Bibliografie tematiche / Congenital heart disease

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Letteratura scientifica selezionata sul tema "Congenital heart disease"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 29 luglio 2024

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Articoli di riviste sul tema "Congenital heart disease"

Martins, Cristiane. "Congenital heart disease". Clinical Cardiology and Cardiovascular Interventions 3, n. 11 (20 novembre 2020): 01–02. http://dx.doi.org/10.31579/2641-0419/097.

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Taksande, Amar, e Sachin Dhamke. "Critical Congenital Heart Disease in Newborns". Pediatric Education and Research 5, n. 2 (2017): 87–95. http://dx.doi.org/10.21088/per.2321.1644.5217.17.

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Petrovna, Askaryans Vera, e Xikmatov Javoxirbek Sherali ogli. "CONGENITAL HEART DEFECTS". Eurasian Journal of Medical and Natural Sciences 03, n. 02 (1 febbraio 2023): 194–99. http://dx.doi.org/10.37547/ejmns-v03-i02-p1-32.

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Abstract (sommario):

Congenital heart defects (TYN), also known as congenital heart anomaly and congenital heart disease, are defects in the structure of the heart or great vessels present at birth. Congenital heart defects are classified as cardiovascular diseases. Signs and symptoms depend on the specific type of defect. Symptoms can be harmless or life-threatening. If present, symptoms may include rapid breathing, bluish skin (cyanosis), low weight, and fatigue. Congenital heart defects do not cause chest pain. Congenital heart defects are often not associated with other diseases. A complication of congenital heart defects is heart failure.

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Siu, S. C. "CONGENITAL HEART DISEASE: Heart disease and pregnancy". Heart 85, n. 6 (1 giugno 2001): 710–15. http://dx.doi.org/10.1136/heart.85.6.710.

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Kelleher, Andrea A. "Adult congenital heart disease (grown-up congenital heart disease)". Continuing Education in Anaesthesia Critical Care & Pain 12, n. 1 (febbraio 2012): 28–32. http://dx.doi.org/10.1093/bjaceaccp/mkr045.

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Allan, L. "CONGENITAL HEART DISEASE: Antenatal diagnosis of heart disease". Heart 83, n. 3 (1 marzo 2000): 367. http://dx.doi.org/10.1136/heart.83.3.367.

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Rathod, Bipin. "Anthropometric Profiles of Children with Congenital Heart Disease". Pediatric Education and Research 5, n. 1 (2017): 23–27. http://dx.doi.org/10.21088/per.2321.1644.5117.5.

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K., Thaslima, e Sunil Mhaske. "Neurodevelopmental Status of Children with Congenital Heart Disease". Indian Journal of Trauma and Emergency Pediatrics 8, n. 2 (2016): 99–102. http://dx.doi.org/10.21088/ijtep.2348.9987.8216.10.

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Qureshi, Shakeel A., e Lee Benson. "Congenital heart disease". Future Cardiology 8, n. 2 (marzo 2012): 143–47. http://dx.doi.org/10.2217/fca.12.22.

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Puri, Kriti, Hugh D. Allen e Athar M. Qureshi. "Congenital Heart Disease". Pediatrics in Review 38, n. 10 (ottobre 2017): 471–86. http://dx.doi.org/10.1542/pir.2017-0032.

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Tesi sul tema "Congenital heart disease"

Rowlinson, Giselle Victoria. "Connexins in congenital heart disease". Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.550483.

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Gap junctions are clusters of transmembrane channels, composed of connexins (Cx), that facilitate electrical and chemical communication between the cytoplasmic compartments of contiguous cells. Three connexins are expressed in cardiac myocytes, Cx40, Cx43 and Cx45. Targeted deletion of these connexin genes in mice results in cardiac malformations and conduction abnormalities. From this background, the question arises as to whether connexins play a role in human congenital heart disease. Atrial and ventricular tissue samples were studied from patients undergoing cardiac surgery. Immunoconfocal microscopy and western blot analysis of atrial tissue revealed that expression of CX40 and CX43 in children and adults with congenital heart disease is the same as that in the normal adult atrium, irrespective of the underlying malformation. Normal adult ventricular working myocytes express only CX43. Study of control ventricular samples in children confirmed that, as in adults, CX43 only is expressed. However, immunoconfocal microscopy of samples from patients with right ventricular outflow obstruction (tetralogy of Fallot and double chambered right ventricle) revealed that in addition to CX43, CX40 is also highly expressed. Expression is heterogeneous and CX40 is eo-localised with CX43. Quantitative western blot analysis showed that up to 10% of the total connexin expressed in these samples is CX40. As patients re-operated following previous repair (with markedly different underlying haemodynamics) still demonstrated high CX40 expression in the working myocardium, these results suggest that a lack of normal CX40 repression during development leads to heart malformations . . Gap junction channels formed from each connexin isofonn have distinctive biophysical properties. Connexin eo-expression further alters these properties. To investigate the functional consequences of the connexin eo-expression patterns observed in the ventricular samples, in vitro cell models were used. Intercellular communication was assessed using cell-to-cell Lucifer Yellow dye transfer in an inducible RLE cell line and conducjion properties were studied in an atrial myocyte (HL-l) cell line. The findings are consistent with the idea that altered function arising from abnormal embryonic connexin expression is a contributor to some types of human cardiac malformation.

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Grech, Victor. "Congenital heart disease in Malta". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286359.

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Khetyar, Maher. "Genetics of congenital heart disease". Thesis, St George's, University of London, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.754064.

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Congenital Heart Disease (CHD) is the leading non-infectious cause of death among children less than one year. CHD is genetically heterogeneous, but analysis of large multi-generational families has led to the identification of a number of genes for CHD. In this project I investigated the molecular genetic basis of CHD in a large Kuwaiti family with clinically diagnosed truncus arteriosus. Using a homozygosity mapping approach I identified a region of interest on chromosome 8p21. I proceeded to sequence candidate genes in this region. One of the novel genes identified was predicted to be the human homolog of mouse Nkx2.6, a gene encoding a homeobox transcription factor expressed in the sinus venosa and the myocardium of the outflow tract in the developing mouse heart. Sanger sequencing identified a Phel51Leu mutation which segregated with disease in the family. Next I investigated whether mutations in Nkx2.6, or the related gene Nkx2.5, were a common cause of type I truncus arteriosus in 12 unrelated individuals. However I found no mutations, suggesting the pattern of inheritance in this phenotype is likely to be complex and potentially multifactorial. Finally I investigated the molecular genetic basis of another congenital heart defect known as Patent Ductus Arteriosus (PDA) in a multigenerational Kuwaiti family with six affected members. A condition known as Char Syndrome is characterized by a combination of major features one of which is PDA and can be caused by mutations in the TFAP2B gene which encodes the Transcription Factor AP-2 Beta. I therefore hypothesised that mutations in TFAP2B may also be responsible for PDA in the Kuwaiti family. I identified a predicted splice site variant in this gene that segregated with disease status. A full clinical history and physical examination confirmed that no affected members of this family have any of the remaining features of Char Syndrome suggesting that mutations in TFAP2B can also cause isolated PDA.

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Bentham, James Robert. "Genetic & molecular mechanisms of congenital heart disease". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496824.

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Lyon, Joy E. "Adults with congenital heart disease : the patients' perspective". Thesis, Bournemouth University, 2006. http://eprints.bournemouth.ac.uk/10535/.

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Over the last 50 years technical and other advances have resulted in more than 90% of children born with congenital heart disease (CHD) surviving and reaching adulthood. This new patient population has been largely overlooked in recent policy and practice developments in health and social care. Evidence available at the start of the study confirmed increased survival and suggested the need for life long follow up. There was found to be limited research exploring the view of what was required by adults with CHD or into psychosocial aspects of living with a heart condition. The purpose of this phenomenological study was to discover the adults' experience of living with CHD. Twenty-eight people, over the age of 20 years, who had undergone surgery for their heart condition, participated in semi-structured interviews during which they recounted their experience of growing up and living with CHD. Five people, who epitomised being well, contributed to second interviews during which they told stories that demonstrated what being well meant for them. Thematic analysis revealed participants had a positive view of themselves and were highly motivated to maintain their health. Their heart condition was an integral part of who they were, but did not dominate their life. Three main areas influenced the positive view held by participants. These were: first the perceptions of wider society, second when the CHD impacted on available choices, and third when hospital attendance occurred. Second interviews revealed `being well' developed through participants' ability to make their own decisions, which was done in a responsible manner, resulting in informants being able to get on with life, engaging in activities of their choosing. The study findings inform proposals for services to develop in ways that can enhance opportunities for adults with CHD to achieve their full potential. Developing skills relevant to `non-patient' activities and managing the misconceptions of wider society are key factors in adults with CHD being able to participate in meaningful activities of their choice. It is essential for health and social care to be delivered in ways that promote patient autonomy and self-management. Areas for further research emerge from the findings. Hearing the way living with CHD is experienced during childhood and adolescence can contribute to transition processes. Hearing the experience of other groups including parents, partners and health professionals, as well as people surviving with other chronic childhood conditions, can add to the findings presented here.

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Hanna, E. J. "Epidemiological and genetic studies in congenital heart disease". Thesis, Queen's University Belfast, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373007.

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Patel, Chirag. "Molecular genetic analysis of familial congenital heart disease". Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4471/.

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Development of the human heart is a complex process controlled by multiple genes (in interacting pathways), many of which are still to be determined. Abnormal heart development results in a spectrum of congenital heart disease (CHD), occurring in isolation or part of a syndrome, and with or without a family history, implying a genetic basis in some individuals. In this project I investigated the molecular genetic basis of CHD, in 23 families with nonsyndromic CHD. Using autozygosity mapping, I initially investigated the molecular basis of CHD in a single large consanguineous family (CHD1), and identified a region of interest containing a candidate gene (GDF1). I proceeded to sequence GDF1 (and genes in the same developmental pathway - NODAL, CFC1, TDGF1, and FOXH1) in 9 kindreds, but did not identify any pathogenic mutations. I then utilised whole exome sequencing (WES) to identify candidate mutations in potential CHD genes (GMFG, WNT11 and DVL2), and investigated these further by conventional sequencing. A novel GMFG nonsense variant was validated in family CHD1 and was absent from ethnically matched controls. Bioinformatics analysis of WES data from 19 affected individuals from 9 kindreds did not identify a frequently mutated candidate gene (or further GMFG candidate mutations), though candidate variants in individual kindreds were identified. Further functional analysis using animal models is required to determine the pathophysiological effect of the GMFG truncating mutation in cardiac development.

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Plymen, C. M. "The right ventricle in adult congenital heart disease". Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1431817/.

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Heart failure (HF) and sudden cardiac death (SCD) in congenital heart disease (CHD) is prevalent and can relate to abnormal right ventricular (RV) physiology and abnormalities of QRS duration, and QRS, JT and QT dispersion (d). Characterising disease and identifying factors that may predict adverse outcome in those with either a subpulmonary or subsystemic RV, as well as investigating potential avenues to ameliorate abnormal RV physiology is necessary to improve outcomes in this young population. I undertook several studies during the course of this Thesis to examine and further understand these two separate physiological substrates: In the first I studied the effect of isolated percutaneous (PPVI) pulmonary valve implantation on surface ECG parameters. PPVI represents a pure model of RV mechanical and electrophysiological changes post replacement as compared to surgical replacement: Ninety nine PPVI procedures in patients with CHD (aged 23.1±10 yrs) were studied pre, post and 1-year following PPVI with serial ECG’s and echocardiography/ magnetic resonance imaging (CMR). 43% had pulmonary stenosis, 27% pulmonary regurgitation (PR) and 29% mixed lesions. In those with predominantly PR (n=26), QRS duration decreased significantly (135±27 to 128±29ms; p=0.007). However, in the total cohort no significant change in QRS duration at 1 year was observed (137±29 to 134±29ms). QTc, QRSd, QTd and JTd all significantly reduced at 1 yr (p≤0.001). RV EDV correlated with pre-procedure QRS duration (r=0.34; p<0.002) but there was no correlation after PPVI. This is the first study to report electrical remodelling following isolated PPVI and it confirms that reductions in QRS duration occur post PPVI in PR, as reported for equivalent surgical cohorts. Further, increased homogeneity of repolarisation, in combination with improved conduction, may reduce arrhythmic events in congenital cardiac patients with pulmonary valvular disease. My second study sought to create an epicardial electroanatomic map of the RV and then apply post-operative targeted single and dual site RV temporary pacing with measurement of haemodynamic parameters. I wished to determine the potential role of cardiac resynchronization therapy (CRT) in the setting of RV dysfunction as little is known regarding the potential benefits of CRT in this setting. Sixteen adults (age=32±8 yrs, 6M; 10F) with right bundle branch block (RBBB) and repaired tetralogy of Fallot (ToF; n=8) or corrected congenital pulmonary stenosis (n=8) undergoing surgical pulmonary valve replacement (PVR) for PR underwent intra-operative epicardial RV mapping and haemodynamic assessment of random pacing configurations including site of latest RV activation. I found that the commonest site of latest activation was the RV free wall & dual chamber (DDD) pacing here, alone or combined with RV apical pacing, resulted in significant increases in cardiac output (CO) vs AAI pacing (p<0.01 all measures). DDD RV alternative site pacing significantly improved CO by 16 % vs AAI, and 8.5% versus DDD RV apical pacing (p=0.02). Single site RV pacing targeted to the region of latest activation in patients with RBBB undergoing PVR thus induces acute improvements in haemodynamics and implies that targeted pacing in such patients has therapeutic potential both post-operatively and in the long term. QRS duration is a strong predictor of survival in acquired left ventricular dysfunction, but equivalent data in those with a systemic RV is lacking. My next studies investigated not only the relationship between ECG parameters, arrhythmia burden and outcome in adults with transposition of the great arteries (TGA) late after atrial switch repair, but also the interrelationships between various HF markers in this cohort. Adults with Senning or Mustard palliation of TGA under follow up at a dedicated congenital HF clinic and 13 similar adults who suffered a cardiac death were included for study. Patients were subdivided by arrhythmic history, surgical intervention and death. Assessment included symptom assessment, venous blood sampling for circulating N-terminal pro brain natriuretic peptide (NT-proBNP) levels, measurement of surface ECG and CMR for the assessment of RV systolic function and determination of indexed RV volumes. I found that QRS duration (p=0.0003) and QTc interval (p=0.0009) increase significantly with changing arrhythmia subtype, and that both QRS and QTc were independently associated with increased risk of death: for 1ms increase in QRS HR 15 [95% CI 3.3-68.6] and for QTc HR 10.7 [95% CI 2.3-49] (p<0.0001 for both). QRS >104ms and QTc >406ms had a sensitivity/specificity for predicting death of 96%/66% and 96%/56% respectively. Two year mortality was 36% when QRS<104ms and 88% when >104ms (p<0.0001 for difference). Further, compared to those with uncomplicated surgery, patients with complex surgical history had higher NT-proBNP levels (55±26 vs 20±35pmol/L; P=0.002) and longer QRS duration (116±28ms vs 89±11ms; P=0.0004) whilst showing no difference in NYHA class and RV function. There was a significant relationship between diastolic and systolic RV volumes and both NT-proBNP levels (r=0.43, P=0.01; r=0.53, P=0.001 respectively) and QRS duration (r=0.47, P=0.004; r=0.53, P=0.001 respectively). These findings suggest that QRS width and corrected QTc interval on surface ECG are associated with increased risk of death in adults late after atrial switch repair of TGA. Given that a QRS of only 104ms defines a high risk population, careful examination of the ECG is desirable in all patients and therapy to reduce risk attempted. Further, together with these simple surface ECG parameters, circulating NT-proBNP levels constitute safe, cost effective and widely available surrogate markers of systemic RV function and provide additional information on heart failure status. Both measures hold promise as prognostic markers and their association with long-term outcome should be determined. Lastly, I examined the mechanisms of late RV failure and studied their relationship to subjective quality of life assessment as this are poorly characterised. Equilibrium Contrast CMR imaging was used to quantify extracellular volume (ECV) in the septum and RV free wall of adults presenting to a specialist clinic late after atrial redirection surgery for TGA. These were compared to age and sex matched healthy volunteers. Patients were also assessed with a standardised CMR protocol, NT-proBNP and surface ECG measurement, and cardiopulmonary exercise (CPEX) testing. Patients also completed a Minnesota Living With Heart Failure Questionnaire (MLHFQ) self assessment. I determined that mean septal ECV was significantly higher in patients than controls (0.254±0.036, vs 0.230±0.032; p=0.03). NT-proBNP positively related to septal ECV (p=0.04; r=0.55) but chronotropic index (CI) during CPEX testing negatively related to ECV (p=0.04; r=-0.58). No relationship was seen with other CMR or CPEX parameters. Median MLHFQ score was 6(2-19), median NT-pro BNP 24 (16-43) and mean peak VO2 24±7mL/kg/min. There was a significant positive correlation between MLHFQ score and NT-proBNP (p=0.001, r=0.34) and a significant negative correlation with peak VO2 (p=0.001, r=0.49. ). Septal interstitial expansion is seen in adults late after atrial redirection surgery for TGA. It correlates well with NT-proBNP and CI and may have a role in the development of RV systolic impairment. The MLHFQ correlates highly with NT-proBNP and exercise capacity in patients with systemic RV impairment. The ability of the MLHFQ in predicting HF events and prognosis in adults with CHD needs further evaluation.

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Lipscomb, Sund Kristen. "Adults with Congenital Heart Disease: A Genetic Perspective". University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1252702239.

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Tseng, Stephanie Y. "Altered Erythropoiesis in Newborns with Congenital Heart Disease". University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1592170832331138.

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Più fonti

Libri sul tema "Congenital heart disease"

1940-, Macartney F. J., a cura di. Congenital heart disease. Lancaster, England: MTP Press, 1986.

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Mary, Kearns-Jonker. Congenital Heart Disease. New Jersey: Humana Press, 2006. http://dx.doi.org/10.1385/159745088x.

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Macartney, F. J., a cura di. Congenital Heart Disease. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4872-3.

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Senzaki, Hideaki, e Satoshi Yasukochi, a cura di. Congenital Heart Disease. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-54355-8.

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Bergersen, Lisa, Susan Foerster, Audrey C. Marshall e Jeffery Meadows, a cura di. Congenital Heart Disease. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-77292-9.

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Flocco, Serena Francesca, Angelo Lillo, Federica Dellafiore e Eva Goossens, a cura di. Congenital Heart Disease. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-78423-6.

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M, Bartelings M., Hazekamp M. G, Wenink Arnold C. G e Boerhaave Commissie voor Postacademisch Onderwijs in de Geneeskunde., a cura di. Congenital heart disease. [Leiden?]: Boerhaave Committee for Postgraudate Medical Education, Leiden University, 1998.

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Bartelings, M. M., e Arnold C. G. Wenink. Congenital heart disease. Leiden: Boerhaave Committee for Postgraduate Medical Education, Leiden University Medical Center, 1999.

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1932-, Roberts William C., a cura di. Adult congenital heart disease. Philadelphia: Davis, 1987.

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Butera, Gianfranco, Silvia Schievano, Giovanni Biglino e Doff B. McElhinney, a cura di. Modelling Congenital Heart Disease. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-88892-3.

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Capitoli di libri sul tema "Congenital heart disease"

Galve-Basilio, E. "Congenital heart disease". In Developments in Cardiovascular Medicine, 282–94. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1984-9_15.

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Prapa, Matina, Dimitra Krexi, Anselm Uebing e Michael A. Gatzoulis. "Congenital Heart Disease". In Essential Cardiology, 361–75. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6705-2_20.

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Subirana-Doménech, M., e X. Borrás-Pérez. "Congenital heart disease". In Atlas of Practical Cardiac Applications of MRI, 106–33. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4544-2_10.

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Mee, R. B. B. "Congenital heart disease". In Oesophageal Atresia, 229–39. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-3079-8_15.

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Pillutla, Priya, e Jamil A. Aboulhosn. "Congenital Heart Disease". In Atlas of Cardiovascular Computed Tomography, 339–50. London: Springer London, 2017. http://dx.doi.org/10.1007/978-1-4471-7357-1_17.

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Pieles, Guido E., e A. Graham Stuart. "Congenital Heart Disease". In IOC Manual of Sports Cardiology, 263–74. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119046899.ch24.

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Backer, Carl L., e Constantine Mavroudis. "Congenital Heart Disease". In Surgery, 1315–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-57282-1_59.

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Mocumbi, Ana, Tantchou Tchoumi Jacques Cabral, John Musuku e Serigne A. Ba. "Congenital heart disease". In The Heart of Africa, 35–43. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119097136.ch2.

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Abramzon, Fernando, Maria Jose Bosaleh, Pablo Pollono, Ezequiel Levy Yeyati, Juan Wolcan e Gastón A. Rodríguez-Granillo. "Congenital Heart Disease". In Clinical Atlas of Cardiac and Aortic CT and MRI, 201–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-03682-9_6.

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Vegas, Annette. "Congenital Heart Disease". In Perioperative Two-Dimensional Transesophageal Echocardiography, 219–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-60902-7_10.

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Atti di convegni sul tema "Congenital heart disease"

Sharma, T., A. Aujla, N. Shah, N. Patel e J. Kluger. "Cyanotic Congenital Heart Disease in Adulthood". In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1928.

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Amelia, P., B. Lubis, R. Adriansyah, T. C. L. Tobing, M. Ali e H. Z. Abdillah. "Nutritional Status in Congenital Heart Disease". In International Conference of Science, Technology, Engineering, Environmental and Ramification Researches. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0010102909330935.

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Krishnan, Usha, Erika Berman Rosenzweig, Julia Wynn, Gudrun Aspelund, Marc S. Arkovitz e Wendy Chung. "Congenital Heart Disease In Association With Congenital Diaphragmatic Hernia. Impact On Outcome". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1847.

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Krivec, Uros, Marina Praprotnik, Malena Aldeco, Dusanka Lepej, Ana Kotnik Pirs, Aleksandra Zver, Jana Lozar Krivec, Tomaz Podnar, Jelena Berger e Matevz Srpcic. "Airway abnormalities in children with congenital heart disease". In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4171.

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Kockar, Tuba, Mehmet Gunduz, Sedat Oktem, Semra Gundogdu, Fatma Gamze Demirel, Ayhan Tastekin e Hacer Kamali. "Bronchoscopic findings in children with congenital heart disease". In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1355.

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Ehmann, A. L. S., L. Pruessner, S. Barnow, P. Helm e U. Bauer. "Emotion Regulation in Adults with Congenital Heart Disease". In 52nd Annual Meeting of the German Society for Pediatric Cardiology. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705568.

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Guerin, Sophie, Nathalie Bertille, Diala Khraiche, Damien Bonnet, Francois Goffinet, Nathalie Lelong, Babak Khoshnood e Christophe Delacourt. "Lung function in children with congenital heart disease". In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4676.

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Icheva, V., J. Ebert, U. Budde, G. Wiegand, S. Schober, J. Engel, M. Kumpf et al. "Acquired von Willebrand's Syndrome in Congenital Heart Disease". In The 54th Annual Meeting of the German Society for Pediatric Cardiology (DGPK). Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1743019.

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Hawkins, Stephen M. M., Amy L. Taylor e Christopher M. Rausch. "Restrictive Lung Disease In Pediatric Patients With Structural Congenital Heart Disease". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6128.

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Xu, Xiaowei, Tianchen Wang, Dewen Zeng, Yiyu Shi, Qianjun Jia, Haiyun Yuan, Meiping Huang e Jian Zhuang. "Accurate Congenital Heart Disease Model Generation for 3D Printing". In 2019 IEEE International Workshop on Signal Processing Systems (SiPS). IEEE, 2019. http://dx.doi.org/10.1109/sips47522.2019.9020624.

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Rapporti di organizzazioni sul tema "Congenital heart disease"

Vanreusel, Inne, Wendy Hens, Jan Taeymans, Emeline Van Craenenbroeck, An Van Berendoncks, Bernard Paelinck, Vincent Segers e Jacob J. Briedé. Oxidative Stress in Patients with Congenital Heart Disease: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maggio 2023. http://dx.doi.org/10.37766/inplasy2023.5.0044.

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Review question / Objective: To conduct a systematic review and meta-analysis of clinical controlled studies comparing parameters measuring oxidative stress in blood of patients with congenital heart disease (CHD). Main objective: to review studies on the presence of oxidative stress in both children and adults with CHD. Secondary objectives: - to review methods to assess oxidative stress levels in peripheral blood of CHD - to review factors with the potential to influence oxidative stress levels - to study whether there are therapeutic options targeting oxidative stress in CHD.

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Zhang, Ruizhe, e Qingya Xie. A meta-analysis of cholesteryl ester transfer protein(CETP) gene rs708272(G>A) polymorphism in association with cornoary heart disease risk. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, giugno 2023. http://dx.doi.org/10.37766/inplasy2023.6.0021.

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Review question / Objective: To seek the association of the CETP rs708272 polymorphism with CHD.To figure out if the carriers of allele rs708272-A reduce or increase the risk of CHD in comparison with carriers of allele rs708272-G under allele model, dominant model and recessive model. Condition being studied: The inclusion criteria of CHD:(1)the presence of stenosis≥50% in a minimum of one main segment of coronary arteries (the right coronary artery, left circumfex, or left anterior descending arteries) by coronary angiography.(2) symptoms representing angina pectoris, electrocardiographic changes, and elevations of cardiac enzymes based on the criteria of the World Health Organization. (3) a certifed record of coronary artery bypass graft or percutaneous coronary intervention were included in the study.The exclusion criteria of CHD :patients with congenital heart disease, cardiomyopathy, and valvular disease.Controls:the same populations as the cases and specifed to be without CAD, cardiovascular and cerebrovascular diseases, and peripheral atherosclerotic arterial disease.

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Guo, Xiaozhen, e Xing Wang. Effects of Aerobic Exercise on Cardiopulmonary Function in Postoperative Patients with Congenital Heart Disease：a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2024. http://dx.doi.org/10.37766/inplasy2024.4.0016.

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