Academic literature on the topic 'Chronic heart failure; Cardiac death'

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Journal articles on the topic "Chronic heart failure; Cardiac death"

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Packer, Milton. "Nonarrhythmic Sudden Cardiac Death in Chronic Heart Failure—A Preventable Event?" JAMA Cardiology 4, no. 8 (August 1, 2019): 721. http://dx.doi.org/10.1001/jamacardio.2019.2228.

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Ran, Yuqin, Jingzhou Chen, Ning Li, Weili Zhang, Li Feng, Rongrong Wang, Rutai Hui, Shu Zhang, and Jielin Pu. "Common RyR2 variants associate with ventricular arrhythmias and sudden cardiac death in chronic heart failure." Clinical Science 119, no. 5 (June 4, 2010): 215–26. http://dx.doi.org/10.1042/cs20090656.

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Ca2+ cycling plays a critical role in heart failure and lethal arrhythmias. As susceptibility to sudden cardiac death is considered to be a heritable trait in general population, we have therefore investigated whether potentially functional variants of genes encoding RyR2 (ryanodine receptor 2) and the L-type Ca2+ channel are related to the risk of ventricular arrhythmias and sudden cardiac death in CHF (chronic heart failure) in a case-control study. We found that the A allele of rs3766871 in RYR2 was associated with an increased risk of ventricular arrhythmias in patients with CHF {odds ratio, 1.66 [95% CI (confidence interval), 1.21–2.26]; P=0.002}. During a median follow-up period of 32 months in 1058 (85.0%) patients, 296 (28.0%) patients died from heart failure, of whom 141 (47.6%) had sudden cardiac death. After adjustment for age, gender and suspected risk factors, patients carrying the A allele of rs3766871 had an increased risk of cardiac death {HR (hazard ratio), 1.53 [95% CI, 1.11–2.12]; P=0.010} and sudden cardiac death [HR, 1.92 (95% CI, 1.25–2.94); P=0.003]. Patients carrying the A allele of rs790896 in RYR2 had a reduced risk of sudden cardiac death [HR, 0.65 (95% CI, 0.45–0.92); P=0.015]. In conclusion, the A allele of rs3766871 in RYR2 not only associates with ventricular arrhythmias, but also serves as an independent predictor of sudden cardiac death, and the A allele of rs790896 in RYR2 is a protective factor against sudden cardiac death in patients with CHF.
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Unic-Stojanovic, Dragana, Miroslav Milicic, Petar Vukovic, Srdjan Babic, and Miomir Jovic. "Heart surgery in patients on chronic dialysis." Medical review 66, no. 1-2 (2013): 64–69. http://dx.doi.org/10.2298/mpns1302064u.

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Introduction. Patients on dialysis for end-stage renal failure are subjected to cardiac surgery with increasing frequency. End-stage renal failure is known to be an important risk factor for complications of cardiac operations performed with cardiopulmonary bypass. The aim of this study was to determine the impact of preoperative clinical status and operative variables on perioperative morbidity and mortality in hemodialysis dependent patients subjected to a cardiac surgery. Material and Methods. The following operative variables were examined: urgency, type and duration of surgery and duration of extracorporeal circulation. The study is a retrospective analysis of consecutive patients with end-stage renal failure dependent on maintenance hemodialysis who underwent cardiac surgery during four years. Results. The study included 46 patients. Operations performed included isolated coronary artery bypass grafting (CABG, n = 24), valve surgery alone (n = 6), and combined valve surgery or coronary artery bypass grafting and valve surgery (n = 16). The perioperative mortality rate was 13% with four fatal outcomes in patients who had undergone combined cardiac surgery. We found age > 70 years, preoperative New York Heart Association class IV, preoperative anemia, combined surgery and emergent surgery to be associated with a higher relative risk for perioperative death. Conclusion. Patients on dialysis have an increased morbidity and mortality following cardiac surgery; however, we believe that end-stage renal failure should not be regarded as a contraindication to cardiac surgery or cardiopulmonary bypass.
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Verschure, Derk O., G. Aernout Somsen, Berthe L. F. van Eck-Smit, and Hein J. Verberne. "Renal Function in Relation to Cardiac 123I-MIBG Scintigraphy in Patients with Chronic Heart Failure." International Journal of Molecular Imaging 2012 (May 14, 2012): 1–8. http://dx.doi.org/10.1155/2012/434790.

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The aim of this study was to explore if estimates of renal function could explain variability of 123I-metaiodobenzylguanidine (123I-MIBG) assessed myocardial sympathetic activity. Furthermore estimates of renal function were compared to 123I-MIBG as predictors of cardiac death in chronic heart failure (CHF). Semi-quantitative parameters of 123I-MIBG myocardial uptake and washout were calculated using early heart/mediastinum ratio (H/M), late H/M and washout. Renal function was calculated as estimated Creatinine Clearance (e-CC) and as estimated Glomerular Filtration Rate (e-GFR). Thirty-nine patients with CHF (24 males; age: 64.4±10.5 years; NYHA II/III/IV: 17/20/2; LVEF: 24.0±11.5%) were studied. Variability in any of the semi-quantitative 123I-MIBG myocardial parameters could not be explained by e-CC or e-GFR. During follow-up (60±37 months) there were 6 cardiac deaths. Cox proportional hazard regression analysis showed that late H/M was the only independent predictor for cardiac death (Chi-square 3.2, regression coefficient: −4.095; standard error: 2.063; hazard ratio: 0.17 [95% CI: 0.000–0.950]). Addition of estimates of renal function did not significantly change the Chi-square of the model. Semi-quantitative 123I-MIBG myocardial parameters are independent of estimates of renal function. In addition, cardiac sympathetic innervation assessed by 123I-MIBG scintigraphy seems to be superior to renal function in the prediction of cardiac death in CHF patients.
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Walker, Andrew MN, and Richard M. Cubbon. "Sudden cardiac death in patients with diabetes mellitus and chronic heart failure." Diabetes and Vascular Disease Research 12, no. 4 (April 10, 2015): 228–33. http://dx.doi.org/10.1177/1479164115573225.

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Claydon, Susan M. "Myocardial Degeneration in Chronic Solvent Abuse." Medicine, Science and the Law 28, no. 3 (July 1988): 217–18. http://dx.doi.org/10.1177/002580248802800308.

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Chronic solvent abuse is leading to increasing reports of death from cardiac related causes. This case involves a 21-year-old man who died of acute heart failure. Histological examination of his heart showed extensive chronic damage of the myocardium. He had regularly and frequently abused solvents for five years.
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La Rovere, Maria Teresa, Gian Domenico Pinna, Roberto Maestri, Andrea Mortara, Soccorso Capomolla, Oreste Febo, Roberto Ferrari, et al. "Short-Term Heart Rate Variability Strongly Predicts Sudden Cardiac Death in Chronic Heart Failure Patients." Circulation 107, no. 4 (February 4, 2003): 565–70. http://dx.doi.org/10.1161/01.cir.0000047275.25795.17.

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Moore, Roger K. G., David G. Groves, Pauline E. Barlow, Keith A. A. Fox, Ajay Shah, James Nolan, and Mark T. Kearney. "Heart rate turbulence and death due to cardiac decompensation in patients with chronic heart failure." European Journal of Heart Failure 8, no. 6 (October 2006): 585–90. http://dx.doi.org/10.1016/j.ejheart.2005.11.012.

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Mareev, V. Yu Mareev, and Yu V. Mareev Mareev. "Methods of Prevention of Sudden Death in Chronic Heart Failure." Kardiologiia 9_2015 (September 27, 2015): 72–83. http://dx.doi.org/10.18565/cardio.2015.9.72-83.

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Lei, Li, Steve Mason, Dinggang Liu, Yan Huang, Carolyn Marks, Reed Hickey, Ion S. Jovin, Marc Pypaert, Randall S. Johnson, and Frank J. Giordano. "Hypoxia-Inducible Factor-Dependent Degeneration, Failure, and Malignant Transformation of the Heart in the Absence of the von Hippel-Lindau Protein." Molecular and Cellular Biology 28, no. 11 (February 19, 2008): 3790–803. http://dx.doi.org/10.1128/mcb.01580-07.

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ABSTRACT Hypoxia-inducible transcription factor 1 (HIF-1) and HIF-2α regulate the expression of an expansive array of genes associated with cellular responses to hypoxia. Although HIF-regulated genes mediate crucial beneficial short-term biological adaptations, we hypothesized that chronic activation of the HIF pathway in cardiac muscle, as occurs in advanced ischemic heart disease, is detrimental. We generated mice with cardiac myocyte-specific deletion of the von Hippel-Lindau protein (VHL), an essential component of an E3 ubiquitin ligase responsible for suppressing HIF levels during normoxia. These mice were born at expected frequency and thrived until after 3 months postbirth, when they developed severe progressive heart failure and premature death. VHL-null hearts developed lipid accumulation, myofibril rarefaction, altered nuclear morphology, myocyte loss, and fibrosis, features seen for various forms of human heart failure. Further, nearly 50% of VHL−/− hearts developed malignant cardiac tumors with features of rhabdomyosarcoma and the capacity to metastasize. As compelling evidence for the mechanistic contribution of HIF-1α, the concomitant deletion of VHL and HIF-1α in the heart prevented this phenotype and restored normal longevity. These findings strongly suggest that chronic activation of the HIF pathway in ischemic hearts is maladaptive and contributes to cardiac degeneration and progression to heart failure.
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Dissertations / Theses on the topic "Chronic heart failure; Cardiac death"

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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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Galil, Arise Garcia de Siqueira. "Prevalência de anemia e doença renal crônica em portadores de insuficiência cardíaca sistólica num ambulatório de hipertensos e diabéticos." Universidade Federal de Juiz de Fora (UFJF), 2008. https://repositorio.ufjf.br/jspui/handle/ufjf/2837.

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Introdução: A insuficiência cardíaca (IC) tem alta morbimortalidade que decorre de fatores causais e refratariedade ao tratamento. A doença renal crônica (DRC) e a anemia têm se associado a pior prognóstico em pacientes com IC grave, especialmente os hospitalizados. Há, porém, poucos estudos que avaliem a prevalência e as conseqüências da DRC e da anemia em pacientes com IC acompanhados ambulatorialmente. Objetivos: Avaliar a prevalência da DRC e anemia e o impacto de desfechos cardiovasculares em portadores de IC sistólica estágios B e C. Pacientes e Métodos: Foram estudados pacientes adultos, com idade >18 anos e diagnóstico de IC sistólica e com fração de ejeção (EF) ≤45%, selecionados do ambulatório do Serviço de Hipertensão, Diabetes e Obesidade do SUS de Juiz de Fora e acompanhados por 12 meses. A anemia foi definida como hemoglobina <12,0g/dl nas mulheres e <13,0g/dl nos homens. A reserva de ferro foi considerada adequada quando índice de saturação da transferrina encontrava-se ≥20% e a ferritina ≥100ηg/dl. A filtração glomerular foi estimada pela fórmula do estudo MDRD e a DRC foi definida como proposto pelo K/DOQI da National Kidney Foundation americana. Considerou-se com desfechos cardiovasculares (CV) a ocorrência de hospitalização e/ou morte decorrente da IC. Os dados demográficos, de exame físico e laboratorial foram obtidos do prontuário dos pacientes. Resultados: Foram avaliados 83 pacientes, com idade média de 62,7±12 anos, sendo 56,6% do sexo feminino. A média da fração de ejeção (FE) foi de 37,8+7,9% e a maioria dos indivíduos (60,2%) estava no estágio C. A prevalência de anemia foi de 24,09%; 30,30% no estágio B e 20% no estágio C. A prevalência de DRC foi elevada, presente em 49,4% da amostra, 42,4% no estágio B da IC e 54% no estágio C. Todos os pacientes com anemia tinham reserva de ferro normal e 68,6% apresentavam DRC concomitante. Os desfechos CV ocorreram em 26,5% da amostra. Na estratificação dos pacientes nos estágios B e C da IC e presença ou não de DRC, evidenciou que 100% e 64,7% apresentaram desfechos, respectivamente. Na análise multivariada, após ajustes para fatores prognósticos no período basal, o diagnóstico de DRC aumentou em 3,6 vezes a possibilidade de desfechos (IC 95%1,04-12,67, p=0,04), enquanto os níveis mais elevados de sódio sérico (R 0,807, IC95%0,862-0,992, p=0,03) e da fração de ejeção (R 0,925, IC95% 0,862-0,942, p= 0,03) se mostraram protetores. Conclusão: Na coorte de pacientes estudada, composta de pacientes com IC estágios B e C, a ocorrência de anemia foi compatível com a observada em outros estudos e com tendência de se associar com menor filtração glomerular. A DRC foi prevalente e independentemente se associou a maior risco de hospitalizações e mortes secundárias à descompensação cardíaca, especialmente nos pacientes assintomáticos.
Introduction: Chronic heart failure (CHF) has a high morbidity and mortality which are consequent to etiologic factors and no response to treatment. Anemia and chronic kidney disease (CKD) have been associated to worse outcome in patients with severe hospitalized CHF. So far, there is few studies that assessed the prevalence and the consequences of anemia and CKD in outpatients with CHF. Aim: To study the prevalence of CKD and anemia and the impact of CV end points in patients with systolic CHF followed in an outpatient clinic. Methods: This is prospective cohort study, dealing with adult patients older than 18 years of age and diagnosis of systolic CHF and ejection fraction (EF) ≤45%, selected from the Hypertension, Diabetes and Obesity Outpatient Clinic of SUS of Juiz de Fora. Anemia was defined as hemoglobin <12,0g/dL in women and <13g/dL in men and women after the menopause. Normal iron store was defined when transferring saturation index was >20% and/or ferritin >100ηg/dL. The glomerular filtration rate was estimated from serum creatinine usinf the MDRD study formula, and CKD was defined as suggested by the K/DOQI of National Kidney Foundation. CV endpoints were defined as death or hospitalization due to CHF, in 12 months follow up. Demographic and clinical date were obtained from the patients’ charts. Results: Eight three patients were studied, the mean age was 62.7±12 years, and 56.6% were female. The EF was 37,8+7,9%, and the majority of the patients had stage C CHF (60,2%). The prevalence of anemia was 24,1%; 30,3% in stage B and 50% in stage C. CKD was diagnosed in 49.4% of the patients, 42,4% of the stage B and 54% in the stage C. All patients with anemia had normal iron storage, and 68,6% had concomitant CKD. Cardiovascular endpoints were observed in 26.5% of the patients. When the sample was stratified in stages B and C of CHF and presence or absence of CKD, it was found that 100% and 64.7% had CV endpoints, respectively. After adjustments for all other prognostic factors at baseline, it was observed that the diagnosis of CKD increased in 3.6 folds the hazard of CV endpoints (CI 95% 1,04-12,67, p=0,04), whereas higher ejection fraction (R 0,925, IC 95% 0,862-0,942, p= 0,03) and serum sodium (R 0,807, IC 95% 0,862-0,992, p=0,03) were protectors. Conclusion: In this cohort of outpatients with CHF stages B and C, the occurrence of anemia was low and frequently associated with concomitant CKD. On the other hand, CKD was prevalent and independently associated with heightened risk for hospitalization and death secondary of cardiovascular causes, mainly in asymptomatic patients.
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Steele, Ian Conrad. "Pathophysiology of chronic cardiac failure." Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337046.

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Bosco-Lévy, Pauline. "Heart failure in France : chronic heart failure therapeutic management and risk of cardiac decompensation in real-life setting." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0348.

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En France, environ un million de personnes seraient touchées par l’insuffisance cardiaque (IC) ; on recense près de 70 000 décès liés à l’IC, et plus de 150 000 hospitalisations et cela, malgré une prise en charge thérapeutique bien codifiée. Ces chiffres devraient s’accroitre dans les années futures du fait notamment du vieillissement de la population.L’objectif de ce travail était d’étudier l’utilisation des traitements pharmacologiques indiqués dans le traitement de l’IC (beta bloquant, inhibiteur de l’enzyme de conversion, anti-aldostérone, antagoniste des récepteurs à l’angiotensine II, diurétiques, digoxine, ivabradine) en situation réelle de soin, et d’identifier les facteurs cliniques ou pharmacologiques associés à la survenue d’un épisode de décompensation cardiaque.Un premier travail a permis de mesurer la fiabilité des bases de données médico-administratives françaises pour identifier des patients IC.Une deuxième étude a permis d’estimer que 17 à 37% de patients IC n’étaient exposés à aucun traitement de l’IC dans l’année suivant une première hospitalisation pour IC.Les troisième et quatrième parties de cette thèse ont mis en évidence qu’environ un quart des patients IC étaient réhospitalisés dans les 2 ans suivant une première hospitalisation. Les principaux facteurs cliniques prédictifs de cette réhospitalisation étaient l’âge, l’hypertension artérielle, la fibrillation auriculaire et le diabète. L’association retrouvée entre l’utilisation de fer bivalent et la réhospitalisation pour IC, souligne l’importance du risque lié à la présence d’une anémie ou d’une déficience en fer dans la survenue d’un épisode de décompensation cardiaque.Ces résultats permettent de reconsidérer la prise en charge thérapeutique chez les patients IC et mettent en avant la nécessité de renforcer la surveillance des patients les plus à risque de décompenser leur IC
In France, around one million persons would be affected by heart failure (HF); there are nearly 70 000 deaths related to HF and more than 150 000 hospitalizations despite a well defined treatment management. These numbers should increase in the next years due in particular to the ageing of the population.The objective of this work was to study the use of the pharmacological treatments indicated in HF (beta-blocker, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone antagonist, diuretics, digoxin, ivabradine) in real-world setting and to identify the clinical or pharmacological predictors associated with a new episode of cardiac decompensation.A first work has enabled to estimate the accuracy of French claims databases in identifying HF patients.A second study estimated that 17 to 37% HF patients were not exposed to any HF treatment in the year following an incident HF hospitalization.The third and fourth parts of this thesis showed that almost one forth of HF patients was rehospitalized within the 2 years following a first hospitalization. The main clinical predictors of rehospitalization were age, high blood pressure, atrial fibrillation and diabetes. The association found between bivalent iron use and HF rehospitalization underlines the importance of the risk related to anemia or iron deficiency in the occurrence of a cardiac exacerbation episode.These results allow to reconsider the treatment management of HF patients and highlight the need to reinforce the surveillance of patients with a highest risk of cardiac exacerbation
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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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Stewart, Simon. "Optimising therapeutic efficacy in acute and chronic cardiac disease states /." Title page, contents and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phs851.pdf.

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Morley-Davies, A. J. "Predicting death in chronic heart failure : electrocardiographic, autonomic and neuroendocrine risk assessment." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272860.

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Coats, Andrew J. S. "Doppler aortic velocimetry and the assessment of cardiac function in chronic heart failure." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305499.

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Lancaster, Jordan, and Jordan Lancaster. "Development and Testing of a Tissue Engineered Cardiac Construct for Treatment of Chronic Heart Failure." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/621361.

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There is a growing epidemic of chronic heart failure (CHF) in the developed world. The costs associated with providing care is profound and despite our best efforts, new, more effective treatments for CHF are needed; 50% of patients diagnosed with CHF are dead within 5 years. Current paradigms rely heavily on pharmacologic interventions, which merely help manage the disease. Surgical interventions may also be considered for late stage CHF patients such as heart transplant or left ventricular assist device (LVAD) but require burdensome and invasive surgical procedures. In addition they are costly, and require the need for life long immunosuppressive and anticoagulant therapies respectively. Despite our best intentions, the long-term prognosis for CHF patients remains poor. With over a decade of clinical investigation taken place, data from cell-based therapy trials remains inconsistent. While demonstrating safety, limited efficacy has been reported and to date, no stem cell therapy has been approved by the FDA. Despite these shortcomings important lessons have been learned that can be applied to future developments. Retrospective analysis of early cell-based clinical trial data has suggested that variations in isolated cell number, viability, and potency from donor to donor in autologous preparations yielded wide discrepancies in functional outcomes. In addition, sub culturing adult stem cells, even for short periods of time in 2D polystyrene environments void of complementary cell populations and extra cellular matrix protein interactions, may alter the therapeutic potential of a given cell. As a solution, allogeneic approaches where donor cell quality and potency can be assessed and optimized may help achieve functional benefits. Furthermore, co-dosing with multiple cell populations or developing 3D sub-culture environments that more closely mimic the in vivo milieu may ultimately yield more potent therapeutic cell populations. While these alterations may improve cell-based therapy outcomes, other solutions have been proposed such as tissue engineering. While the concept of tissue engineering is not new, advancements in biomaterials, bioreactor design and cell sources have greatly enhanced the reality of these preparations. Previously, one of the greatest limitations to tissue engineering is overcoming the cell requirements for developing and testing where millions if not billions of cells are required. Cell sourcing limitations appear to have been solved with the discovery and development of induced pluripotent stem cell (iPSC) derived cell populations. First reported in 2007, they have the ability to generate embryonic like pluripotent stem cells without the ethical concerns of embryonic stem cells. These iPSCs hold tremendous potential for drug toxicology / screening, personalized medicine and cell therapies. The body of work described in this dissertation looks at developing and testing a tissue engineered cardiac patch to treat heart failure. For which, an emphasis has been to provide 1) structural support for engrafted cells and 2) a rapidly inducible vascular supply once implanted in vivo. Biomaterials were sourced that facilitate infill by multiple cell populations in 3D culture and the establishment of extra cellular matrix deposits. Together, these patches enhanced cellular development in vitro and result in long term functional improvements in small animal models for CHF. Additional feasibility work was performed in large animal models to permit upscaling and development of surgical implantation techniques to demonstrate clinical applicability
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Sundararaman, Srividya. "Cell-Taught Gene Therapy for the Preservation and Regeneration of Cardiac Tissue Following Chronic Heart Failure." Cleveland State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=csu1294157257.

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Books on the topic "Chronic heart failure; Cardiac death"

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Chronic cardiac disease: Optimizing therapeutic efficacy in heart failure. London: Whurr, 2002.

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Rahimi, Kazem. Chronic heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0092.

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The European Society of Cardiology defines heart failure as a clinical syndrome in which patients have the following features: symptoms typical of heart failure (breathlessness, fatigue, ankle swelling); signs typical of heart failure (tachycardia, tachypnoea, pulmonary crackles, pleural effusion, raised jugular venous pressure, peripheral oedema, hepatomegaly); and objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heat sound, cardiac murmurs, abnormality on the echocardiogram, raised natriuretic peptide concentration). Heart failure results in activation of the sympathetic nervous system and the renin–aldosterone–angiotensin system, and release of a number of hormones such as natriuretic peptides, and cytokines, including tumour necrosis factor amongst others. While neurohormone activation is initially compensatory and helps in the short term to maintain circulatory needs, ultimately it has detrimental effects on the myocardium and compromises its function further. These mechanisms are therefore therapeutic targets to improve symptoms and lessen the risk of death.
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Slaughter, Mark S. Cardiac Surgery in Chronic Renal Failure. Wiley & Sons, Incorporated, John, 2008.

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Slaughter, Mark S. Cardiac Surgery in Chronic Renal Failure. Wiley & Sons, Incorporated, John, 2008.

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Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Chronic heart failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0754_update_004.

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The diagnosis and management of chronic heart failure are discussed. Medical therapy and indications for cardiac resynchronization therapy (CRT), implantable cardioverter-defibrillators (ICD), left ventricular assist devices (LVAD), and transplantation are presented. Recommendations by the ACC/AHA and ESC on the management of patients with heart failure have been summarized and tabulated.
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Goldsmith, David J. Cardiovascular disease and chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0098.

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Even after as full a statistical adjustment as can be made for traditional cardiovascular risk factors has been undertaken, impaired kidney function and raised concentrations of albumin in urine each increase the risk of cardiovascular disease (CVD) by two- to fourfold, the degree increasing with severity. If the patient is also suffering from diabetes (as either the cause of CKD or a complication of it), the risks of CVD increase two- to fourfold again. CKD patients should, therefore, be acknowledged as having perhaps the highest cardiovascular risk of any patient cohort. CVD is underdiagnosed and undertreated in these patients. In early CKD the manifestations of CVD are similar to those of other patients. In late CKD and particularly in patients on dialysis the epidemiology is different. Left ventricular hypertrophy is very common and sudden cardiac death is greatly increased in incidence. Heart failure is a common complication. Calcification of valves and vessels becomes increasingly common and bad CVD outcomes are associated with hyperphosphataemia and other manifestations. The mechanisms by which risks are increased are not fully understood. The evidence base for the effectiveness of established therapies for CVD is relatively light in patients with CKD, but there is evidence for benefit of lipid-lowering therapies and most nephrologists believe that blood pressure and volume control are important for good long-term outcomes. Evidence of impact on CVD of interventions to alter mineral bone disease is disappointingly weak.
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S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.

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S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.

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S, Slaughter Mark, ed. Cardiac surgery in chronic renal failure. Malden, Mass: Blackwell Futura, 2007.

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10

Bakris, George L. The Kidney in Heart Failure. Springer, 2014.

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Book chapters on the topic "Chronic heart failure; Cardiac death"

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Verschure, Derk O., K. Nakajima, and Hein J. Verberne. "123I-mIBG in the Risk Stratification of Sudden Cardiac Death in Chronic Heart Failure." In Nuclear Cardiology, 567–85. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62195-7_24.

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Böhm, Michael, and Erland Erdmann. "Therapy with Cardiac Glycosides." In Chronic Heart Failure, 115–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-85913-7_8.

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Guindo, J., A. Bayés de Luna, P. Torner, J. Bartolucci, and R. Estiarte. "Treatment of heart failure." In Sudden Cardiac Death, 255–65. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-009-0573-3_22.

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Keck, E. W. "Quality of Life of Infants and Children with Cardiac Disease and Cardiac Failure Both Before and After Cardiac Surgery." In Chronic Heart Failure, 132–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76433-2_11.

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Piepoli, Massimo F. "Congestive Heart Failure: Stable Chronic Heart Failure Patients." In Cardiac Rehabilitation Manual, 187–205. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84882-794-3_10.

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Piepoli, Massimo F. "Congestive Heart Failure: Stable Chronic Heart Failure Patients." In Cardiac Rehabilitation Manual, 207–26. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47738-1_10.

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Marín-García, José. "Cardiac Remodeling and Cell Death in Heart Failure." In Heart Failure, 213–31. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-147-9_11.

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Horie, Minoru, Hidetada Yoshida, Hideo Otani, Tomohiko Ai, Toshihisa Nishimoto, Tetsuya Haruna, Yutaka Kono, and Shigetake Sasayama. "Long QT Syndrome as a Cause of Cardiac Sudden Death." In Heart Failure, 105–13. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68331-5_9.

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Rychlik, R., D. Urbahn, and P. Potthoff. "The Questionnaire as a Tool for the Empirical Assessment of Quality of Life in Patients with Cardiac Failure." In Chronic Heart Failure, 165–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76433-2_13.

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Marban, Eduardo, and Gordon F. Tomaselli. "Sudden Cardiac Death in Heart Failure." In Medical Science Symposia Series, 357–67. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5022-4_40.

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Conference papers on the topic "Chronic heart failure; Cardiac death"

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Palacios, Saúl, Iwona Cygankiewicz, Antoni Bayés-de-Luna, Juan Pablo Martínez, and Esther Pueyo. "Sudden Cardiac Death Prediction in Chronic Heart Failure Patients by Periodic Repolarization Dynamics." In 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.209.

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Ram�rez, Julia, Michele Orini, Esther Pueyo, and Pablo Laguna. "T-wave Morphology Restitution Dependency with Heart Rate Range and Its Association with Sudden Cardiac Death in Chronic Heart Failure." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.221-009.

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Ram�rez, Julia, Michele Orini, Esther Pueyo, and Pablo Laguna. "Comparison of ECG T-wave Duration and Morphology Restitution Markers for Sudden Cardiac Death Prediction in Chronic Heart Failure." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.224-267.

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Martin, Alba, Iwona Cygankiewicz, Antoni Bayes-de-Luna, Pablo Laguna, Enrico G. Caiani, and Juan Pablo Martinez. "Index of T:wave Variation as a Predictor of Sudden Cardiac Death in Chronic Heart Failure Patients with Atrial Fibrillation." In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.002-366.

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Lenis, Gustavo, Robert Menges, Julia Ramirez, Iwona Cygankiewicz, Antoni Bayes de Luna, Juan Pablo Martinez, Pablo Laguna, and Olaf Doessel. "Postextrasystolic T Wave Change to Stratify Risk of Pump Failure Death in Patients with Chronic Heart Failure." In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.011-402.

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Naftali, Sara, Idit Avrahami, and Amir Landesberg. "Quantification of the hemodynamics inside a novel Synchronized Therapeutic Cardiac Assist Device for Chronic Heart Failure." In 2006 International Conference on Information Technology: Research and Education. IEEE, 2006. http://dx.doi.org/10.1109/itre.2006.381546.

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Kume, K., K. Amano, S. Yamada, T. Kanazawa, K. Hatta, and N. Kuwaba. "AB0489 Tofacitinib improves left ventricular mass and cardiac output in rheumatoid arthritis patients with chronic heart failure." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.1037.

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Mannion, T., L. Devaney, S. Fall, M. Carey, A. Jago, S. Fay, R. Pharithi, E. Egom, and V. Maher. "15 The relationship between the buckberg index and functional capacity in stable chronic heart failure patients." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 5th – Saturday October 7th 2017, Millennium Forum, Derry∼Londonderry, Northern Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2017. http://dx.doi.org/10.1136/heartjnl-2017-ics17.15.

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Uzbekova, Nelly, Sergey Kityan, and Nodira Badalbaeva. "CLINICAL STATUS AND STRUCTURAL AND FUNCTIONAL CARDIAC PARAMETERS IN PATIENTS WITH CHRONIC HEART FAILURE WITH PRESERVED EJECTION FRACTION." In ADVANCED DISCOVERIES OF MODERN SCIENCE: EXPERIENCE, APPROACHES AND INNOVATIONS. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-09.04.2021.v2.21.

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Verduri, Alessia, Bianca Beghé, Martina Garofalo, Sara Balduzzi, Michela Schito, Valentina Ruggieri, Alessandro Fucili, Leonardo M. Fabbri, Enrico Clini, and Piera Boschetto. "LATE-BREAKING ABSTRACT: Risk factors for hospitalization and death in elderly smokers with chronic obstructive pulmonary disease (COPD) and/or chronic heart failure (CHF)." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3712.

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Reports on the topic "Chronic heart failure; Cardiac death"

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Treadwell, Jonathan R., James T. Reston, Benjamin Rouse, Joann Fontanarosa, Neha Patel, and Nikhil K. Mull. Automated-Entry Patient-Generated Health Data for Chronic Conditions: The Evidence on Health Outcomes. Agency for Healthcare Research and Quality (AHRQ), March 2021. http://dx.doi.org/10.23970/ahrqepctb38.

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Background. Automated-entry consumer devices that collect and transmit patient-generated health data (PGHD) are being evaluated as potential tools to aid in the management of chronic diseases. The need exists to evaluate the evidence regarding consumer PGHD technologies, particularly for devices that have not gone through Food and Drug Administration evaluation. Purpose. To summarize the research related to automated-entry consumer health technologies that provide PGHD for the prevention or management of 11 chronic diseases. Methods. The project scope was determined through discussions with Key Informants. We searched MEDLINE and EMBASE (via EMBASE.com), In-Process MEDLINE and PubMed unique content (via PubMed.gov), and the Cochrane Database of Systematic Reviews for systematic reviews or controlled trials. We also searched ClinicalTrials.gov for ongoing studies. We assessed risk of bias and extracted data on health outcomes, surrogate outcomes, usability, sustainability, cost-effectiveness outcomes (quantifying the tradeoffs between health effects and cost), process outcomes, and other characteristics related to PGHD technologies. For isolated effects on health outcomes, we classified the results in one of four categories: (1) likely no effect, (2) unclear, (3) possible positive effect, or (4) likely positive effect. When we categorized the data as “unclear” based solely on health outcomes, we then examined and classified surrogate outcomes for that particular clinical condition. Findings. We identified 114 unique studies that met inclusion criteria. The largest number of studies addressed patients with hypertension (51 studies) and obesity (43 studies). Eighty-four trials used a single PGHD device, 23 used 2 PGHD devices, and the other 7 used 3 or more PGHD devices. Pedometers, blood pressure (BP) monitors, and scales were commonly used in the same studies. Overall, we found a “possible positive effect” of PGHD interventions on health outcomes for coronary artery disease, heart failure, and asthma. For obesity, we rated the health outcomes as unclear, and the surrogate outcomes (body mass index/weight) as likely no effect. For hypertension, we rated the health outcomes as unclear, and the surrogate outcomes (systolic BP/diastolic BP) as possible positive effect. For cardiac arrhythmias or conduction abnormalities we rated the health outcomes as unclear and the surrogate outcome (time to arrhythmia detection) as likely positive effect. The findings were “unclear” regarding PGHD interventions for diabetes prevention, sleep apnea, stroke, Parkinson’s disease, and chronic obstructive pulmonary disease. Most studies did not report harms related to PGHD interventions; the relatively few harms reported were minor and transient, with event rates usually comparable to harms in the control groups. Few studies reported cost-effectiveness analyses, and only for PGHD interventions for hypertension, coronary artery disease, and chronic obstructive pulmonary disease; the findings were variable across different chronic conditions and devices. Patient adherence to PGHD interventions was highly variable across studies, but patient acceptance/satisfaction and usability was generally fair to good. However, device engineers independently evaluated consumer wearable and handheld BP monitors and considered the user experience to be poor, while their assessment of smartphone-based electrocardiogram monitors found the user experience to be good. Student volunteers involved in device usability testing of the Weight Watchers Online app found it well-designed and relatively easy to use. Implications. Multiple randomized controlled trials (RCTs) have evaluated some PGHD technologies (e.g., pedometers, scales, BP monitors), particularly for obesity and hypertension, but health outcomes were generally underreported. We found evidence suggesting a possible positive effect of PGHD interventions on health outcomes for four chronic conditions. Lack of reporting of health outcomes and insufficient statistical power to assess these outcomes were the main reasons for “unclear” ratings. The majority of studies on PGHD technologies still focus on non-health-related outcomes. Future RCTs should focus on measurement of health outcomes. Furthermore, future RCTs should be designed to isolate the effect of the PGHD intervention from other components in a multicomponent intervention.
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