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Academic literature on the topic 'Ischaemic heart disease'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Ischaemic heart disease"

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Shah, Dr Aashka M. "Fibrinogen and Ischaemic Heart Disease." International Journal of Scientific Research 3, no. 6 (June 1, 2012): 257–58. http://dx.doi.org/10.15373/22778179/june2014/81.

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Saeid, Feyzizadeh, Javadi Aniseh, Badalzadeh Reza, and Vafaee S. Manouchehr. "Signaling mediators modulated by cardioprotective interventions in healthy and diabetic myocardium with ischaemia–reperfusion injury." European Journal of Preventive Cardiology 25, no. 14 (February 14, 2018): 1463–81. http://dx.doi.org/10.1177/2047487318756420.

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Ischaemic heart diseases are one of the major causes of death in the world. In most patients, ischaemic heart disease is coincident with other risk factors such as diabetes. Patients with diabetes are more prone to cardiac ischaemic dysfunctions including ischaemia–reperfusion injury. Ischaemic preconditioning, postconditioning and remote conditionings are reliable interventions to protect the myocardium against ischaemia–reperfusion injuries through activating various signaling pathways and intracellular mediators. Diabetes can disrupt the intracellular signaling cascades involved in these myocardial protections, and studies have revealed that cardioprotective effects of the conditioning interventions are diminished in the diabetic condition. The complex pathophysiology and poor prognosis of ischaemic heart disease among people with diabetes necessitate the investigation of the interaction of diabetes with ischaemia–reperfusion injury and cardioprotective mechanisms. Reducing the outcomes of ischaemia–reperfusion injury using targeted strategies would be particularly helpful in this population. In this study, we review the protective interventional signaling pathways and mediators which are activated by ischaemic conditioning strategies in healthy and diabetic myocardium with ischaemia–reperfusion injury.
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Fox, K., and D. G. Julian. "Ischaemic heart disease." Current Opinion in Cardiology 1, no. 4 (July 1986): 451–52. http://dx.doi.org/10.1097/00001573-198607000-00001.

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Julian, D. G., and K. Fox. "Ischaemic heart disease." Current Opinion in Cardiology 1, no. 6 (1986): 825–26. http://dx.doi.org/10.1097/00001573-198611000-00001.

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&NA;. "Ischaemic heart disease." Current Opinion in Cardiology 1, no. 6 (1986): 963–76. http://dx.doi.org/10.1097/00001573-198611000-00029.

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Julian, D. G. "Ischaemic heart disease." Current Opinion in Cardiology 2, no. 6 (November 1987): 947–48. http://dx.doi.org/10.1097/00001573-198711000-00001.

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&NA;. "Ischaemic heart disease." Current Opinion in Cardiology 3, no. 4 (July 1988): 561–651. http://dx.doi.org/10.1097/00001573-198803040-00012.

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&NA;. "Ischaemic heart disease." Current Opinion in Cardiology 3, no. 4 (July 1988): 561–651. http://dx.doi.org/10.1097/00001573-198807000-00012.

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Crouse, JohnR. "ISCHAEMIC HEART DISEASE." Lancet 341, no. 8850 (April 1993): 931–32. http://dx.doi.org/10.1016/0140-6736(93)91218-b.

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Peters, David, P. G. F. Nixon, Wayne Perry, and Val Hopwood. "Ischaemic heart disease." Complementary Therapies in Medicine 2, no. 1 (January 1994): 14–20. http://dx.doi.org/10.1016/0965-2299(94)90154-6.

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Dissertations / Theses on the topic "Ischaemic heart disease"

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O'Sullivan, Christine Ann. "Electromechanical changes in ischaemic heart disease." Thesis, Imperial College London, 2006. http://hdl.handle.net/10044/1/8251.

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In coronary artery disease,. resting electrical and mechanical function of the left ventricle may vary according to different presentations. Stress or exercise in these patients results in electrical disturbances, which may havc mechanical consequences. The objectives ofthis thesis were: I) to assess the effect of the presence and location of Q wave myocardial infarction on left ventricular segmental mechanical function and identify patterns ofdisturbances. 2) to study the acute implications of induction of localised myocardial infarction at the proximal ventricular septum on ventricular performance. 3) to determine the effect of pharmacological stress on left and right ventricular behaviour in patients with coronary artery disease. AIl patients were studied by Doppler echocardiography using conventional measurements, as well as detailed assessment of long axis function and 12 lead surface EeG's. The foHowing groups ofpatients were studied: a). 72 patients with old Q wave MI; 35 anterior and 37 inferior. b) 54 patients with old anterior MI; 39 Q wave and 15 non-Q wave MI. c) 20 symptomatic patients with hypertrophic obstructive cardiomyopathy before and after non-surgical septal reduction therapy. d) . 27 patients with coronary artery disease, at rest and during dobutamine stress to assess left ventricular fune:tion. e) 33 patients with triple coronary artery disease at rest and at peak dobutamine stress to assess right ventricular function. The normal septal Q wave was' absent in 94% of anterior and 8% of inferior MI patients. Long axis amplitude and shortening and lengthening velocities were globaIly reduced in anterior and inferior myocardial infarction and the onset of shortening and lengthening were delayed by 30-40ms and 20-30 ms respectively in the two patient groups. Post ejection ~hortening was localised to the septum in the majority of patients with anterior myocardial infarction, but was generalised in patients with inferior infarction. 1) The normal septal Q wave was absent in 10% of control subjects and in 46% of patients with non-Q wave myocardial infarction. Q wave anterior MI was associated with a scarred septum and dilated LV cavity. Long axis amplitude was not different from normal in non-Q wave-infarction, but its onset ofshortening and lengthening was delayed by 20ms. Post ejection shortening occurred more frequently in Q wave infarction (76%) compared with non-Q wave infarction (21 %). These .abnormalities were localised to the left rand septal sites in non-Q wave infarction in contrast to their global distribution in Q wave infarction. . 2) Induction of localised upper septal myocardial infarction with alcohol resulted in broadening of the QRS (by 35ms), RBBB in 80% of patients, development of reduced septal long axis amplitude, and accentuated post ejection shortening at the septal long axis site. 3) In contrast to controls, dobutamine stress results in progressive broadening of QRS duration and prolongation of the QTc interval in patients with coronary artery disease, with corresponding reductions in long axis amplitude of motion and peak lengthening .velocity. 4) In patients with triple vessel coronary disease, dobutamine stress results in right ventricular long axis ischaemic disturbances similar to those seen on the left. Failure ofright ventricular long axis amplitude to increase by 2 mm was 88% specific for detecting right ventricular ischaemic dysfunction, which also correlated with the attenuated cardiac output at peak stress r= 0.56, p
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Claesson, Maria. "Women's hearts : ischaemic heart disease and stress management in women." Doctoral thesis, Umeå : Department of Public Health and Clinical Medicine, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-725.

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Horan, P. G. "Unravelling the genetic basis of ischaemic heart disease." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426746.

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Byrne, Conor James. "Ischaemic and pharmacological preconditioning of the uraemic heart." Thesis, Queen Mary, University of London, 2011. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8831.

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The incidence and mortality from cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) far exceeds that seen in the general population. Whilst a number of risk factors and associations have been identified in patients with CKD that may contribute to the increased risk of CVD, our understanding of the underlying pathophysiology remains poor. It has previously been reported that uraemic animals sustain larger myocardial infarcts and that this ‘reduced ischaemia tolerance’ may in part explain the excess mortality from CVD seen in CKD patients. The aim of this work was to establish an in vivo model of uraemic myocardial infarction in order to further explore the pathophysiology of uraemic CVD with particular focus on ameliorating myocardial ischaemia-reperfusion injury using ischaemic and pharmacological preconditioning. An increase in myocardial infarct size was demonstrated in the sub-total nephrectomy model of chronic uraemia, confirming previous reports in the literature. However, infarct size was not found to be increased in adenine diet induced renal failure. In addition, it was demonstrated for the first time, that the techniques of ischaemic preconditioning (IPC) and remote ischaemic preconditioning (RIPC) are both efficacious and not attenuated by chronic uraemia induced by sub-total nephrectomy or adenine diet (IPC only). Investigations were undertaken using an agent (a HIF stabiliser, FG4497) to induce pharmacological preconditioning in both animals with renal insufficiency and those without. These studies demonstrate that stabilisation of hypoxia inducible factor (HIF) may be a promising strategy to induce pharmacological preconditioning. It is hoped that this work may lay the foundations for future investigations to determine why sub-totally nephrectomised rats have larger infarcts whilst those with adenine induced renal failure, with a substantially greater degree of renal dysfunction, do not. Moreover, it is hoped that; by demonstrating that uraemia 3 does not prevent or attenuate the myocardial protection afforded by ischaemic preconditioning, the recruitment of patients with CKD will be encouraged to clinical trials of both ischaemic preconditioning and other therapies to limit myocardial infarction.
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Awad, Wael Ibrahim Issa. "Ischaemic preconditioning in the neonatal rat heart." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391636.

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O'Kane, Peter Danny. "The role of nitric oxide in ischaemic heart disease." Thesis, King's College London (University of London), 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420333.

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Mackie, Eileen Elizabeth. "Exercise and haemostasis in health and ischaemic heart disease." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433574.

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Teece, Stewart. "The assessment of ischaemic heart disease in the emergency department." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499952.

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Wright, Robert Anthony. "Hyperinsulinaemia, insulin resistance and endogenous fibrinolysis in ischaemic heart disease." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/21618.

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The work presented in this thesis has explored the hypotheses that disturbances of insulin and of endogenous fibrinolysis are a feature of patients with established ischaemic heart disease and investigated the potential manipulation of these by an inhibitor of the angiotensin converting enzyme. The possibility that the presence of either a previous myocardial infarction or of heart failure might influence the development of hyperinsulinaemia was studied. Only patients with heart failure showed fasting hyperinsulinaemia, whereas the increased insulin response to an oral glucose load in those with heart failure or previous myocardial infarction was similar, and greater than the response in patients with stable angina. Hyperinsulinaemia has been previously associated with impaired peripheral muscle glucose uptake and metabolism and might contribute to the development of muscular fatigue on exertion in patients with previous myocardial infarction or with heart failure. Amongst patients with ischaemic heart disease who had a normal fasting plasma glucose, one fifth had impaired glucose tolerance on formal testing and this group exhibited significantly greater fasting and stimulated hyperinsulinaemia. Including all patients, there was an inverse relationship between left ventricular ejection fraction and fasting plasma insulin concentration. Impaired endogenous fibrinolysis has been associated with an adverse prognosis in patients with ischaemic heart disease. The effect of captopril upon tissue-type plasminogen activator and on plasminogen activator inhibitor type 1 was investigated in patients with recent uncomplicated myocardial infarction. Captopril caused a significant reduction in antigen levels of both type plasminogen activator and on plasminogen activator inhibitor type 1. This may help to explain the reduction in acute coronary syndromes that has been associated with the use of captopril following acute myocardial infarction.
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See, Hoe Louise. "Mechanisms and Clinical Utility of Sustained Ligand-Activated Preconditioning." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/365566.

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Ischaemic heart disease (IHD) remains a leading cause of global morbidity and mortality, with persistent prevalence in Western populations, and a growing incidence in the developing world. Myocardial ischaemic injury is alleviated through surgical intervention, detrimentally exposing the heart to reperfusion injury. This inevitable and paradoxical injury has driven a field of cardioprotective research aimed at limiting cell death, enhancing standard reperfusion protocols and improving long-term patient outcomes from ischaemia/reperfusion (I/R) injury. Despite promising laboratory results, clinical translation of cardioprotective interventions remains an unrealised goal. Notably, age, co-morbidities and chronic pharmacotherapy negatively influence the efficacy of cardioprotective interventions aimed at limiting I/R injury. Thus, effective interventions that reduce myocardial I/R injury in the settings of ageing and disease are fundamental. Based upon this fundamental premise, this doctoral project investigates a novel opioid therapy termed sustained ligand-activated preconditioning (SLP). Previous work demonstrated that SLP is superior to conventional cardioprotection through engagement of alternative signalling pathways, and exhibits potent and prolonged efficacy in young to aged hearts. Studies executed in this doctorate aimed to further delineate the specific mechanisms involved in generation of the protected SLP phenotype, and determine the clinical utility of SLP using other relevant models of disease and chronic pharmacotherapy.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Books on the topic "Ischaemic heart disease"

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Perrins, E. J. Ischaemic heart disease. Guildford: Update - Siebert, 1987.

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Bray, Colin. Ischaemic heart disease. London: Update, 1986.

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Rankin, A. C. Ischaemic heart disease. Guildford: Update-Siebert, 1988.

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M, Fox Kim, ed. Ischaemic heart disease. Lancaster, England: MTP Press, 1987.

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Fox, Kim M., ed. Ischaemic Heart Disease. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3211-1.

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Meade, T. W. Haemostatic variables, thrombosis and ischaemic heart disease. Amsterdam: Excerpta Medica, 1995.

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Gunnell, David. The invasive management of ischaemic heart disease. Bristol: Health Care Evaluation Unit, University of Bristol, 1994.

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de Luna, A. Bays, and M. Fiol-Sala, eds. The Surface Electrocardiography in Ischaemic Heart Disease. Oxford, UK: Blackwell Publishing, 2007. http://dx.doi.org/10.1002/9780470696248.

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Edwards, Eric William. Population variation for risk variables in ischaemic heart disease. Oxford: OxfordPolytechnic, 1992.

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Porter, Marilyn. Human plasma glutathione peroxidase as a risk factor for ischaemic heart disease. Manchester: University of Manchester, 1996.

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Book chapters on the topic "Ischaemic heart disease"

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Aronow, Wilbert S. "Ischaemic Heart Disease." In Cardiovascular Disease and Health in the Older Patient, 152–71. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118451786.ch7.

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Fry, John, Gerald Sandler, and David Brooks. "Ischaemic Heart Disease." In Disease Data Book, 20–48. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4149-6_2.

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Collison, Damien, and Keith G. Oldroyd. "Ischaemic Heart Disease." In Textbook of Vascular Medicine, 355–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16481-2_33.

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Aronow, Wilbert S. "Ischaemic Heart Disease." In Pathy's Principles and Practice of Geriatric Medicine, 437–47. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781119952930.ch37.

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Ross, Donald N., Terence A. H. English, and Roxane McKay. "Ischaemic Heart Disease." In Principles of Cardiac Diagnosis and Treatment, 231–43. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-1470-3_8.

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Fry, John. "Ischaemic Heart Disease." In Common Diseases, 151–60. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4924-9_17.

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Michaud, Katarzyna. "Ischaemic Heart Disease." In Cardiac Pathology, 137–51. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24560-3_7.

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Marmot, M. G., and J. I. Mann. "Epidemiology of ischaemic heart disease." In Ischaemic Heart Disease, 1–31. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3211-1_1.

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Davies, M. J. "Pathology of ischaemic heart disease." In Ischaemic Heart Disease, 33–68. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3211-1_2.

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Hoffman, J. I. E. "Coronary physiology and pathophysiology." In Ischaemic Heart Disease, 69–89. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3211-1_3.

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Conference papers on the topic "Ischaemic heart disease"

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Haxhibeqiri-Karabdić, Ilirijana, Emir Kabil, and Haris Vranić. "ISCHAEMIC HEART DISEASE – SURGICAL TREATMENT AND POST-OPERATIVE COMPLICATIONS." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-07.

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Xing, Ruiming, and James Meng. "Machine Learning for Ischaemic Heart Disease Diagnostic Analysis." In 2022 IEEE 4th Eurasia Conference on Biomedical Engineering, Healthcare and Sustainability (ECBIOS). IEEE, 2022. http://dx.doi.org/10.1109/ecbios54627.2022.9944997.

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Patel, Anant R. C., Gavin C. Donaldson, Alexander J. Mackay, Jadwiga A. Wedzicha, and John R. Hurst. "Health Status In Patients With Chronic Obstructive Pulmonary Disease And Comorbid Ischaemic Heart Disease." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2614.

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Marshall, Adele H., Laura A. Hill, and Frank Kee. "Continuous Dynamic Bayesian networks for predicting survival of ischaemic heart disease patients." In 2010 IEEE 23rd International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2010. http://dx.doi.org/10.1109/cbms.2010.6042637.

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Kuang, Silin, and See Meng Khoo. "Obstructive sleep apnoea and nocturnal arrhythmias in patients with ischaemic heart disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4178.

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Jathanna, Nikesh, Kevin Strachan, Bara Erhayiem, Xin Chen, and Shahnaz Jamil-Copley. "15 Scar Radiomic Feature Associations with Clinical Endpoints in Ischaemic Heart Disease." In British Society of Cardiovascular Magnetic Resonance (BSCMR) Annual Congress 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2023. http://dx.doi.org/10.1136/heartjnl-2022-bscmr.15.

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Banks, MJ, EJ Flint, PA Bacon, and GD Kitas. "OP0013 Prevalence, clinical expression and causes of ischaemic heart disease in rheumatoid arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1022.

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Ashraf, Saadia, and Amber Ashraf. "Study Of Risk Factors For Arrhythmias Among Chronic Obstructive Pulmonary Disease Patients Having Ischaemic Heart Disease." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2461.

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Katz, D., S. Tiosano, D. Comaneshter, A. D. Cohen, and H. Amital. "SAT0690 The association between sarcoidosis and ischaemic heart disease – a big data analysis." 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.6887.

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Larsen, Ann Dyreborg, Harald Hannerz, Karen Albertsen, Hermann Burr, Martin Lindhardt Nielsen, Jan Hyld Pejtersen, and Anne Helene Garde. "1252 Long weekly working hours and risk of ischaemic heart disease and stroke." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.1367.

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Reports on the topic "Ischaemic heart disease"

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Zhou, Zhuo, Guixing Xu, Liuyang Huang, Hao Tian, Fengyuan Huang, Yilin Liu, Mingsheng Sun, and Fanrong Liang. Effectiveness and Safety of Electroacupuncture for Depression: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0068.

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Review question / Objective: Is electroacupuncture a safe therapy for the treatment of depression? Is electroacupuncture effective for the treatment of depression, as compared with sham control, or conventional drugs？ Condition being studied: Depression is a mood disorder that causes sufferers to feel sadness, decreased interest, guilt, self-blame, loss of energy, and experience sleep disorders such as insomnia. People suffering from depression even feel they have no way out and have suicidal thoughts. In the United States, the prevalence of a major depressive disorder is 16.2%1-3. The 2010 Global Burden of Disease Study identified major depression as the second leading cause of disability worldwide and a leading cause of the burden of suicide and ischaemic heart disease. At present, depression patients are mainly treated with antidepressants, but the efficacy is extremely unstable. Studies have shown that acupuncture can help improve symptoms in patients with depression, but these clinical studies have not been systematically evaluated, and further confirmation is needed to confirm the efficacy of electroacupuncture in treating depression.
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