Relevant bibliographies by topics / Cardiac injury

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cardiac injury'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Cardiac injury"

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N, Dublin, H. K. Chow, and Y. C. Lim. "Penetrating Cardiac Injury." Journal of Health and Translational Medicine 4, no. 2 (December 27, 1999): 117–18. http://dx.doi.org/10.22452/jummec.vol4no2.12.

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Schultz, Jess M., and Donald D. Trunkey. "Blunt cardiac injury." Critical Care Clinics 20, no. 1 (January 2004): 57–70. http://dx.doi.org/10.1016/s0749-0704(03)00092-7.

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O'Connor, J., M. Ditillo, and T. Scalea. "Penetrating Cardiac Injury." Journal of the Royal Army Medical Corps 155, no. 3 (September 1, 2009): 185–90. http://dx.doi.org/10.1136/jramc-155-03-02.

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HEALEY, MARK A., REA BROWN, and DAVID FLEISZER. "Blunt Cardiac Injury." Journal of Trauma: Injury, Infection, and Critical Care 30, no. 2 (February 1990): 137–46. http://dx.doi.org/10.1097/00005373-199002000-00002.

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&NA;. "BLUNT CARDIAC INJURY." Journal of Trauma: Injury, Infection, and Critical Care 33, no. 5 (November 1992): 649–50. http://dx.doi.org/10.1097/00005373-199211000-00001.

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Iserson, Kenneth V., and Dan Judkins. "BLUNT CARDIAC INJURY." Journal of Trauma: Injury, Infection, and Critical Care 36, no. 3 (March 1994): 462. http://dx.doi.org/10.1097/00005373-199403000-00050.

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Hsieh, Hung-Jen, Pan-Fu Kao, Hsuan-Li Huang, and Yu-Hsiang Chou. "Cardiac Stab Injury." Clinical Nuclear Medicine 35, no. 2 (February 2010): 121–22. http://dx.doi.org/10.1097/rlu.0b013e3181c7be78.

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Giurgius, Magdy, Fahad Al Asfar, Piyaray M. Dhar, and Nema Al Awadi. "Penetrating Cardiac Injury." Medical Principles and Practice 15, no. 1 (December 9, 2005): 80–82. http://dx.doi.org/10.1159/000089392.

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Banki, Nader M., and Jonathan G. Zaroff. "Neurogenic cardiac injury." Current Treatment Options in Cardiovascular Medicine 5, no. 6 (December 2003): 451–58. http://dx.doi.org/10.1007/s11936-003-0034-8.

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Bock, Jeremy S., and R. Michael Benitez. "Blunt Cardiac Injury." Cardiology Clinics 30, no. 4 (November 2012): 545–55. http://dx.doi.org/10.1016/j.ccl.2012.07.001.

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Dissertations / Theses on the topic "Cardiac injury"

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Bourke, L. T. "Cardiac injury in lupus." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1458423/.

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Systemic lupus erythematosus (SLE) carries a significantly enhanced risk of developing cardiovascular disease (CVD) and remains a leading cause of death in these patients, accounting for ~25% of all causes of mortality. Although there is clear evidence li nking accelerated atherosclerosis to SLE (and consequently an increase in cardiovascular events), another factor that may contribute to CVD related morbidity and mortality is reperfusion injury that occurs post - ischaemia. This is termed ischaemic / reperfu sion (I/R) injury and is a known important contributor to the size of the eventual infarct in the heart, which in animal studies has been shown to account for up to 40 - 50% of the final infarct size. Hydroxychloroquine (HCQ), originally an anti - malarial dr ug, is now used to treat autoimmune disorders, including SLE. HCQ has been shown to modulate inflammation in rheumatic diseases such as SLE and rheumatoid arthritis as well as have potential cardiovascular benefits in these patients. One of the keys aims o f this thesis was to explore the potential use of HCQ in reducing cardiac I/R injury. HCQ was found to be cardioprotective in an in vitro neonatal cardiomyocytes simulated I/R injury model as well as in an in vivo cardiac I/R injury model. This was found to be through an ERK - dependent mechanism which was blocked in the presence of the ERK inhibitor U0126 both in vitro and in vivo . Another relevant question addressed in this thesis was if I/R injury is enhanced in lupus. There is evidence from an autoimmune prone mouse model that lupus IgG are pathogenic in mesenteric I/R injury . However, no study as yet has investigated human lupus IgG in a heart model. IgG was purified from the serum of SLE patients (aPL +ve vs aP L – ve), antiphospholipid syndrome (APS) patients, juvenile onset SLE (JSLE) patients and healthy volunteers. The pre - treatment of neonatal rat cardiomyocytes with IgG from all 3 patient groups enhanced simulated I/R injury. However, the most pathogenic wer e those who were aPL positive. Interestingly, JSLE patients who were all aPL negative, enhanced I/R injury to similar levels as those who tested positive in the adult patient cohort. An enhanced p38 MAPK phosphorylation was observed in the presence of aPL positive IgG and this pathogenic effect was blocked in the presence of the p38 inhibitor SB23580. The results ob tained in this thesis have identified a potential role for HCQ in the cardiovascular field as a cardioprotective therapeutic in myocardial I/R injury. Additionally , IgG purified from patients with SLE , APS and JSLE have been shown to accelerate myocardial I/R injury.
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Wall, Johanna Martine. "Trauma-induced secondary cardiac injury." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/43998.

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Trauma-induced secondary cardiac injury (TISCI) represents an under recognised complication of severe injury with haemorrhage. A limited number of clinical studies have supported the development of adverse cardiac events, such as arrhythmia, in association with biomarker proven TISCI. Pre-clinical studies using small animal models have provided insights into potential mechanisms and key effector molecules involved in the development of TISCI, but there remains a general lack of understanding regarding the in vivo functional implications of this indirect cardiac injury resulting from trauma-haemorrhage. This project aimed to investigate the implications of cardiac injury on myocardial systolic function. A robust, translatable model of TISCI was developed, which reflected the cardiac biomarker profile identified in clinical studies and, for the first time, demonstrated a significant, dose-dependent rise in Heart-type Fatty Acid Binding Protein (H-FABP) in response to trauma-haemorrhage. Non-invasive echocardiography was used to determine the acute myocardial response to injury and haemorrhage and also to assess the response of the left ventricle to resuscitation after an antecedent 60-minute period of trauma-haemorrhage. The functional studies presented here have enabled real time visualisation of the impact of trauma-haemorrhage upon systolic left ventricular function over 1 to 6 hours, both with and without resuscitation. Having established the trends in in vivo systolic function over time, further studies were then conducted to test the combination of adenosine, lidocaine and magnesium (ALM) as a cardiovascular rescue agent in TISCI. ALM, as an adjunct to fluid resuscitation, has shown great promise as a therapeutic agent which improves haemodynamic outcomes, reduces the volume of resuscitation fluid required and favours survival in the murine model of TISCI.
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De’Ath, Henry D. I. "Trauma associated cardiac injury & dysfunction." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8466.

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The existence of a trauma induced secondary cardiac injury (TISCI) remains in doubt. The risk factors and pathological processes that lead to its development are not known, whilst the effects of TISCI on injured patient outcome are uncertain. Concurrently, the incidence of coronary heart disease (CHD) in a trauma population and its influence on mortality are inconclusive. The aim of this research project was to address these specific areas of uncertainty. Critically injured patients (n=135) were retrospectively investigated for the incidence and nature of adverse cardiac events (ACEs), and levels of the cardiac specific biomarkers Troponin I, B-type Natriuretic Peptide and Heart-type Fatty Acid Binding Protein were measured. Biomarkers and cardiac events were evaluated against outcome. Thereafter, the relationship of pro-inflammatory cytokines with TISCI was explored. A prospective cohort study of 199 trauma patients followed, to confirm the existence of TISCI and describe its clinical features, risk factors and outcomes. Finally, coronary artery calcium, as a marker of CHD, was evaluated on 432 CT scans of the chest of trauma patients aged 45 years or over, and its association with survival after injury was established. ACEs and early biomarker rises occurred in trauma patients and both were unrelated to the severity of chest injury. Each was associated with higher mortality, and confirmed the existence of TISCI. Risk factors for the development of the condition included increasing age, worsening tissue injury and shock. A relationship with cytokines was demonstrated, and implicated acute inflammation in the pathogenesis of TISCI. Calcification on CT scans revealed the incidence of CHD in an injured cohort approached 70%, although its presence did not impact survival. There exists a trauma induced secondary cardiac injury which was related to poorer outcome. The condition was associated with inflammation. CHD was widespread in older trauma patients but was not associated with increased in-hospital mortality.
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Caroll, Patricia A. "Markers of cardiac injury in ultraendurance runners." Thesis, University of Hawaii at Manoa, 2003. http://hdl.handle.net/10125/6969.

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Wasilewski, Melissa Anne. "ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/525634.

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Biomedical Sciences
Ph.D.
Heart failure (HF) is a prevalent disease affecting over 5.1 million people in the United States and over 23 million people worldwide. Many of the symptoms associated with HF are associated with neurohormonal responses to the decrease in cardiac output and systemic blood pressure, such as the activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. Current treatment guidelines recommend using drugs that block β-adrenergic receptor (βAR) signaling (e.g. β- blockers) or RAAS signaling (e.g. angiotensin receptor blockers/ARBs or angiotensin converting enzyme inhibitors/ACEi’s) Additionally, clinical studies have demonstrated that drugs blocking these neurohormones from properly signaling have decreased hospitalizations, morbidity, and mortality in these HF patients; and these are the only classes of pharmacological therapies that have been shown to reduce patient mortality. Interestingly, the neurohormone arginine vasopressin (AVP) has been implica
Temple University--Theses
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Maharsy, Wael. "Enhancing Cardiomyocyte Survival in Drug Induced Cardiac Injury." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23384.

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Cardiotoxicity associated with many cancer drugs is a critical issue facing physicians these days and a huge hurdle that must be overcome for a side effects-free cancer therapy. Survival of cardiac myocytes is compromised upon the exposure to certain chemotherapeutic drugs. Unfortunately, the mechanisms implicated in cardiac toxicity and the pathways governing myocyte survival are poorly understood. The following thesis addresses the mechanisms underlying the cardiotoxicity of two anticancer drugs, doxorubicin (DOX) and Imatinib mesylate (Gleevec). Transcription factor GATA-4, has recently emerged as an indispensable factor in the adult heart adaptive response and cardiomyocyte survival. Therefore, the specific aim of this project was to determine the role of GATA-4, its upstream regulators, as well as partners in survival. A combination of cell and molecular techniques done on in vivo, and ex vivo models were utilized to tackle these issues. In this study, we confirmed the cardiotoxicity of the anticancer drug, Imatinib mesylate and found to be age dependent. GATA-4, already known to be implicated in DOX-induced toxicity, was confirmed as an Imatinib target. At the molecular level, we identified IGF-1 and AKT as upstream regulators of GATA-4. Moreover, we confirmed ZFP260 (PEX-1), a key regulator of the cardiac hypertrophic response, as a GATA-4 collaborator in common prosurvival pathways. Collectively, these results provide new insights on the mechanisms underlying drug-induced cardiotoxicity and raise the exciting possibility that cancer drugs are negatively affecting the same prosurvival pathway(s), in which GATA-4 is a critical component. Therapeutic interventions aimed at enhancing GATA-4 activity may be interesting to consider in the context of treatments with anticancer drugs.
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Patel, Nikil. "Causes of brain injury associated with cardiac interventions." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/33073.

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Background& Objective: Brain injury after cardiac surgery is a serious concern for patients and their families. Thousands of air bubbles enter the cerebral circulation during cardiac surgery, but whether these are harmful to the brain and impact adversely on cognition remains subject of speculation. The purpose of this study was to use MRI to characterise new and pre-existing cerebral ischaemic lesions in patients undergoing cardiac surgery, and to test whether the accumulation of new lesions adversely affects cognition. This study also draws upon recent advances in intra-operative bubble sizing to investigate whether high volumes of macro-bubbles have potential to result in new MRI lesions or increased risk of cognitive decline following surgery. Methods: The burden of pre-existing versus new ischaemic lesions was quantified based on analysis of 3T MR images and compared with the results of cognitive testing. Intraoperative Doppler ultrasound recordings were used to estimate the number, volume and diameters of bubbles entering the middle cerebral artery during surgery for comparison with MRI and cognitive outcome. Results: Post-operative lesions were identified in 31% of patients. Patients with pre-existing lesions were 10 times more likely to receive new lesions after surgery. Forty six percent of patients experienced postoperative cognitive decline, which was independent of whether new lesions were present. Intra-cardiac patients received over 16 times the total volume of air, 7 times as many macro-bubbles, 5 times as many emboli following aortic cross-clamp removal, and over twice as many emboli overall than CABG patients, but there were no significant differences in MRI or cognitive outcome. Conclusions: New MRI lesions and high numbers of intra-operative macro-bubbles are common during cardiac surgery, but we found no evidence of any adverse effect on cognition.
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Naganathar, Sriveena. "Trauma induced secondary cardiac injury clinical manifestations and underlying mechanisms." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/54467.

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Since 1933, studies have explored the concept of trauma induced secondary cardiac injury (TISCI), yet till 2012, it had not been defined as the incidence of cardiac events and rise in cardiac biomarkers following traumatic injury. Despite, improvements in early outcomes, trauma patients have reduced long-term mortality with cardiac disease being the major contributor. Although many putative mechanisms have been suggested for TISCI, the underpinning pathophysiology still remains unclear. In this thesis, a prospective study of 290 critically injured patients identifies a 13% incidence of adverse cardiac events (ACE) with consistently raised serum h-FABP levels in these patients. H-FABP was found to be a good predictor of ACE through ROC analysis and a h-FABP of 16.8 ng/ml used to define trauma induced secondary cardiac injury (TISCI). TISCI was associated with longer hospital stay and higher mortality. Patients who developed ACE had higher plasma levels of adrenaline and noradrenaline with a correlating increase in plasma h-FABP. On multivariate analysis, hypertension was the only independent risk factors for ACE. The increase in serum cardiac biomarkers was reflected by an increase in serum h- FABP in our group's trauma hemorrhage murine models. The hearts of these models were used in the experiments that form the last experimental chapter of this thesis. Protein expression studies confirm this increase in serum h-FABP by evidence of concurrent leaching in the cardiac tissue, along with Troponin I. Myocardial injury was evident on electron microscopy with evidence of interstitial and organelle oedema, myofibrillar degeneration, nuclear condensation and changes in mitochondrial morphology. Immunohistochemistry and western blotting protein studies demonstrate the translocation of the mitochondrial death-related protein AIF to the cytosol and nucleus, where it becomes its active pro-apoptotic form. This thesis propositions the utility of the cardiac biomarker h-FABP in predicting ACE and outcomes in critically injured patients. Although increasing serum noradrenaline and adrenaline levels are associated with higher incidence of ACE and biochemical evidence of cardiac injury with rising h-FABP levels, multivariate analysis negates their value as independent predictors of ACE. Leaching out of the proteins h-FABP and Troponin I in the murine cardiac tissue confirmed the value of serum measurements of these proteins as markers of cardiac injury. This was associated with widespread ultrastructural myocardial damage in the TH mice with changes in mitochondrial morphology. The mitochondrial damage seen is associated with the translocation of the mitochondrial death-related protein AIF to the cytosol and the nucleus where I propose its canonical signaling leading to nuclear degradation and cell death is the driver of cardiac dysfunction.
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Hiraumi, Yoshimi. "Granulocyte colony-stimulating factor protects cardiac mitochondria in the early phase of cardiac injury." Kyoto University, 2009. http://hdl.handle.net/2433/126456.

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Khan, Areeg Ismail Ahmed Abdulla. "Novel translational strategies to treat cardiac injury and dysfunction." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8445.

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There is ample evidence of the crucial role of PI3K/Akt dependent signalling in cardiac function, cellular growth and cell apoptosis. The PI3K/Akt pathway mediates cardioprotective effects in experimental models of cardiovascular disease. For example, activation of this pathway ameliorates the sepsis-induced cardiac dysfunction, whereas its activation in myocardial ischaemia/reperfusion (I/R) limits cardiac injury. This thesis investigates the role of two drugs, which activate the PI3K/Aktpathway, namely the haematopoietic cytokine erythropoietin and the anti-malarial drug artesunate, in a mouse animal model of experimental sepsis-induced cardiac dysfunction and in a rat model of regional myocardial I/R injury, respectively. Using a clinically relevant model of caecal ligation and puncture in mice, I demonstrated that aged (8 months) C57BL/6 mice (receiving fluid resuscitation and antibiotic therapy) developed significant cardiac dysfunction (within 24 h), while younger mice (2 months) did not. Erythropoietin attenuated the impaired systolic contractility (in vivo and ex vivo) caused by endotoxaemia (lipopolysacchride 9 mg kg-1; young mice) and sepsis (aged mice). These beneficial effects were associated with activation of Akt and endothelial nitric oxide synthase survival pathways and inhibition of the glycogen synthase kinase 3β, nuclear factor-κB and interleukin 1β pro-inflammatory pathways, secondary to activation of the β-common receptor. A single bolus administration of artesunate at the start of reperfusion in a rat model of myocardial I/R significantly attenuated the infarct size. This effect was mediated via activation of pro-survival pathways (PI3K/Akt and ERK 1/2 and STAT-3) and inhibition of the glycogen synthase kinase 3β and nuclear factor-κB pro-inflammatory pathways. Thus, in this thesis I have demonstrated that pharmacological activation of the PI3K/Akt pathway by erythropoietin and artesunate in sepsis and myocardial I/R, respectively, plays a vital role in the amelioration of cardiac dysfunction and injury.
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Books on the topic "Cardiac injury"

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František, Kolář, ed. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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Ostadal, Bohuslav. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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Ošt’ádal, Bohuslav, and František Kolář. Cardiac Ischemia: From Injury to Protection. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4757-3025-8.

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American College of Emergency Physicians and American Academy of Orthopaedic Surgeons, eds. First aid, CPR, and AED essentials. 6th ed. Burlington, MA: Jones & Bartlett Learning, 2013.

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Initiative, Acute Dialysis Quality, Conference on Biomarkers in AKI (10th : 2011 : Dublin, Ireland), and Conference on CRS (11th : 2012 : Venice, Italy), eds. ADQI consensus on AKI biomarkers and cardiorenal syndromes. Basel: Karger, 2013.

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Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.

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Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.

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Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.

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Volpe, Joseph, Richard Jonas, and Jane Newburger. Brain Injury and Pediatric Cardiac Surgery. Taylor & Francis Group, 2019.

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Friedhelm, Beyersdorf, ed. Ischemia-reperfusion injury in cardiac surgery. Georgetown, Tx: Landes Bioscience, 2000.

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Book chapters on the topic "Cardiac injury"

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Nicholson, Kristina J., Ravi K. Ghanta, Matthew J. Wall, and Andrew B. Peitzman. "Cardiac Injury." In Thoracic Surgery for the Acute Care Surgeon, 207–25. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48493-4_15.

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Carrel, Thierry. "Cardiac Injury." In Cardiac Surgery, 1009–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-52672-9_32.

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Tesoriero, Ron. "Cardiac Injury." In The Shock Trauma Manual of Operative Techniques, 173–94. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2371-7_10.

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Biffl, Walter L., and Ernest E. Moore. "Blunt Cardiac Injury." In Thoracic Trauma and Critical Care, 281–88. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1127-4_37.

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Grande, Antonino M., and Alessandro Mazzola. "Penetrating Cardiac Injury." In Operative Techniques and Recent Advances in Acute Care and Emergency Surgery, 307–17. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-95114-0_22.

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Tesoriero, Ronald. "Cardiac Injury: Techniques." In The Shock Trauma Manual of Operative Techniques, 233–61. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-27596-9_10.

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Manley, Nathan R., and George O. Maish. "Blunt Cardiac Injury." In Clinical Algorithms in General Surgery, 637–39. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98497-1_156.

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Chaubey, Vikas P., Kevin B. Laupland, Christopher B. Colwell, Gina Soriya, Shelden Magder, Jonathan Ball, Jennifer M. DiCocco, et al. "Blunt Cardiac Injury." In Encyclopedia of Intensive Care Medicine, 358. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1238.

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von Schmilowski, Eva, and Howard Swanton. "Cardiac Catheter Laboratory." In Management of Myocardial Reperfusion Injury, 103–33. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-84996-019-9_6.

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Dean, Kenneth J. "Cardiac Troponin T as a Marker of Myocardial Injury." In Cardiac Markers, 205–27. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4612-1806-7_13.

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Conference papers on the topic "Cardiac injury"

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Juntao, F., W. Lijuan, Z. Xiaoman, L. Shangyu, L. Hui, L. Tiewei, and L. Ping. "26 Exenatide alleviate adriamycin-induced cardiac injury." In Irish Cardiac Society Annual Scientific Meeting & AGM, Thursday October 4th – Saturday October 6th 2018, Galway Bay Hotel, Galway, Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-ics.26.

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Gollmann-Tepeköylü, C., M. Graber, L. Pölzl, F. Nägele, J. Hirsch, N. Bonaros, M. Grimm, S. Schneeberger, T. Resch, and J. Holfeld. "RNA Release Triggers Ischemia/Reperfusion Injury in Cardiac Transplantation." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705467.

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Bastin, Anthony J., Andrew J. Slack, Simon Finney, Mark J. D. Griffiths, Marlies Ostermann, and Timothy W. Evans. "Acute Kidney Injury After Cardiac Surgery: Utility Of Acute Kidney Injury Network And RIFLE Criteria." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4547.

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Sequeira, M., O. Bhadra, D. Kalbacher, N. Schofer, F. Deuschl, A. Schäfer, Y. Schneeberger, et al. "Percutaneous Management of Vascular Injury after Transfemoral Aortic Valve Implantation." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678873.

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Tong, H., MI Gilmour, JM Samet, and RB Devlin. "Ultrafine Ambient Particulate Matter Enhances Cardiac Ischemia and Reperfusion Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3147.

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BULBOL, GUILHERME ANDRADE, RAFAEL MARQUES FIGUEIREDO, HENZO THEODORO FONSECA SILVA, JOELMA MOREIRA BELAS TORRES, GABRIEL ANTONIO LIMA CERQUEIRA, VIVIANE SANTOS FERREIRA, IGOR OLIVEIRA SILVA, et al. "ATYPICAL MITRAL INJURY IN RHEUMATIC CARDIAC DISEASE: A CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-035.

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Beardsley, Brayden, Abigayle Brewer, Matthew Gummersbach, Zachary Houck, Stephen Humbert, Edward J. O'Rourke, Nicholas Verham, Benjamin Lobo, and Donald Brown. "Using Intraoperative Variables to Predict Acute Kidney Injury Following Cardiac Surgery." In 2019 Systems and Information Engineering Design Symposium (SIEDS). IEEE, 2019. http://dx.doi.org/10.1109/sieds.2019.8735604.

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Huenges, K., M. Salem, B. Panholzer, C. Friedrich, J. Schöttler, F. Schoeneich, T. Pühler, J. Cremer, and A. Haneya. "Influence of Acute Kidney Injury in Patients with Acute Aortic Dissection Type A." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678855.

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Shin, Hyun-Chool, Shanbao Tong, Soichiro Yamashita, Xiaofeng Jia, Romergryko G. Geocadin, and Nitish V. Thakor. "Quantitative EEG Assessment of Brain Injury and Hypothermic Neuroprotection after Cardiac Arrest." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260739.

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Shin, Hyun-Chool, Shanbao Tong, Soichiro Yamashita, Xiaofeng Jia, Romergryko G. Geocadin, and Nitish V. Thakor. "Quantitative EEG Assessment of Brain Injury and Hypothermic Neuroprotection after Cardiac Arrest." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4398882.

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Reports on the topic "Cardiac injury"

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Alternative sedative reduces the risk of acute kidney injury following cardiac surgery. National Institute for Health Research, July 2018. http://dx.doi.org/10.3310/signal-000613.

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