja terveyshaittojen välisiä yhteyksiä globaalisti, ja määritettiin kylmäjaksojen ja sydänperäisen äkkikuoleman (SÄK) välisiä yhteyksiä Pohjois-Suomessa. Yhdeksän eri puolella maailmaa toteutetun tutkimuksen tulosten meta-analyysissa satunnaisvaikutusten malli osoitti yhteyden kylmäjaksojen ja kaikkien tai luonnollisien syiden (RR 1.10; 95% CI: 1.04–1.17), sydän- ja verisuonisairauksien (RR 1.11; 95% CI: 1.03–1.19), ja hengityselimistön sairauksien (RR 1.21; 95% CI: 0.97–1.51) kuolleisuuden välillä. Viitteellistä näyttöä havaittiin muista terveyshaitoista. Tutkittaessa 51-vuoden koordinaattikohtaista säätä case-crossover-asetelmassa oikeuslääketieteellisesti vahvistettujen SÄK-tapausten kotiosoitteissa, ehdollisen logistisen regression mukaan SÄK:n riski oli yhteydessä kuolemaa edeltävään kylmäjaksoon (OR 1.33; 95% CI: 1.00–1.78). Lisääntyvä kylmien päivien lukumäärä ennen kuolemaa lisäsi riskiä keskimäärin 19% päivää kohden (OR 1.19; 95% CI: 1.07–1.32). Yhteys kausikohtaisten kylmäjaksojen ja SÄK:n välillä oli vahvin syksyllä ja talvella, ja heikoin keväällä ja kesällä. Yhteys oli vahvempi kylmäjaksojen ja iskeemisen SÄK:n (OR 1.55; 95% CI: 1.12–2.13) kuin kylmäjaksojen ja ei-iskeemisen SÄK:n (OR 0.68; 95% CI: 0.32–1.45) välillä (Q-statistic 3.85, p 0.05). Iskeemisen SÄK:n kokeneilla yhteys vaikutti vahvemmalta tapauksilla joilla ei ollut aiempaa iskeemisen sydänsairauden diagnoosia, kuin tapauksilla jotka oli diagnosoitu elinaikana. Yhteys vaikutti vahvemmalta vaikea-asteisesta sepelvaltimostenoosia sairastavilla (OR 1.60; 95% CI: 1.11–2.30), kuin lievempi-asteisessa stenoosissa (OR 0.97; 95% CI: 0.37–2.55). Aspiriini, β-salpaajat, ja nitraatit vaikuttivat vähentävän iskeemisen SÄK:n riskiä kylmäjakson aikana. Yhteenvetona, kylmäjaksot lisäsivät iskeemisen SÄK:n riskiä, ja potilaat vailla iskeemisen sydänsairauden diagnoosia ja lääkityksiä vaikuttivat olevan alttiimpia kylmäjaksojen haittavaikutuksille. Tulokset viittaavat sepelvaltimostenoosin keskeiseen rooliin kylmään liittyvän SÄK:n patogeneesissä. Varhainen iskeemisen sydänsairauden diagnoosi ja siihen liittyvä sydäntä suojaava lääkitys voisivat vähentää säähän liittyviä SÄK:a
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Kageyama, Shoichi. "Graft Reconditioning With Nitric Oxide Gas in Rat Liver Transplantation From Cardiac Death Donors." Kyoto University, 2014. http://hdl.handle.net/2433/193570.
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MARCANTONI, ILARIA. "Alternanza elettrocardiografica: identificazione automatica e significato clinico. electrocardiographic alternans: automatic identification and clinical significance." Doctoral thesis, Università Politecnica delle Marche, 2021. http://hdl.handle.net/11566/287750.
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L'alternanza elettrocardiografica (ECGA) è un indice non invasivo di rischio cardiaco che riflette un fenomeno elettrofisiologico, palesandosi come alternanza dell'onda P/complesso QRS/onda T (PWA/QRSA/TWA, rispettivamente) sull'elettrocardiogramma. Scopo di questa tesi di dottorato è approfondire il ruolo clinico e l'applicabilità dell'ECGA. L'obiettivo è presentare il primo metodo automatico per identificare e misurare in modo affidabile tutte le forme di ECGA. Infatti, i metodi esistenti si concentrano solo sulla TWA. Il metodo di correlazione è stato aggiornato ed è stato sviluppato il metodo del filtro match adattivo migliorato per fornire sia l'ampiezza dell'alternanza (µV) che l'area (µV∙ms). È stato riscontrato che TWA sale 6h, 7h e 8h dopo la somministrazione di dofetilide, suggerendo una maggiore vulnerabilità ad aritmie indotte da dofetilide. Alta TWA in prossimità di crisi epilettiche (prima: 31µV; durante: 46µV; dopo: 30µV) ha suggerito una maggiore instabilità elettrica e quindi vulnerabilità all'aritmia. TWA in condizioni fetali e pretermine non patologiche (ECG fetale diretto: 9µV; ECG fetale indiretto: 11µV; ECG pretermine: 26µV) ha suggerito un collegamento della TWA a un incompleto sviluppo, essendo correlata al rapporto età gestazionale sul peso alla nascita (0.76, p=0,02). In un paziente con ponte miocardico, TWA era l'alternanza prevalente e correlava con la frequenza cardiaca (0.72, p minore di 0.01), suggerendo una condizione di rischio più elevato. In un paziente emodialitico, l'ECGA era maggiore prima (51µV) e durante (53µV) rispetto a dopo (28µV) l’emodialisi, suggerendo un rischio più basso dopo il trattamento. Inoltre, sono state ottenute misurazioni ECGA affidabili sia in condizioni simulate che sperimentali. La TWA era prevalente nei pazienti con insufficienza cardiaca con defibrillatore cardiaco impiantato per la prevenzione primaria (PWA: 545µV∙ms; QRSA: 762µV∙ms; TWA: 1382µV∙ms). Studi futuri valuteranno il ruolo prognostico dell'ECGA.Electrocardiographic alternans (ECGA) is a noninvasive cardiac risk index that reflects an electrophysiological phenomenon, manifesting as P-wave/QRS-complex/T-wave alternans (PWA/QRSA/TWA, respectively) on the electrocardiogram. Aim of this PhD thesis is to provide insights on ECGA clinical role and applicability. The specific objective is to present the first automatic method to reliably identify and measure all ECGA forms. Indeed, current existent methods only focus on TWA. To this aim, here, the correlation method was upgraded, and the enhanced heart-rate adaptive match filter method was developed to provide both alternans amplitude (µV) and area (µV∙ms). TWA was found to increase 6h, 7h and 8h after administration of dofetilide drug, suggesting a higher predisposition to dofetilide-induced arrhythmias. High TWA in proximity of epileptic seizures (before: 31µV; during: 46µV; after: 30µV) suggested a higher electrical instability that rises arrhythmia vulnerability. TWA in the non-pathological fetal and preterm conditions (direct fetal ECG: 9µV; indirect fetal ECG: 11µV; preterm ECG: 26µV) suggested a TWA link to a state of incomplete development, being related to gestational-age to birth-weight ratio (0.76, p=0.02). In a patient with myocardial bridging, TWA was the prevalent alternans and correlated with heart rate (0.72, p less than 0.01), suggesting a higher risk condition. In a hemodialytic patient, ECGA was higher before (51µV) and during (53µV) hemodialysis than after (28µV), suggesting a lower risk condition after the treatment. Additionally, reliable ECGA measurements were obtained in both simulated and experimental conditions. TWA was prevalent in heart failure patients with implanted cardioverter defibrillator for primary prevention (PWA: 545µV∙ms; QRSA: 762µV∙ms; TWA: 1382µV∙ms). Future studies will assess prognostic role of ECGA.
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Opstal, Jurren Marie van. "Drug-induced torsade de pointes arrhythmias and sudden cardiac death in the remodeled canine heart." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2002. http://arno.unimaas.nl/show.cgi?fid=7511.
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Sen-Chowdhry, Srijita. "New perspectives on arrhythmogenic right ventricular dysplasia/cardiomyopathy and sudden cardiac death in the young." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612987.
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Jundi, Hala. "Elucidating ryanodine receptor domain interactions in sudden cardiac death : towards the development of novel therapeutic strategies." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/55106/.
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Interdomain Interactions within the complex three-dimensional architecture of the cardiac ryanodine receptor (RyR2) are pivotal in channel regulation. Acquired or genetic abnormalities that perturb these stabilising intra-molecular interactions are pathogenic. This laboratory identified the interacting- or l-Domain of human RyR2 that mediated interaction between cytoplasmic and transmembrane (TM) assemblies. To further elucidate the precise roles of functional motifs within the l-Domain, three contiguous fragments spanning RyR2 amino acid residues 3722-4610 were synthesised using a cell-free system. One fragment termed IDB (amino acid residues 4353-4499) profoundly modulated cellular Ca2+ cycling and resulted in the remarkable normalisation of intercellular synchrony following its microinjection into ouabain-treated cardiomyocyte monolayers. These phenomena were linked to IDB- mediated stabilisation of RyR2 and were fully corroborated using IDB purified from a bacterial expression system. Bioinformatic analysis revealed striking structural homology between sub-fragments of the RyR2 l-Domain and l-Domain-like regions of inositol 1,4,5- trisphosphate receptors (IP3R). Recombinant expression of l-domain sub-fragments in RyR- null human embryonic kidney (HEK) cells remodelled carbachol-evoked Ca2+-responses and suppressed homeostatic Ca2+ signalling events indicating that IDB also modulated IP3R signalling mechanisms. In both HL-1 and HEK cells, IDB-dependent Ca2+ modulation extended to surrounding cells that were not microinjected with recombinant protein. This so- called 'bystander effect' was mediated by the transfer of signalling molecules via direct cell- to-cell coupling (gap junctions) and also by the extracellular transmission of diffusible effectors. This thesis supports the concept that RyR2 stabilisation rescues pathogenic Ca2+ dysregulation and suggests that there is substantial merit in developing further epitope-targeting strategies for the therapeutic normalisation of Ca2+ cycling in cardiac disease.
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Cruz, Frederic Anthony Silo. "Features or forensic pathology in sudden cardiac death: are there histologic indicators of acute myocardial ischemia?" Thesis, Boston University, 2013. https://hdl.handle.net/2144/12079.
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Thesis (M.S.)--Boston UniversityThe following thesis proposes the question if current scientific data supports the hypothesis that an acute myocardial infarction, not identified by gross symptoms, can be visualized by using apoptotic signaling biomarkers as a diagnostic tool to complement a post-mortem autopsy. The biochemistry and mechanisms of irreversible cellular death is presented and supported through published experimental, clinical and case studies. Furthermore, the aforesaid biomarkers have been observed in the cardiac myocyte in elevated levels associated with hypoxic ischemia. In addition, the physical characteristic of DNA fragmentation is addressed to visualize apoptotic injury due to hypoxic ischemic conditions. Although the quality of evidence lacked published data to suggest one immunochemical staining method positively identifies a myocardial infarction, there is adequate data to suggest that a combination of staining methods can be utilized as a tool to positively identify and diagnose an acute myocardial infarction.