Relevant bibliographies by topics / Acute myocarditi

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

Academic literature on the topic 'Acute myocarditi'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Acute myocarditi"

1

Wang, Haipeng, Bin Zhao, Huan Yang, Tianyi Qian, Bo Han, Haipeng Jia, Jing An, Junyu Zhao, Ximing Wang, and Cuiyan Wang. "Identifying myocardial injuries in “normal-appearing” myocardium in pediatric patients with clinically suspected myocarditis using mapping techniques." PeerJ 8 (November 4, 2020): e10252. http://dx.doi.org/10.7717/peerj.10252.

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Background Mapping techniques using cardiac magnetic resonance imaging have significantly improved the diagnostic accuracy for myocarditis with focal myocardial injuries. The aim of our study was to determine whether T1 and T2 mapping techniques could identify diffuse myocardial injuries in “normal-appearing” myocardium in pediatric patients with clinically suspected myocarditis and to evaluate the associations between diffuse myocardial injuries and cardiac function parameters. Methods Forty-six subjects were included in this study: 20 acute myocarditis patients, 11 subacute/chronic myocarditis patients and 15 control children. T2 values, native T1 values and the extracellular volume (ECV) of “normal-appearing” myocardium were compared among the three groups of patients. Associations between diffuse myocardial injuries and cardiac function parameters were also evaluated. Results The ECV of “normal-appearing” myocardium was significantly higher in the subacute/chronic myocarditis group than in the control group (30.1 ± 0.9 vs 27.0 ± 0.6, P =0.004). No significant differences in T1 and T2 values between the acute myocarditis and control groups were found. In the subacute/chronic myocarditis group, a significant association between ECV and left ventricle ejection fraction was found (P=0.03). Conclusions Diffuse myocardial injuries are likely to occur in subacute/chronic myocarditis patients with prolonged inflammatory responses. Mapping techniques have great value for the diagnosis and monitoring of myocarditis.
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Yermola, Yu A., A. A. Galyshevskaya, A. A. Davydova, A. A. Beketov, T. P. Makalish, and M. A. Kriventsov. "Myocardial lesions in patients with COVID-19. Autopsy case series." CLINICAL AND EXPERIMENTAL MORPHOLOGY 11, no. 4 (2022): 59–69. http://dx.doi.org/10.31088/cem2022.11.4.59-69.

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Introduction. Morphological data on SARS-CoV-2-associated heart damage and its mechanisms are rather limited. However, clinical and morphological features of myocardial lesions in COVID-19 patients have been described and include myocardial ischemia, acute coronary syndrome, and acute myocarditis. The prevailing features of myocardial lesions and their consequences are still controversial. The aim of our research was to evaluate the morphological features of myocardial lesions in patients with severe COVID-19, using routine histological examination and immunohistochemistry (CD45) to confirm myocardial inflam-matory infiltration. Materials and methods. We analyzed samples of the left ventricular myocardium obtained during autopsy examination of 48 patients with severe COVID-19 who died from SARS-CoV-2-associated pneumonia. We used histological description and immunohistochemical methods. Results. The results revealed several histopathological features of COVID-19-associated myocardial lesions, including acute ischemia (25% of cases) and mild inflammatory changes termed borderline myocarditis (18.75% of cases). Other significant findings in the myocardium included microcirculatory vessel thrombosis. Conclusion. The study confirms the existing data on damage to myocardium in severe COVID-19. However, further studies are warranted. It may contribute to the development of new management strategies for severe COVID-19 patients. Keywords: SARS-CoV-2, heart, ischemia, myocarditis
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Chetrit, Michael, and Matthias G. Friedrich. "The unique role of cardiovascular magnetic resonance imaging in acute myocarditis." F1000Research 7 (July 30, 2018): 1153. http://dx.doi.org/10.12688/f1000research.14857.1.

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This article addresses the specific diagnostic information provided by cardiovascular magnetic resonance (CMR) in patients with suspected acute myocarditis. It gives an overview of the current evidence of the ability of CMR to detect myocardial inflammation and discusses the added value as well as its limitations in clinical settings. Because of the large variety of symptoms and the limited specificity of other non-invasive procedures, the identification of myocardial inflammation is of paramount importance. Because of its accuracy in imaging ventricular volumes and function and its unique ability to visualize myocardial edema, scar, and other tissue abnormalities, CMR has emerged as the prime non-invasive diagnostic tool in patients with acute myocarditis. The presence of myocardial inflammation is not specific to viral myocarditis or other forms of acute myocardial injury, and the regional distribution within the myocardium helps differentiate acute myocarditis from other diseases. The currently recommended diagnostic criteria (Lake Louise Criteria) include markers for hyperemia/capillary leak, edema, and inflammatory scarring. Their diagnostic accuracy of close to 80% is satisfactory to rule in myocarditis, yet the negative predictive value is less than 70%. Novel CMR techniques, especially T1 and T2 mapping, have been shown to further improve the diagnostic utility.
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Zdravković, Marija, Slobodan Klašnja, Maja Popović, Predrag Đuran, Andrea Manojlović, Milica Brajković, Olivera Marković, Igor Jovanović, Marija Branković, and Višeslav Popadić. "Cardiac magnetic resonance imaging in early diagnostics of myocardial inflammation after COVID-19: Case series and literature review." Srpski medicinski casopis Lekarske komore 2, no. 4 (2021): 323–36. http://dx.doi.org/10.5937/smclk2-34913.

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Although, in the beginning, it was considered a respiratory infection with bilateral pneumonia as its main manifestation, COVID-19 is more of a multisystemic disease with various extrapulmonary manifestations. Cardiovascular manifestations are caused by direct viral involvement or by the effects of different cytokines on the myocardium and can occur during the acute phase of the disease or in the post-acute stadium. The most common cardiovascular symptoms in the post-acute COVID-19 stadium are fatigue, shortness of breath, chest pain, and palpitations. Routine cardiovascular diagnostics in these patients is usually without significant findings, although underlying myocardial inflammation may be present. Myocardial damage can also be the substrate for the worsening of heart failure and different potentially life-threatening arrhythmias, which is extremely important for further treatment and prognosis. Cardiac magnetic resonance imaging is a sophisticated, non-radiating imaging modality that can provide important information regarding left and right ventricle volumes and function, tissue characterization, and scar quantification. It is the golden standard in non-invasive diagnostics of myocarditis. In patients with prior COVID-19 infection and cardiovascular symptoms, typical signs of myocarditis, including myocardial edema, necrosis, and myocardial scarring, may be seen in cardiac magnetic resonance. Also, there are sophisticated cardiac magnetic resonance imaging modalities that can register subtle changes in the myocardium, in terms of myocardial inflammation, without visible signs in standard sequences. We present a case series of patients with different myocardial inflammation patterns, followed by a comprehensive review of potential pathophysiological mechanisms, complications, treatment and prognosis of patients with myocarditis or pericarditis after COVID-19.
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Meseck, Emily K., Bradley L. Njaa, Nicholas J. Haley, Edward H. Park, and Stephen C. Barr. "Use of a Multiplex Polymerase Chain Reaction to Rapidly Differentiate Neospora Caninum from Toxoplasma Gondii in an Adult Dog with Necrotizing Myocarditis and Myocardial Infarct." Journal of Veterinary Diagnostic Investigation 17, no. 6 (November 2005): 565–68. http://dx.doi.org/10.1177/104063870501700607.

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This report describes a 3-year-old male castrated Mastiff dog that died unexpectedly with locally extensive, acute, necrotizing myocarditis and myocardial infarction. Intralesional protozoal tachyzoites in the affected myocardium were confirmed to be Neospora caninum by a novel multiplex polymerase chain reaction (PCR) and immunohistochemistry. Protozoal organisms were not identified in other tissues by histology, immunohistochemistry, or PCR. The multiplex PCR assay was used to quickly provide preliminary results on fresh myocardium to differentiate N. caninum and Toxoplasma gondii. Neosporosis is an uncommon cause of myocarditis in adult dogs and differential diagnoses for myocarditis in this population of dogs are reviewed.
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Valevičienė, Nomeda, Žaneta Petrulionienė, Birutė Petrauskienė, Gediminas Lauraitis, Sigita Glaveckaitė, Darius Palionis, Algirdas Tamošiūnas, and Aleksandras Laucevičius. "Differentiation of Acute Myocarditis and Acute Myocardial Infarction by the Regional Distribution of Myocardial Irreversible Injury Using Cardiovascular Magnetic Resonance Imaging." Medicina 48, no. 3 (April 4, 2012): 18. http://dx.doi.org/10.3390/medicina48030018.

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Background and Objective. In this study, we have sought for differences between cardiovascular magnetic resonance patterns of acute myocarditis and acute myocardial infarction. Material and Methods. A prospective analysis of 110 consecutive patients was performed. The presence, precise location, and pattern of late gadolinium enhancement (LGE) by cardiovascular magnetic resonance were investigated. Results. The subendocardial LGE pattern was much more frequent in the myocardial infarction group (76.7%) than myocarditis group (10.0%) (P<0.001). Meanwhile, midmyocardial LGE was much more typical of myocarditis (65.0%) than acute myocardial infarction (1.1%) (P<0.001), and epicardial LGE was also much more typical of myocarditis (55.0%) than acute myocardial infarction (0.0%) (P<0.001). Midmyocardial and epicardial LGE patterns were defined as a nonischemic LGE pattern more typical of myocarditis. Logistic regression analysis revealed that the subendocardial and midmyocardial LGE locations played the greatest role in differentiation between acute myocarditis and acute myocardial infarction. A statistical model based on midmyocardial LGE distribution and age showed a sensitivity of 90% and a specificity of 93.3% in differentiating between acute myocarditis and acute myocardial infarction. Conclusion. Our findings suggest that in clinical practice, differentiation between acute myocardial infarction and acute myocarditis can be done based on the subendocardial and midmyocardial LGE location. The presence of subendocardial LGE was found to be strongly associated with acute myocardial infarction; meanwhile, the presence of midmyocardial LGE indicated acute myocarditis. However, other clinical factors should also be taken into account when making the final diagnosis.
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Amano, Yasuo, Masaki Tachi, Hitomi Tani, Kyoichi Mizuno, Yasuhiro Kobayashi, and Shinichiro Kumita. "T2-Weighted Cardiac Magnetic Resonance Imaging of Edema in Myocardial Diseases." Scientific World Journal 2012 (2012): 1–7. http://dx.doi.org/10.1100/2012/194069.

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The purpose of this paper is to describe imaging techniques and findings of T2-weighted magnetic resonance imaging (MRI) of edema in myocardial diseases. T2-weighted cardiac MRI is acquired by combining acceleration techniques with motion and signal suppression techniques. The MRI findings should be interpreted based on coronary artery supply, intramural distribution, and comparison with delayed-enhancement MRI. In acute myocardial diseases, such as acute myocardial infarction and myocarditis, the edema is larger than myocardial scarring, whereas the edema can be smaller than the scarring in some types of nonischemic cardiomyopathy, including hypertrophic cardiomyopathy. T2-weighted MRI of edema identifies myocardial edema associated with ischemia, inflammation, vasculitis, or intervention in the myocardium and provides information complementary to delayed-enhancement MRI.
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Stirrat, Colin G., Shirjel R. Alam, Thomas J. MacGillivray, Calum D. Gray, Marc R. Dweck, Kevin Dibb, Nick Spath, et al. "Ferumoxytol-enhanced magnetic resonance imaging in acute myocarditis." Heart 104, no. 4 (October 6, 2017): 300–305. http://dx.doi.org/10.1136/heartjnl-2017-311688.

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ObjectivesUltrasmall superparamagnetic particles of iron oxide (USPIO)-enhanced MRI can detect tissue-resident macrophage activity and identify cellular inflammation within tissues. We hypothesised that USPIO-enhanced MRI would provide a non-invasive imaging technique that would improve the diagnosis and management of patients with acute myocarditis.MethodsTen volunteers and 14 patients with suspected acute myocarditis underwent T2, T2* and late gadolinium enhancement (LGE) 3T MRI, with further T2* imaging at 24 hours after USPIO (ferumoxytol, 4 mg/kg) infusion, at baseline and 3 months. Myocardial oedema and USPIO enhancement were determined within areas of LGE as well as throughout the myocardium.ResultsMyocarditis was confirmed in nine of the 14 suspected cases of myocarditis. There was greater myocardial oedema in regions of LGE in patients with myocarditis when compared with healthy volunteer myocardium (T2 value, 57.1±5.3 vs 46.7±1.6 ms, p<0.0001). There was no demonstrable difference in USPIO enhancement between patients and volunteers even within regions displaying LGE (change in R2*, 35.0±15.0 vs 37.2±9.6 s−1, p>0.05). Imaging after 3 months in patients with myocarditis revealed a reduction in volume of LGE, a reduction in oedema measures within regions displaying LGE and improvement in ejection fraction (mean −19.7 mL, 95% CI (−0.5 to −40.0)), −5.8 ms (−0.9 to −10.7) and +6% (0.5% to 11.5%), respectively, p<0.05 for all).ConclusionIn patients with acute myocarditis, USPIO-enhanced MRI does not provide additional clinically relevant information to LGE and T2 mapping MRI. This suggests that tissue-resident macrophages do not provide a substantial contribution to the myocardial inflammation in this condition.Clinical trial registration NCT02319278; Results.
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Nana-Leventaki, E., M. Nana, N. Poulianitis, D. Sampaziotis, D. Perrea, D. Sanoudou, D. Rontogianni, and K. Malliaras. "Cardiosphere-Derived Cells Attenuate Inflammation, Preserve Systolic Function, and Prevent Adverse Remodeling in Rat Hearts With Experimental Autoimmune Myocarditis." Journal of Cardiovascular Pharmacology and Therapeutics 24, no. 1 (July 30, 2018): 70–77. http://dx.doi.org/10.1177/1074248418784287.

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Background: Cardiosphere-derived cells (CDCs) have yielded promising efficacy signals in early-phase clinical trials of ischemic and nonischemic cardiomyopathy. The potential efficacy of CDCs in acute myocarditis, an inflammatory cardiomyopathy without effective therapy, remains unexplored. Given that CDCs produce regenerative, cardioprotective, anti-inflammatory, and anti-fibrotic effects (all of which could be beneficial in acute myocarditis), we investigated the efficacy of intracoronary delivery of CDCs in a rat model of experimental autoimmune myocarditis. Methods: Lewis rats underwent induction of experimental autoimmune myocarditis by subcutaneous footpad injection of purified porcine cardiac myosin supplemented with Mycobacterium tuberculosis on days 1 and 7. On day 10, rats were randomly assigned to receive global intracoronary delivery of 500 000 CDCs or vehicle. Global intracoronary delivery was performed by injection of cells or vehicle into the left ventricular (LV) cavity during transient occlusion of the aortic root. Rats were euthanized 18 days after infusion. Cardiac volumes and systolic function were assessed by serial echocardiography, performed on days 1, 10, and 28. Myocardial inflammation, T-cell infiltration, and cardiac fibrosis were evaluated by histology. Results: Experimental autoimmune myocarditis was successfully induced in 14/14 rats that completed follow-up. Left ventricular ejection fraction (LVEF) and volumes were comparable on days 1 and 10 between groups. CDC infusion resulted in increased LVEF (81.5% ± 3% vs 65.4% ± 8%, P < .001) and decreased LV end-systolic volume (43 ± 15 vs 100 ± 24 μL, P < .001) compared to placebo administration at 18 days post-infusion. Cardiosphere-derived cell infusion decreased myocardial inflammation (7.4% ± 7% vs 20.7% ± 4% of myocardium, P = .007), cardiac fibrosis (16.6% ± 13% vs 38.1% ± 3% of myocardium, P = .008), and myocardial T-cell infiltration (30.4 ± 29 vs 125.8 ± 49 cells per field, P = .005) at 18 days post-infusion compared to placebo administration. Conclusion: Intracoronary delivery of CDCs attenuates myocardial inflammation, T-cell infiltration, and fibrosis while preventing myocarditis-induced systolic dysfunction and adverse remodeling in rats with experimental autoimmune myocarditis.
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Adeboye, Adedayo, Deya Alkhatib, Asra Butt, Neeraja Yedlapati, and Nadish Garg. "A Review of the Role of Imaging Modalities in the Evaluation of Viral Myocarditis with a Special Focus on COVID-19-Related Myocarditis." Diagnostics 12, no. 2 (February 21, 2022): 549. http://dx.doi.org/10.3390/diagnostics12020549.

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Viral myocarditis is inflammation of the myocardium secondary to viral infection. The clinical presentation of viral myocarditis is very heterogeneous and can range from nonspecific symptoms of malaise and fatigue in subclinical disease to a more florid presentation, such as acute cardiogenic shock and sudden cardiac death in severe cases. The accurate and prompt diagnosis of viral myocarditis is very challenging. Endomyocardial biopsy is considered to be the gold standard test to confirm viral myocarditis; however, it is an invasive procedure, and the sensitivity is low when myocardial involvement is focal. Cardiac imaging hence plays an essential role in the noninvasive evaluation of viral myocarditis. The current coronavirus disease 2019 (COVID-19) pandemic has generated considerable interest in the use of imaging in the early detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related myocarditis. This article reviews the role of various cardiac imaging modalities used in the diagnosis and assessment of viral myocarditis, including COVID-19-related myocarditis.
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Dissertations / Theses on the topic "Acute myocarditi"

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VARRENTI, MARISA. "PROGNOSTIC PERFORMANCE OF CLINICAL PRESENTATION AND CARDIAC MAGNETIC RESONANCE IMAGING PARAMETERS IN PATIENTS WITH ACUTE MYOCARDITIS." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/392357.

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BACKGROUND: L'identificazione di marcatori affidabili associati a eventi dopo una miocardite acuta (AM) è clinicamente rilevante per pianificare un futuro follow-up. Abbiamo cercato di chiarire la performance prognostica dei marcatori di risonanza magnetica cardiaca (CMRI) precedentemente descritti, tra cui l'aumento tardivo del gadolinio settale (LGE), rispetto all'evidenza della frazione di eiezione ventricolare sinistra (LVEF) <50% sulla CMRI basale, rispetto alla presentazione clinica complicata (CCP) della AM (definita come la presenza di aritmie ventricolari sostenute [SVT] o LVEF <50% al primo ecocardiogramma di presentazione fulminante). METODI: Abbiamo valutato 248 pazienti AM con insorgenza di sintomi cardiaci <30 giorni prima del ricovero, aumento della troponina e CMRI coerente con la diagnosi di miocardite (tempo mediano dal ricovero alla CMRI di 6 giorni). I pazienti sono stati raccolti retrospettivamente tra febbraio 2006 e aprile 2019 da 6 ospedali Lombardi con un follow-up mediano di 1708 giorni (primo - terzo quartile [Q1-Q3], 1000-2751). Abbiamo valutato la performance prognostica di LGE settale vs. LVEF<50% su CMRI vs. CCP. RISULTATI: La popolazione dello studio aveva un'età mediana di 34 anni (Q1-Q3: 23-41) con una prevalenza maschile dell'87,1% e una LVEF mediana del 61% (Q1-Q3, 55-66%) alla CMRI basale. Tredici pazienti (5,2%) hanno sperimentato almeno un evento cardiaco maggiore (tra cui morte cardiaca, trapianto di cuore (N=1), arresto cardiaco resuscitato (N=3), SVT (N=5), o ricovero per insufficienza cardiaca (N=5). Tra questi 13 pazienti, 10 (76,9%) avevano LGE settale, 8 (61,5%) avevano LVEF<50%, su CMRI, e 12 (92,3%) avevano un CCP. La migliore performance per questi marcatori prognostici era il valore predittivo negativo (NPV) che variava tra 0,98 e 0,99 per CCP, mentre il valore predittivo positivo era basso, tra 0,14 e 0,25 per LVEF<50%. CONCLUSIONI: Abbiamo confermato che il tasso di eventi cardiaci maggiori dopo una AM è relativamente basso, e LGE settale, LVEF<50% su CMRI, e CCP sono significativamente associati agli eventi nel follow-up. Il risultato più rilevante è l'alto NPV di questi marcatori per identificare i pazienti senza eventi dopo una AM. Questa osservazione può aiutare i medici a monitorare i pazienti dopo una AM ed impostare un corretto monitoraggio nel follow-up sulla base di tali dati all'esordio.
BACKGROUND: Identifying reliable markers associated with events after acute myocarditis (AM) is clinically relevant to planning a future follow-up. We aimed to clarify the prognostic performance of previously described cardiac magnetic resonance imaging (CMRI) markers including septal late gadolinium enhancement (LGE), versus evidence of left ventricular ejection fraction (LVEF)<50% on baseline CMRI, vs. complicated clinical presentation (CCP) of AM (defined as the presence of sustained ventricular arrhythmias [SVT] or LVEF <50% on the first echocardiogram of fulminant presentation). METHODS: We assessed 248 AM patients with onset of cardiac symptoms <30 days before admission, increased troponin, and CMRI consistent with myocarditis (median time from admission to CMRI of 6 days). The patients were retrospectively collected between February 2006 and April 2019 from 6 hospitals with a median follow-up of 1708 days (first to third quartile [Q1-Q3], 1000-2751). We assessed the prognostic performance of septal LGE vs. LVEF<50% on CMRI vs. CCP. RESULTS: The study population had a median age of 34 years (Q1-Q3: 23-41) with a male prevalence of 87.1% and a median LVEF of 61% (Q1-Q3, 55-66%) on baseline CMRI. Thirteen patients (5.2%) experienced at least one major cardiac event (including cardiac death, heart transplantation (N=1), aborted cardiac death (N=3), SVT (N=5), or heart failure hospitalization (N=5). Among these 13 patients, 10 (76.9%) had septal LGE, 8 (61.5%) had LVEF<50%, on CMRI, and 12 (92.3%) had a CCP. The best performance for these prognostic markers was the negative predictive value (NPV) ranging between 0.98 and 0.99 for CCP, while predictive value was low, ranging between 0.14 and 0.25 for LVEF<50%. CONCLUSIONS: We confirmed that the rate of major cardiac events after an AM is relatively low, and septal LGE, LVEF<50% on CMRI, and CCP are significantly associated with events. The most relevant finding is the high NPV of these markers to identify patients without events after an AM. This observation can help clinicians to monitor the patients after an AM, in fact, patients without these markers had an uneventful follow-up.
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Kannan, Harsha. "The Inflammasome in Acute Myocarditis." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3108.

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Acute myocarditis is an acute inflammatory syndrome characterized by myocardial damage and dysfunction often due to a viral infection followed by a variable development over time. There are currently no specific treatments and standard treatments for heart failure are generally applied. The inflammasome is a recently identified macromolecular structure that occupies a central role in the amplification of the inflammatory response and promotion of cell death during acute and chronic infections. We hypothesized the formation of the inflammasome in acute myocarditis. To investigate, samples of patients were collected from the Cardiomyopathy Registry in Trieste, with 12 cases of biopsy-proven myocarditis and 11 cases of autopsy-proven myocarditis stained for major components of the inflammasome through immunofluorescence; 10 of the 12 (83.3%) biopsy cases and 8 of the 11 (72.7%) autopsy cases presented formation of the inflammasome in a variety of cells including resident cells (i.e. cardiomyocytes, endothelial cells, fibroblasts) and infiltrating cells (i.e. leukocytes) while varying in intensity and distribution. Control samples of 5 subjects not presenting with any acute cardiac events showed no formation of the inflammasome. While further studies should look to elucidate the correlation of inflammasome-formation and progression of disease, this finding paves the way for further insight into the pathophysiology of acute myocarditis.
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Ruparelia, Neil. "Monocytes in acute myocardial infarction." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:02ad6ebd-a8c2-4cb6-a1f7-0cdf8cec59ed.

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Acute myocardial infarction (AMI) results in the activation of the innate immune system with monocytes playing critical roles in both the initial inflammation following myocardial ischaemia and subsequent recovery. Monocytes are a heterogeneous cell population and observations from experimental models demonstrate that immediately following myocardial injury, classical inflammatory monocytes, which are highly phagocytic, are recruited to ischaemic myocardium from the bone marrow and spleen and peak at 48 hours. This is followed by the recruitment of non-classical monocytes that are involved in repair and healing, peaking at day 5. The monocyte response in humans following AMI is currently poorly understood. Due to their central role in the pathogenesis of AMI, monocytes are attractive both as potential biomarkers to inform of extent of myocardial injury (and recovery) and also as therapeutic targets with the specific targeting of monocytes in experimental models resulting in reduced infarction size and improved LV remodelling. However, in spite of these promising results and our greater understanding of the pathogenesis of AMI, no immune-modulating therapeutic has been translated into routine clinical practice. We therefore hypothesized that characterisation of the monocyte response to AMI by flow cytometry and gene expression profiling in both experimental models and humans would give novel insights into underlying biological processes and function (both locally in the myocardium and systemically), identify novel therapeutic targets, enable their use as cellular biomarkers of disease, and test conservation between species validating the experimental model for future investigation. Classical inflammatory monocytes were found to significantly increase in the peripheral blood 48 hours following AMI in both mice and humans, with the magnitude of the monocyte response correlating with the extent of myocardial injury in both species. Gene expression profiling of peripheral circulating monocytes following AMI identified a number of candidate genes, biological pathways and upstream regulators that were conserved between species and that could represent novel therapeutic targets. Furthermore, in an experimental model of AMI, leukocytes appeared to have effects beyond the ischaemic myocardium, with leukocyte recruitment in remote myocardium and in kidneys associated with elevated inflammatory markers and endothelial activation.
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Buchanan, Lynne M. "Psychophysiological recovery after acute myocardial infarction /." Thesis, Connect to this title online; UW restricted, 1989. http://hdl.handle.net/1773/7244.

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McNeill, Albert John. "Thrombolytic therapy in acute myocardial infarction." Thesis, Queen's University Belfast, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356866.

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Graham, Lee Nicholas. "Sympathetic mechanisms following acute myocardial infarction." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403027.

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Dawkins, Sam. "MicroRNA release in acute myocardial infarction." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:a0a82298-45e5-4f66-b368-446cad9726ae.

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Coronary heart disease (CHD) is the single biggest cause of death in the United Kingdom1. Primary percutaneous coronary intervention (primary PCI) has transformed the early treatment of acute myocardial infarction (MI), improving outcome by rapidly re-opening the occluded coronary artery, with a larger mortality benefit and reduced risk compared with thrombolysis. Despite these advances, and even with the optimal treatment, some patients still sustain substantial myocardial damage leading to mortality and morbidity. MicroRNAs (miRs) are short non-coding RNAs with a role in regulating protein synthesis. Some miRs are cardiospecific, can be detected in plasma after a myocardial infarction and show promise as biomarkers and insights into the mechanisms of myocardial injury. In this work, as part of the Oxford Acute MI (OxAMI) Programme, a cohort of patients recruited at the time of ST elevation MI underwent detailed clinical and microRNA analysis at the time of myocardial infarction. This work was validated using separate discovery and validation cohorts. The source of detected miRs was further analysed in an in-vitro endothelial cell culture model and by measuring miRs released into the venous drainage of the heart, the coronary sinus. In the Discovery Cohort, miRs previously shown to be increased in myocardial infarction (e.g. miR-1, -133a, -499) were detectible in plasma after myocardial infarction, and this was confirmed in the validation cohort. Other miRs with a similar relationship were also identified (e.g. miR-30a, -378a, 125b). Microvascular obstruction was found to be associated with increased infarct size and also with release of microRNAs correlating with infarct size suggesting a link between microvascular obstruction and myocardial necrosis. Analysis of paired coronary artery and coronary sinus samples showed that these miRs increased down the myocardial gradient, suggesting myocardial release. The culmination of this work was to use the experimental findings from circulating plasma, cultured endothelial cells and coronary sinus experiments to design a microRNA panel using a blood sample taken six hours after admission to use in a regression model which was more predictive of final infarct size than troponin alone.
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Hulaga, O. I. "Eplerenone use in acute myocardial infarction." Thesis, БДМУ, 2022. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/19567.

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Jackson, Melanie H. "The neutrophil in acute myocardial infarction." Thesis, University of Edinburgh, 1992. http://hdl.handle.net/1842/19869.

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The aim of this thesis was to determine if the neutrophil played a significant role in acute myocardial infarction in man. Firstly methods for isolating and radiolabelling neutrophils were developed. These, along with measurement of established markers of neutrophil activation and free radical activity were used to assess neutrophil involvement in myocardial infarction in man. The single-step isolation procedure developed provided a simple and easy means of isolating an essentially 'pure' preparation of cells with a minimum of 'handling'. That this method resulted in isolation of a viable cell population was evidenced by normal kinetics and uptake into sites of infection and inflammation in vivo. In collaboration with others it was shown that the acute inflammatory response to myocardial infarction may be imaged in man using radiolabelled autologous neutrophils. The time interval from onset of pain to injection of labelled cells was the only factor shown to determine the outcome of imaging and suggests that the stimulus for cell recruitment may be early and transient. Detection of increased neutrophil elastase by radioimmunoassay and the non-peroxide diene conjugated isomer of linoleic acid by high performance liquid chromatography in the plasma of these patients demonstrated increased neutrophil activation and free radical activity in acute myocardial infarction in man. Coronary reperfusion, effected by intravenous thrombolysis, might be thought to be associated with increased neutrophil activation but the results showed a reduction in the intensity of the inflammatory response as assessed by uptake of radiolabelled autologous neutrophils, abolition of the late peak of neutrophil activation and a similar degree of free radical activity between patients treated with and without thrombolysis. This is consistent with a reduction rather than an exaggeration of the inflammatory response and conflicts with current views on 'reperfusion injury'.
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Abraham, Sherin. "Preventing Acute Myocardial Infarction Readmission Rates." ScholarWorks, 2019. https://scholarworks.waldenu.edu/dissertations/7579.

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Unplanned readmissions to the hospital are a problem faced by most health care organizations in the United States; hospitals are penalized for such readmissions. The project site identified high readmission rates for patients who were discharged after acute myocardial infarction (AMI), making careful transition home a necessity for post-AMI patients. The focus of this quality improvement (QI) project was implementation of an early follow-up appointment of AMI patients following discharge. The purpose of this project was to evaluate the effectiveness of changing follow-up appointments for patients with an AMI from 14-30 days to 7-14 days post discharge to reduce unplanned readmission rates. Bandura’s self- efficacy theory provided the theoretical framework for this project. An evaluation of the QI project was completed by comparing patient readmission rates 6 months before and 6 months after implementation of the early follow-up appointments. Data analysis demonstrated that the readmission rate was not improved in the first 6 months post QI project implementation. Using the plan-do-check-act process, a multifactorial approach was recommended to refine the QI project and address the system-wide readmission rates. The implications of this project for positive social change include providing early analysis of the readmission QI project, which allowed the hospital to restructure the QI approach and improve the plan for preventing readmission.
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Books on the topic "Acute myocarditi"

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G, Nayler Winifred, Parratt James R, and International Society for Heart Research. European Section. Meeting., eds. Myocardial response to acute injury. Houndmills, Basingstoke: Macmillan Academic and Professional, 1991.

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R, Parratt James, and Nayler W. G. 1930-, eds. Myocardial response to acute injury. Basingstoke: Macmillan Press, 1992.

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J, Gersh Bernard, and Rahimtoola Shahbudin H, eds. Acute myocardial infarction. 2nd ed. NewYork: Chapman & Hall, 1996.

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David, McCall, ed. Acute myocardial infarction. New York: Churchill Livingstone, 1991.

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M, Califf Robert, ed. Acute myocardial infarction and other acute ischemic syndromes. St. Louis: Mosby, 1996.

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1954-, Topol Eric J., ed. Acute coronary intervention. New York: Liss, 1988.

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Minatoguchi, Shinya. Cardioprotection Against Acute Myocardial Infarction. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0167-8.

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Parratt, James R., ed. Myocardial Response to Acute Injury. London: Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-12522-7.

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G, Julian Desmond, and Braunwald Eugene, eds. Management of acute myocardial infarction. London: Saunders, 1994.

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Vermeer, Frank. Thrombolysis in acute myocardial infarction. Assen/Maastricht: Van Gorcum, 1987.

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Book chapters on the topic "Acute myocarditi"

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Pelargonio, S. "Acute Myocarditis." In Pediatric Cardiology, 961–63. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4613-8598-1_257.

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Ni, Xianda, and Jing Ping Sun. "Acute Eosinophilic Myocarditis." In Comparative Cardiac Imaging, 299–304. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119453192.ch53.

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Binayke, Rachana, Heena Desai, Pradeep Vaideeswar, and Smita Divate. "Acute Leptospiral Myocarditis." In Tropical Cardiovascular Pathology, 193–97. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3720-0_34.

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Jiang, Jiangang, and Dao Wen Wang. "Treatments of Fulminant Myocarditis in Acute Phase." In Fulminant Myocarditis, 227–50. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-5759-8_15.

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Stack, Richard S., and Robert K. Stack. "Methods for Detecting Salvage of Jeopardized Myocardium Following Intracoronary Thrombolysis in Acute Myocardial Infarction." In Acute Coronary Care, 335–41. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-3828-4_34.

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Ginsberg, Fredric, and Joseph E. Parrillo. "Acute Heart Failure and Myocarditis." In Acute Heart Failure, 183–99. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84628-782-4_18.

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Spratt, Kelly A., Tanya Y. Huehns, and Robert L. Wilensky. "Acute Myocardial Infarction." In Unstable Coronary Artery Syndromes Pathophysiology, Diagnosis and Treatment, 143–97. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5715-9_5.

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Kim, Jeong A., Sang Il Choi, and Tae-Hwan Lim. "Acute Myocardial Infarction." In Practical Textbook of Cardiac CT and MRI, 155–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-36397-9_11.

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Cole, Jason H., and Nanette K. Wenger. "Acute Myocardial Infarction." In Encyclopedia of Women’s Health, 40–42. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-0-306-48113-0_14.

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Davies, G. J. "Acute Myocardial Infarction." In Care of the Critically Ill Patient, 285–95. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3400-8_19.

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Conference papers on the topic "Acute myocarditi"

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Kordenat, K., and J. Leasure. "PROTECTIVE EFFECT OF CARNITINE (ST-261, SIGMA-TAU) IN ACUTE MYOCARDIAL INFARCTION IN DOGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643012.

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Limitation of infarct size (IS), using ST-261, was evaluated in a group (I) of eight dogs, during acute MI. Another group (II) served as the control group. The protocol for both groups was the same except that each dog in the treated group was ST-261 as a single bolus (25 mg/kg, in 20ml normal saline), before inducing an occluding thrombus in the mid-LAD, using a closed-chest model, under x-ray visualization. Percentages of total (gms) myocardium at jeopardy (TMJW) and myocardial necrosis (TMNW), delineated by fluoroscein and TTC dyes, respectively, were calculated and compared to the total ventricular myocardial weight (TVMU), by computer technique for both groups at 3 Hrs post-occlusion of the LAD. Mean serum total CPK (CPK-t) and isozymes (mb-band) were measured before and up to 3 Hrs post-occlusion, as were various hemodynamic and mean precordial (21 lead) ST-segment and T-wave amplitudes. There was 14% less TMJU (p<0.05) and 41% less TMNW (p<0.01) in Group I compared to Group II. The mean % of CPK-mb/CPK-t decreased in I and increased in II over the 3 Hrs of observation. Mean HR decreased (p<0.01) in I compared to II at 3 Hrs postocclusion. The sum of the mean T-wave amplitudes from the precordial electrode sites was less in I at 3 Hrs. It is felt that ST-261 had a protective effect on the myocardium during acute myocardial infarction.
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Mehri, Sounira, Wided Khamlaoui, and Mohamed Hammami. "Acute myocardial infarction." In the Fourth International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3234698.3234741.

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Murray, R. G., J. Jagger, M. K. Davies, and W. A. Littler. "THROMBOLYTIC THERAPY IN ACUTE MYOCARDIAL INFARCTION: THE SCOPE IN A DISTRICT GENERAL HOSPITAL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642985.

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Despite the interest in thrombolytic therapy in acute’ myocardial infarction, it has been reported.that only a small minority of patients considered for thrombloysis would be suitable. .To determine the demand for such therapy in a District General Hospital, data were collected for patients admitted with chest pain to our Coronary Care Unit over a six month period. Of 197 patients admitted with chest pain 131 patients (67%) were proven to have acute myocardial infarction. Criteria for thrombolytic therapy included presentation within six hours of the onset of symptoms, ST elevation ≥ 0.2 mV in 2 or more ECG leads and age ≤ 70 years. Sixty-seven (51%) of the 131 patients with subsequently proven acute myocardial infarction were eligible for thrombolysis. Criteria for thrombolysis were not fulfilled in 41 patients with acute myocardial infarction; 17 (13%) presented later than six hours, 15 (12%) failed to meet the ECG criteria and 9 (7%) were over 70 years. A further 12 (9%) patients were excluded for cardiogenic shock, patients had peptic ulcers, one patient sustained a recent acute myocardial infarction 2 weeks previously and data from 8 patients were lost.These results suggest that around 50% of patients with acute myocardial infarction and 34% of all patients presenting with chest pain would be suitable for thrombolytic therapy. These data do not support the view that such treatment may only be applicable to a small number of patients with acute myocardial infarction.
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Darella, Amanda Xavier, Stefany Elias, and Gladys Lentz Martins. "Aortic dissection and stroke associated with COVID-19: case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.242.

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Case Report A 58-year-old man, previously healthy, presented with headache, myalgia, retrosternal chest pain associated with paresthesia and paresis in upper limbs and lower limbs of acute onset. He denies fever, cough, dyspnea, or contact with patients with COVID-19. There was a difference in blood pressure and pulse in the upper limbs. No particularities in the neurological examination were noted. The electrocardiogram and enzymes of myocardial necrosis did not show abnormalities. PCR for SARS-CoV-2 was positive. Chest computed angiotomography showed acute type IA aortic dissection. The patient underwent cardiac surgery, without complications. After 48 hours of the procedure, the patient progresses with a lower level of consciousness, left hemiplegia, and anisocoria. The brain computed tomography showed extensive ischemic injury in the right middle cerebral artery territory. The patient underwent decompression craniectomy. The patient was discharged from the hospital, maintaining hemiplegia on the left side of the body. Discussion SARS-CoV-2 is a RNA virus responsible for the current COVID-191 pandemic. Moderate to severe forms of the disease may present with acute respiratory distress syndrome (ARDS), myocarditis, and thrombotic events such as pulmonary venous thromboembolism and ischemic stroke2. There are few reports in the literature about acute aortic dissection in patients with COVID-193,4. Acute aortic dissection is characterized by rupture of the intimal layer of the vessel with exposure of the middle layer and cystic necrosis and formation of a false lumen5. The mechanisms associated with thromboembolic phenomena in SARSCoV-2 infection remain poorly elucidated in the literature. This case report highlights a patient with severe complications of COVID-19, with the viral trigger being a possible contributor to the condition of acute aortic dissection and stroke.
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Machado Filho, Delfino da Costa, and Thelma da Costa. "Acute pulmonary edema associated with acute coronary syndrome - a case report." In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-001.

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Abstract Objective: To report manifestation of acute myocardial infarction with supradenive lament in evolved TS, associated with acute hypertensive pulmonary edema in an adult and smoker patient. Detailing of the case: A 55-year-old smoker (60 years/pack), with a history of myocardial infarction for 15 days, was admitted to the cardiac emergency on 18/07/2022, in severe acute pulmonary edema associated with arterial hypertension. The electrocardiogram (ECG) showed extensive anterior ST-segment unevenness. After measures to stabilize the hemodynamic condition, he underwent cardiac catheterization and angioplasty to the artery responsible for the cardiac event. He underwent a control echocardiogram that showed segmental alterations and an important reduction in the ventricular ejection fraction. Conclusions: Acute myocardial infarction is one of the main causes of morbidity and mortality in Brazil, however, if this emergency is conducted appropriately, within the time limit stipulated by the ACLS protocol, many lives will be saved.
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Gabriela, Doros, Popoiu Anca, Ionac Adina, Olariu Cristina, Ardelean Andrada, Gafencu Mihai, and Miclaus Gratian. "P91 Myocarditis mimicking acute myocardial infarction with normal coronary arteries minca in an adolescent with duchenne disease." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.179.

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Mehri, Sounira, and Mohamed Hammami. "Clinical and biochemical factors associated with acute myocardial infarction: Risk factors for acute myocardial infarction." In 2017 International Conference on Engineering & MIS (ICEMIS). IEEE, 2017. http://dx.doi.org/10.1109/icemis.2017.8273109.

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Suthar, K. D., K. Shah, S. Patel, S. Ghosh, R. Jiyani, and K. Patel. "Scrub Typhus Infection Complicated with Acute Myocarditis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6968.

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Song, C., V. Bedi, B. C. Buragamadagu, and J. Nair. "Suspected COVID-19 Induced Acute Viral Myocarditis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4104.

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Villemant, D., P. Barriot, and P. Bodenan. "THROMBOLYSIS AND ACUTE MYOCARDIAL INFARCTION (AMI)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642981.

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AMI is a major cause of morbidity and mortality in modern society Conventional treatment has no benefic effect on the size of infarct, alteration of left ventricular (LV) function and mortality. Intravenous (IV) thrombolysis reduces in hospital mortality by 23 % if infused within 3 hours of ischemia, 47 % if within 1 hour. It reduces the size of infarct by 51 % if reperfusion occurs within 1 hour of ischemia, 31 % if between 1 and 2 hours and 13 % if between 2 and 4 hours. The preservation of LV function is of 28 to 42%. These benefic effects, thanks to IV thrombolysis, can be obtained only if reperfusion occurs within 3 or 4 hours of ischemia. Unfortunately, a french prospective study “ENIM 84” estimates that the mean delay between onset of chest pain and arrival at hospital is 10,3 hours.Goals of the study were to show that “at home” thrombolysis: 1) is a feasible and a safe technique, 2) is responsible of a significant saving of time, 3) preserves LV function according to the precocity of treatment.Two groups of patients (pts) are compared : group A : 62 pts had “at home” thrombolysis by a trained medical staff aboard a mobile emergency care unit. Group B : 53 pts had thrombolysis at arrival at CCU. Protocol is simular in both groups : An IV infusion of 1 5 M iu of streptokinase over 45 to 60 min after an IV bolus of 100 mg Hydrocortisone. Criteriae and contra-indications are those usually used for thrombolysis. Radionuclide angiography was performed 4 days and 1 month after AMI to evaluate global and regional ejection fraction (EF). Only 1 hemorrhagic complication (a mild melaena) and 2 reversible ventricular fibrillations were reported. Reperfusion arrythmias were frequent (55 %) but do not need treatment. The number of candidates for thrombolysis is then increased. The saving of time is 73 min. Difference between the 4 days and 1 month EF is not significant in pts with conventional treatment or if reperfusion occurs after 4 hours of ischemia 48 ± 11 % vs 51 ± 13 %.But it is significant if before 4 hours 49 ± 11 % vs 56 ± 12 % and highly significant if before 2 hours 48 ± 12 % vs 59 ± 10 %.
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Reports on the topic "Acute myocarditi"

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Dejong, Marla J., Kyungeh An, Candace C. Cherrington, and Debra K. Moser. Predictors of Symptom Appraisal for Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada427523.

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Naydenov, Stefan, Nikolay Runev, Emil Manov, Nadya Naydenova, Mikhail Matveev, and Plamen Krastev. Diagnostic Potential of Signal-Averaged Orthogonal Electrocardiography in Acute Myocardial Infarction. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, February 2021. http://dx.doi.org/10.7546/crabs.2021.02.16.

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De Jong, Marla J. A Cross-Sectional Examination of Changes in Anxiety Early After Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada416443.

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De Jong, Marla J., Kyungeh An, Sharon McKinley, Bonnie J. Garvin, and Lynne A. Hall. Using a 0-10 Scale for Assessment of Anxiety in Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada424770.

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Liu, Xiaofang, and Dichuan Liu. Effects of the sacubitril/valsartan on cardiac remodeling in patients with Acute Myocardial Infarction: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0044.

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Li, Peng, Na jia, Bing Liu, and Qing He. Effect of cardiac shock wave therapy on adverse cardiovascular event for patients with coronary artery disease: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0103.

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Review question / Objective: We have previously demonstrated that cardiac shock wave therapy (CSWT) effectively improves myocardial perfusion in patients with coronary artery disease (CAD). In this study, we want to address whether CSWT could decrease the risk of adverse cardiovascular events in CAD patients unsuitable for revascularization. Eligibility criteria: Trials are considered eligible if they meet these criteria: (1) patients included are diagnosed as refractory angina or ischemic heart failure; (2) the study i a randomized controlled trial (RCT) or a prospective cohort study; (3) intervention consisted of CSWT; (4) patients in the control group are treated with optimal medical therapy, (5)the primary outcome of interest Is rate of MACE. Exclusion criteria were (1) patients with acute myocardial infarction, (2) repeated CSWT, (3) with coronary artery revascularization, (4) without primary outcome, (5) retrospective study, and (6)duplicated data.
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Xie, Xiao-Li. Identification of Key Genes and Pathways in First Acute Myocardial Infarction Based on Gene Expression Profiling by Bioinformatics Analysis. Science Repository, June 2019. http://dx.doi.org/10.31487/j.jicoa.2019.02.02.

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Dai, Xiao-Ce, Lan Ma, Yun-Tao Zhao, Wan-Jie Gu, and Ying Dai. Association between off-hours admission and short-term and long-term mortality in acute myocardial infarction: a meta-analysis and meta-regression. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2020. http://dx.doi.org/10.37766/inplasy2020.6.0041.

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Krastev, Plamen. Dynamics of Left Ventricular Ejection Fraction under Revascularization of Patients with Acute Myocardial Infarction with ST-T Elevation and Single Coronary Artery Disease. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, 2021. http://dx.doi.org/10.7546/crabs.2021.05.16.

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Krastev, Plamen, Violeta Groudeva, Filip Abedinov, Peter Nikolov, Hristo Angelov, and Iliyan Petrov. Early versus Late Primary Percutaneous Coronary Angioplasty in Patients with Acute Myocardial Infarction and Single Vessel Coronary Disease - Factors for Overall Patients Survival Rate. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, July 2020. http://dx.doi.org/10.7546/crabs.2020.07.16.

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