Journal articles: 'Acute myocarditi'

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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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Pan, Hai-Yan, Hua-Mei Sun, Lu-Jing Xue, Min Pan, Yi-Ping Wang, Hiroshi Kido, and Jian-Hua Zhu. "Ectopic trypsin in the myocardium promotes dilated cardiomyopathy after influenza A virus infection." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 6 (September 15, 2014): H922—H932. http://dx.doi.org/10.1152/ajpheart.00076.2014.

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We have previously reported that ectopic trypsin in the myocardium triggers acute myocarditis after influenza A virus (IAV) infection. As myocarditis is a common precursor to dilated cardiomyopathy (DCM), the aim of the present study was to investigate the influence of trypsin on the progression of DCM after IAV infection. IAV-infected mice treated with saline or trypsin inhibitor were euthanized on days 0, 9, 20, 40 and 60 postinfection. Trypsin expression colocalized with myocardial inflammatory loci and IAV-induced myocarditis peaked on day 9 postinfection and alleviated by day 20 but persisted until day 60 postinfection, even though replication of IAV was not detected from day 20 postinfection. Similar time courses were observed for the activation of pro-matrix metalloproteinase (pro-MMP)-9 and expression of the proinflammatory cytokines IL-6, IL-1β, and TNF-α. Degradation of collagen type I, proliferation of ventricular interstitial collagen, and expression of collagen type I and III mRNA increased significantly during acute and chronic phases; collagen type III mRNA increased more significantly than collagen type I mRNA. Cardiac function progressively deteriorated with progressive left ventricular dilation. The trypsin inhibitor aprotinin suppressed pro-MMP-9 activation and cytokine release, alleviated myocardial inflammation, and restored collagen metabolism during acute and chronic phases of myocarditis. This effectively prevented ventricular dilation and improved cardiac function. These results suggest that ectopic trypsin in the myocardium promoted DCM through chronic activation of pro-MMP-9, persistent induction of cytokines, and mediation of collagen remodeling. Pharmacological inhibition of trypsin activity might be a promising approach for the prevention of viral cardiomyopathy.

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Wantania, Frans E. N., Ribka E. Wowor, and Ridwan Tandiawan. "Severe Acute Respiratory Syndrome Coronavirus Associated Myocarditis." Open Access Macedonian Journal of Medical Sciences 9, F (August 22, 2021): 299–304. http://dx.doi.org/10.3889/oamjms.2021.6498.

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Myocardial injury is common in patients with coronavirus disease 2019 (COVID-19). Among COVID-19 related myocardial injuries, etiology may vary, including myocarditis, myocardial infarct, sepsis-associated myocardial injury, and/or stress-induced cardiomyopathy. More data from prospective cohorts and case series are needed to understand the exact mechanism of COVID-19 associated myocardial injuries. It is clinically suspected that myocarditis is the cause of myocardial injury. However, myocarditis has a heterogeneous clinical presentation and tends to be underdiagnosed in critically ill COVID-19 patients. Due to the potential of rapid deterioration in the patient’s condition, it is imperative to recognize myocarditis as a sequel to COVID-19, and a multidisciplinary team should be formed for managing all clinically suspected patients with COVID-19 associated myocarditis. Further studies are needed to recognize better and understand the relationship between myocarditis and COVID-19.

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Lin, Chun-Chi, Dong-Haur Phua, Jou-Fang Deng, and Chen-Chang Yang. "Aconitine intoxication mimicking acute myocardial infarction." Human & Experimental Toxicology 30, no. 7 (October 11, 2010): 782–85. http://dx.doi.org/10.1177/0960327110385960.

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Introduction: Cardiotoxicity in acute aconitine intoxication is well known; however, elevation of troponin I level and abnormal scintigraphy findings had not previously been reported. Case report: A 60-year-old man developed chest tightness, syncope and convulsion after ingesting processed Aconitum carmichaeli (Chuanwu) extract for treatment of headache. Electrocardiogram showed first degree atrioventricular (AV) block. Troponin I level was elevated at 14.8 ng/mL 13 hours post-ingestion. Creatine kinase was also increased to 414 U/L. However, echocardiography did not show any abnormal cardiac wall motion. Tc-99m-PYP scintigraphy revealed diffusely increased uptake in the myocardium, suggesting the presence of myocardial necrosis or myocarditis. Discussion: Aconitine poisoning can mimic acute myocardial infarction with chest tightness and elevated cardiac enzymes. Increased cardiac markers and myocardial insult seen in this patient were likely to be related to the toxicity of aconitine. Care should be taken in making the diagnosis in such instances. Management is primarily supportive.

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Lenzo, Jason C., Geoffrey R. Shellam, and Cassandra M. Lawson. "Ganciclovir and Cidofovir Treatment of Cytomegalovirus-Induced Myocarditis in Mice." Antimicrobial Agents and Chemotherapy 45, no. 5 (May 1, 2001): 1444–49. http://dx.doi.org/10.1128/aac.45.5.1444-1449.2001.

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ABSTRACT The cardiovascular disease myocarditis is characterized by inflammation and necrosis of cardiac muscle. This disease has been associated with various viral etiologies, including cytomegalovirus (CMV). Murine CMV (MCMV) infection of adult BALB/c mice produces a disease with acute and chronic phases similar to that found in humans. In our murine model, we have investigated the therapeutic efficacy of antiviral drug administration on myocarditis. Two drugs commonly used for CMV treatment, ganciclovir and cidofovir, were subjected to trials, with both drugs showing potent antiviral activity against MCMV both in vitro and in vivo. The acute phase of myocarditis was significantly reduced when antiviral therapy commenced 24 h postinfection. Such treatment also reduced the severity of the chronic phase of myocarditis. In contrast, antiviral treatment commencing after the acute phase had no effect on chronic myocarditis. Reinfection of mice with MCMV caused exacerbation of myocardial inflammation. Such an increase in severity of myocarditis could be prevented with either ganciclovir or cidofovir treatment, but the preexisting inflammation and necrosis of the myocardium persisted. These data highlight possible therapeutic uses of antiviral drugs in viral myocarditis as well as further elucidating the pathogenic nature of the disease.

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Imazio, Massimo, Karin Klingel, Ingrid Kindermann, Antonio Brucato, Francesco Giuseppe De Rosa, Yehuda Adler, and Gaetano Maria De Ferrari. "COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or myocarditis?" Heart 106, no. 15 (June 4, 2020): 1127–31. http://dx.doi.org/10.1136/heartjnl-2020-317186.

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The initial mechanism for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is the binding of the virus to the membrane-bound form of ACE2, which is mainly expressed in the lung. Since the heart and the vessels also express ACE2, they both could become targets of the virus. However, at present the extent and importance of this potential involvement are unknown. Cardiac troponin levels are significantly higher in patients with more severe infections, patients admitted to intensive care units or in those who have died. In the setting of COVID-19, myocardial injury, defined by an increased troponin level, occurs especially due to non-ischaemic myocardial processes, including severe respiratory infection with hypoxia, sepsis, systemic inflammation, pulmonary thrombosis and embolism, cardiac adrenergic hyperstimulation during cytokine storm syndrome, and myocarditis. At present, there are limited reports on definite diagnosis of myocarditis caused by SARS-CoV-2 in humans and limited demonstration of the virus in the myocardium. In conclusion, although the heart and the vessels are potential targets in COVID-19, there is currently limited evidence on the direct infection of the myocardium by SARS-CoV-2. Additional pathological studies and autopsy series will be very helpful to clarify the potentiality of COVID-19 to directly infect the myocardium and cause myocarditis.

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Ussov, W. Yu, G. A. Ignatenko, T. A. Bergen, T. A. Shelkovnikova, K. R. Bril, V. V. Khovrin, A. S. Maksimova, O. I. Belichenko, and G. E. Trufanov. "Computational evaluation of mechano-elastic properties and of paramagnetic contrast enhancement of thoracic aortic wall in acute myocardial infarction and in non-coronarogenic myocardial damage, from the data of dynamic ECG-gated MRI (MR-elastometry)." Translational Medicine 8, no. 6 (February 22, 2022): 43–58. http://dx.doi.org/10.18705/2311-4495-2021-6-43-58.

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Background. The state of the aorta is a key factor in the prognosis of the patient’s life, since the distension of the ascending aorta in systole determines the blood supply to the myocardium in diastole. Paramagnetic contrast-enhanced MRI provides a reliable assessment of pathological neoangiogenesis, however, in fact, studies of the aorta are performed descriptively, without calculating mechanical strength and extensibility. Objective. To develop and clinically test on the patients with atherosclerotic lesions and myocarditis a method for quantitative assessment of extensibility and mechanical elasticity of the aortic wall.Design and methods. Were examined 12 patients with acute myocardial infarction with ST segment elevation, as a control group 11 patients without clinical and instrumental signs of atherosclerosis of large arteries and aorta. All underwent MRI of the chest and heart with paramagnetic contrast enhancement (PMCE) and ECG synchronization. The indices of aortic distensibility, distensibility normalized to pulse BP, Young’s modulus of the aortic wall, systolic distension of the ascending aorta (mL), index of strengthening of the aortic wall in PMCE were calculated.Results. Ascending aortic distensibility decreased in patients with myocarditis and acute infarction. Young’s modulus and distensibility of the ascending aorta significantly correlated with the value of the aortic wall enhancement index in PMCE. Myocardial damage in acute infarction and myocarditis was noted with a decrease in systolic expansion of the ascending aorta below 10 ml due to its reduced elasticity.Conclusion. There is a relationship between pathological accumulation of a paramagnet in the wall of the ascending aorta, a decrease in its elasticity, a decrease in the volume of systolic aortic dilation, and the development of hypoperfusion myocardial damage. Magnetic resonance elastometry of the aortic wall makes it possible to assess violations of aortic distensibility and predict the development of ischemic damage in the myocardium of the left ventricle.

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Bogdan, T. V., V. O. Onishchenko, O. V. Savchenko, and O. V. Slobodianyk. "The case report of myocarditis caused by COVID-19." Likarska sprava, no. 1-2 (May 25, 2021): 9–13. http://dx.doi.org/10.31640/jvd.1-2.2021(2).

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Introduction. Myocarditis is known to occur in 5–25 % of COVID-19 cases and is associated with increased mortality. According to studies, even a mild course of COVID-19 is associated with a high risk of cardiovascular disease. Possible mechanisms of myocarditis are a combination of direct viral damage to the myocardium and the human immune response to the affected myocardium. Along with acute manifestations, as fulminant myocarditis, COVID-19 may also be associated with an increased risk of long-term cardiovascular complications. Case report and discussion. The article presents a case of myocarditis that developed five weeks after active coronovirus infection in patient I., 47 years old, Ukraine, Kyiv. She described such symptoms as palpitations, shortness of breath, fever, general malaise. According to magnetic resonance imaging (MRI) of the heart: signs of focal myocarditis; according to laboratory tests, an increase in the level of acute phase indicators; according to Holter monitoring of the electrocardiogram (HM ECG) – AV blockade of the II degree (Mobitz II). The patient was prescribed : eplerinone, bisoprolol fumorate, rivaroxaban, trimetazidine. After four months of treatment, the condition of the patient gradually improved. Positive dynamics was revealed according to HM ECG and MRI of the heart. Thus, the patient was diagnosed with long-term consequences of coronavirus infection – focal myocarditis. Conclusions. Coronavirus infection causes myocardial damage with the development of myocarditis. Myocarditis can develop both in the acute period of the disease and in the long term. Scientists and physicians should pay attention to the possible consequences of COVID-19 from the first contact with the patient, and conduct long-term follow-up of patients in the long term.

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Omori, Taku, Shiro Nakamori, Keiko Ohta-Ogo, Akimasa Matsuda, Yoshito Ogihara, Norikazu Yamada, Kyoko Imanaka-Yoshida, Masaaki Ito, and Kaoru Dohi. "Autopsy study of pulmonary capillary hemangiomatosis with inflammatory cell infiltration into the myocardium." Pulmonary Circulation 10, no. 4 (October 2020): 204589402096060. http://dx.doi.org/10.1177/2045894020960600.

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Pulmonary capillary hemangiomatosis is a rare form of pulmonary artery hypertension; to date, only few descriptions of myocardial pathology in pulmonary capillary hemangiomatosis have been reported in the literature. We report the case of a Japanese female patient who was diagnosed with pulmonary capillary hemangiomatosis combined with acute myocardial inflammation on performing autopsy. She was admitted to our hospital because of acute pneumonia and subsequently suddenly developed severe hypoxemia with breathing difficulty and died 13 days after admission. At autopsy, the histology of the lung was consistent with pulmonary capillary hemangiomatosis. Additionally, a diffuse severe infiltration of inflammatory cells was associated with edema in the myocardium. Myocytolysis was limited and fibrosis was absent. To the best of our knowledge, pulmonary capillary hemangiomatosis with acute myocarditis-like histological findings has been described for the first time through our case.

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Ford, Jordan, Laura McEndaffer, Randall Renshaw, Alex Molesan, and Kathleen Kelly. "Parvovirus Infection Is Associated With Myocarditis and Myocardial Fibrosis in Young Dogs." Veterinary Pathology 54, no. 6 (August 16, 2017): 964–71. http://dx.doi.org/10.1177/0300985817725387.

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Perinatal parvoviral infection causes necrotizing myocarditis in puppies, which results in acute high mortality or progressive cardiac injury. While widespread vaccination has dramatically curtailed the epidemic of canine parvoviral myocarditis, we hypothesized that canine parvovirus 2 (CPV-2) myocardial infection is an underrecognized cause of myocarditis, cardiac damage, and/or repair by fibrosis in young dogs. In this retrospective study, DNA was extracted from formalin-fixed, paraffin-embedded tissues from 40 cases and 41 control dogs under 2 years of age from 2007 to 2015. Cases had a diagnosis of myocardial necrosis, inflammation, or fibrosis, while age-matched controls lacked myocardial lesions. Conventional polymerase chain reaction (PCR) and sequencing targeting the VP1 to VP2 region detected CPV-2 in 12 of 40 cases (30%; 95% confidence interval [CI], 18%–45%) and 2 of 41 controls (5%; 95% CI, 0.1%–16%). Detection of CPV-2 DNA in the myocardium was significantly associated with myocardial lesions ( P = .003). Reverse transcription quantitative PCR amplifying VP2 identified viral messenger RNA in 12 of 12 PCR-positive cases and 2 of 2 controls. PCR results were confirmed by in situ hybridization, which identified parvoviral DNA in cardiomyocytes and occasionally macrophages of juvenile and young adult dogs (median age 61 days). Myocardial CPV-2 was identified in juveniles with minimal myocarditis and CPV-2 enteritis, which may indicate a longer window of cardiac susceptibility to myocarditis than previously reported. CPV-2 was also detected in dogs with severe myocardial fibrosis with in situ hybridization signal localized to cardiomyocytes, suggesting prior myocardial damage by CPV-2. Despite the frequency of vaccination, these findings suggest that CPV-2 remains an important cause of myocardial damage in dogs.

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Takahashi, T., S. Saegusa, H. Sumino, T. Nakahashi, K. Iwai, S. Morimoto, and T. Kanda. "Adiponectin Replacement Therapy Attenuates Myocardial Damage in Leptin-deficient Mice with Viral Myocarditis." Journal of International Medical Research 33, no. 2 (March 2005): 207–14. http://dx.doi.org/10.1177/147323000503300208.

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The effects of adiponectin replacement therapy on myocardial damage were studied in leptin-deficient (OB) mice with acute viral myocarditis. Encephalomyocarditis virus was injected intraperitoneally into OB and wild-type (WT) mice. One subgroup of OB mice received no intervention and another subgroup received daily adiponectin replacement, simultaneously with viral inoculation. Differences in heart weight, cardiac histological score, numbers of infiltrating or apoptotic cells in the myocardium and the immunoreactivity of adiponectin receptors in myocytes were determined. The reactivity of adiponectin receptor 1 in myocytes from OB mice on day 4 and day 8 after viral inoculation was significantly decreased compared with that in myocytes from WT mice; the OB mice also had elevated cardiac weights and severe inflammatory myocardial damage. Adiponectin replacement in OB mice inhibited the development of severe myocarditis by augmenting myocyte adiponectin receptor 1 reactivity. Exogenously administered adiponectin may inhibit the progression of viral myocarditis through binding to the adiponectin receptor 1 in leptin-deficient conditions.

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Magalhães, Maycon Juglas Linhares, Lucas de Pádua Gomes de Farias, Luciana de Pádua Silva Baptista, Marcio Campos Sampaio, Patrícia O. Guimarães, Antonio Claudio Amaral do Baruzzi, Pedro Gabriel Melo de Barros e Silva, and Valter Furlan. "Acute Myocarditis Associated with Acute Myocardial Infarction." Radiology: Cardiothoracic Imaging 3, no. 1 (February 1, 2021): e200469. http://dx.doi.org/10.1148/ryct.2021200469.

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Jedidi, Maher, Samia Tilouche, Tasnim Masmoudi, Maha Sahnoun, Youssef Chkirbène, Sarra Mestiri, Lamia Boughamoura, Mohamed Ben Dhiab, and Mohamed Kamel Souguir. "Infant acute myocarditis mimicking acute myocardial infarction." Autopsy and Case Reports 6, no. 4 (2016): 15–19. http://dx.doi.org/10.4322/acr.2016.052.

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Spodick, David H., Trevor O. Greene, and Gordon Saperia. "Acute Myocarditis Masquerading as Acute Myocardial Infarction." Circulation 91, no. 6 (March 15, 1995): 1886–87. http://dx.doi.org/10.1161/01.cir.91.6.1886.

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van Nierop, J., A. Limburg, and C. E. E. van Ofwegen-Hanekamp. "Myocarditis mimicking acute myocardial infarction." Netherlands Heart Journal 23, no. 10 (July 16, 2015): 502–4. http://dx.doi.org/10.1007/s12471-015-0732-3.

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Hancock, E. William, and Lore Friend. "Myocarditis or Acute Myocardial Infarction?" Hospital Practice 28, no. 11 (November 15, 1993): 109–10. http://dx.doi.org/10.1080/21548331.1993.11442876.

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Buheruk, V. V., O. B. Voloshyna, and І. V. Balashova. "Inflammatory damage to the myocardium in patients with novel coronavirus disease (COVID-19)." Zaporozhye Medical Journal 23, no. 4 (July 1, 2021): 555–65. http://dx.doi.org/10.14739/2310-1210.2021.4.211033.

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The aim. To analyze current evidence about etiology, pathogenesis, clinical manifestation, diagnosis, and treatment of patients with COVID-19 associated myocarditis. Multisystem inflammatory syndrome is possible in COVID-19 including inflammatory damage to the myocardium, which may last over several months and worsen the disease outcome. Mechanisms of inflammatory cardiac damage include direct damage by SARS-CoV-2, massive release of cytokines, dysregulation of the renin-angiotensin system. All these factors can aggravate pre-existing overload of the right heart chambers in patients with multifocal pneumonia, thrombosis of coronary arteries and myocardial ischemia. Inflammation of the myocardium manifests with typical symptoms of myocarditis and pericarditis. It can be accompanied by heart failure with rapid decompensation, arrhythmia, acute coronary syndrome or even sudden death. Laboratory findings in COVID-19 associated myocarditis include high levels of CRP, BNP, NT-proBNP, and D-dimer. Transthoracic echocardiography allows for an assessment of the left ventricular dysfunction and diagnosis of a pericardial effusion. Heart MRI according to the Lake Louise Diagnostic Criteria is the most sensitive diagnostic method in acute myocarditis. Medical imaging is indicated only in cases when results obtained can potentially influence the patient management tactics and should be performed according to the shortest protocol due to high risks of virus transmission. Conclusions. ESC experts (2020) do not provide unanimous recommendations for the treatment of SARS-CoV-2 associated myocarditis, considering a lack of the evidence base. Patient management is limited to adequate treatment of heart failure, arrhythmia, acute coronary syndrome, and prevention of thrombotic complications. Ongoing studies are aiming to evaluate potential place of glucocorticoids, intravenous immunoglobulins, antibodies against IL-6 receptor, colchicine in the treatment of COVID-19.

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Wieczorkiewicz, Paulina, Karolina Supel, Katarzyna Przybylak, Michal Kacprzak, and Marzenna Zielinska. "Acute coronary syndrome versus acute myocarditis in young adults–value of speckle tracking echocardiography." PLOS ONE 17, no. 8 (August 8, 2022): e0271483. http://dx.doi.org/10.1371/journal.pone.0271483.

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Purpose Comparing myocarditis with an acute coronary syndrome (ACS)-like presentation and acute myocardial infarction (AMI) poses an important clinical challenge. The purpose of the study was to investigate the diagnostic value of the clinical, laboratory and especially echocardiographic characteristics including speckle tracking echocardiography (STE) of patients with ACS-like myocarditis and AMI. Methods We conducted a retrospective analysis comparing 69 symptomatic patients (≤ 45 years old), hospitalized at the Department of Interventional Cardiology (Medical University of Lodz, Poland) between April 2014 and June 2021 with an initial diagnosis of ST-segment elevation myocardial infarction. Results 37 patients with the cardiac magnetic resonance–confirmed acute myocarditis and 32 patients diagnosed with AMI based on the clinical presentation, electrocardiogram and the presence of a culprit lesion on the coronary angiography were analysed including echocardiography parameters. On STE analysis an average global longitudinal (GLS), radial and circumferential strain including three—layers observation were significantly lower (absolute value) in patients with AMI versus acute myocarditis (p<0.05). There was no significant difference in Endo/Epi ratio (p = 0.144) between the groups. An average GLS < (-17.5) represented the optimal cut-off value for the myocarditis diagnosis. Conclusion In patients with AMI a significant reduction of global and three-layers strains compared to patients with myocarditis was detected. Furthermore, our analysis also confirmed the discriminative pattern of myocardial injury between the groups.

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Mutovina, Z. Yu, A. V. Gordeev, I. V. Rozanova, and E. A. Galushko. "Severe myocarditis as a cause of the formation of cardiorenal syndrome in a patient with refractory rheumatoid arthritis." Rheumatology Science and Practice 60, no. 4 (September 7, 2022): 495–500. http://dx.doi.org/10.47360/1995-4484-2022-495-500.

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According to modern concepts, myocarditis is an inflammatory disease of the myocardium, diagnosed on the basis of generally accepted histological, immunological, immunohistochemical criteria. Previously, most researchers believed that the most common cardiac extra-articular manifestation of rheumatoid arthritis (RA) is pericarditis. In the last decade, using magnetic resonance imaging (MRI) of the heart, it turned out that myocarditis in patients with rheumatoid arthritis is not a rare manifestation of the disease. Recently, there is increasing evidence that inflammatory cytokines in RA can also directly cause chronic myocardial damage, further contributing to the development of chronic heart failure (CHF). In our clinical case, myocarditis developed in a patient with active refractory rheumatoid arthritis. The myocardial lesion in the patient was characterized by pronounced echocardiographic signs of restrictive cardiomyopathy, a significant decrease in the ejection fraction with the development of heart failure, various rhythm disturbances in combination with acute renal dysfunction, which led to the formation of cardiorenal syndrome (CRS). Complete regression of myocarditis and cattle occurred precisely against the background of effective treatment of refractory rheumatoid arthritis (RA) with basic antirheumatic drugs and the successful use of biological therapy.

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Irina, Pintilie, Scridon Alina, and Șerban Răzvan Constantin. "To Be or Not to Be … Acute Coronary Syndrome." Acta Medica Marisiensis 62, no. 3 (September 1, 2016): 363–67. http://dx.doi.org/10.1515/amma-2016-0029.

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AbstractIntroduction: The association between ST segment abnormalities, elevated cardiac enzymes, and chest pain is usually a marker of acute coronary injury. However, certain other pathologies can sometimes mimic acute coronary syndromes.Case report: A 40-year-old Caucasian male, former smoker, with no other cardiovascular risk factors, presented to the Emergency Department for typical ischemic, prolonged chest pain. The ECG demonstrated inverted T waves in leads I, II, aVL, and V3 to V6. The patient presented high cardiac necrosis markers (troponin I 2.65 ng/ml). Based on these findings, the case was interpreted as non-ST segment elevation myocardial infarction, but coronary angiography excluded the presence of significant coronary lesions. The ventriculography showed an efficient left ventricle, with mild hypokinesia of the two apical thirds of the anterior left ventricular wall. Cardiac magnetic resonance imaging demonstrated areas of hypersignal on the T2-weighted imaging sequence in the left ventricular myocardium, suggestive for acute myocarditis. The patient was started on antiplatelet, beta-blocker, and angiotensin converting enzyme inhibitor, with favorable evolution.Conclusion: This case underlines the polymorphic appearance of acute myocarditis, which can often mimic an acute coronary event.

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Nishikawa, T., S. Ishiyama, K. Takeda, T. Kasajima, S. Abe, T. Shimojo, H. Ito, and M. Hiroe. "Programmed Cell Death (Apoptosis) in the Myocardium with Acute Myocarditis." Microscopy and Microanalysis 3, S2 (August 1997): 63–64. http://dx.doi.org/10.1017/s1431927600007200.

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Acute myocarditis is a potentially lethal disease. However, the precise mechanism of myocardial damage in myocarditis is still unknown, although its pathogenesis seems to be involved in the result of natural killer cells, cytotoxic T cells and autoantibodies. Recently, it has been reported that programmed death of cardiac myocytes can be induced by several pathological conditions including infarction and end-stage cardiac failure. However, little is known about the myocardial cell death in myocarditis. In this study, we investigated whether myocardial cell death via apoptosis occurs in the heart tissue with myocarditis.Since it has been reported that the pathogenesis of the tissue damage in viral myocarditis resembles that in experimental autoimmune myocarditis induced by myosin, we used an experimental model for autoimmune myocarditis induced in Lewis rat with the use of myosin as the antigen. Rats were sacrificed on days 14, 17 and 21 after myosin injection. The tissue specimens were taken from ventricle of the heart.

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Stukalova, O. V., E. M. Gupalo, P. V. Chumachenko, A. N. Samko, E. A. Butorova, R. M. Shakhnovich, N. A. Mironova, et al. "The value of cardiovascular magnetic resonance in myocarditis with different clinical presentation." Terapevticheskii arkhiv 91, no. 4 (April 15, 2019): 28–36. http://dx.doi.org/10.26442/00403660.2019.04.000078.

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Objective: to assess the diagnostic meaning of cardiac magnetic resonance imaging (CMR) in various clinical forms of myocarditis. Materials and methods. 11 (8 men, mean age 32.8±11.1 years) patients (pts), hospitalized with suspected acute coronary syndrome, while an acute myocardial infarction was excluded during the examination (group I); 48 pts (31 men, 43.1±12.7 years), with clinical and instrumental signs of dilated cardiomyopathy (DCM) - group II; and 20 patients (12 men, 39.5±14 years), with episodes of ventricular tachycardia (group III) underwent cardiac magnetic resonance imaging (CMRI). In 38 patients endomyocardial biopsy (EMB) was performed. Results and discussion. According to EMB, signs of active myocarditis were revealed in 10 (34.5%) group II pts and in 3 (37.5%) group III pts; signs of resolved myocarditis - in 8 (27.6%) patients in group II and in 3 (37.5%); minimal morphological changes - in 11 (37.9%) patients of group II and in 2 (25%) patients of group III. In 9 (81.9%) patients of group I MRI data allowed to establish the diagnosis of acute myocarditis. Signs of active inflammation from MRI data were detected in myocardium 5 (10.4%) in group II pts and 7 (35%) in group III pts. In 22 (45.8%) pts in group II and 10 (50%), CMR data corresponded to the picture of resolved myocarditis. In 21 (43.8%) cases of group II and 3 (15%) of group III, MRI revealed minimal structural changes. In pts with clinical and instrumental signs of DCM and/or ventricular tachycardia MRI allows to identify signs of "active myocarditis" with a sensitivity of 37.5% with a specificity of 83.4%. At the same time, in cases of resolved myocarditis and minimal morphological changes MRI has high sensitivity (70 and 71.5%) and specificity (71.5 and 75%, respectively). Conclusion. CMR has high diagnostic significance in patients with infarct-like course of myocarditis. In patients with clinical syndrome of dilated cardiomyopathy or arrhythmias, the sensitivity of MRI in detecting active myocarditis is low (37.5%) with high specificity (83.4%). In cases of minimal structural changes in the myocardium and resolved inflammation, CMR is a good alternative to EMB.

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Bridgman, Paul G. "Asymmetric myocardial thickening during acute myocarditis." Heart, Lung and Circulation 12, no. 3 (January 2003): 199–200. http://dx.doi.org/10.1046/j.1444-2892.2003.00221.x.

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Mottard, N., N. Mewton, E. Bonnefoy, M. Abdellaoui, D. Revel, and G. Kirkorian. "Acute Myocarditis Mimicking Lateral Myocardial Infarction." Anaesthesia and Intensive Care 36, no. 5 (September 2008): 739–42. http://dx.doi.org/10.1177/0310057x0803600520.

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Chakko, Simon, David Woska, Eduardo de Marchena, Azorides R. Morales, and Agustin Castellanos. "Myocarditis simulating acute transmural myocardial infarction." Catheterization and Cardiovascular Diagnosis 21, no. 1 (September 1990): 10–12. http://dx.doi.org/10.1002/ccd.1810210104.

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Dec, G. William, Howard Waldman, James Southern, John T. Fallon, Adolph M. Hutter, and Igor Palacios. "Viral myocarditis mimicking acute myocardial infarction." Journal of the American College of Cardiology 20, no. 1 (July 1992): 85–89. http://dx.doi.org/10.1016/0735-1097(92)90141-9.

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Miklozek, Candace L., Clyde S. Crumpacker, Henry D. Royal, Patricia C. Come, John L. Sullivan, and Walter H. Abelmann. "Myocarditis presenting as acute myocardial infarction." American Heart Journal 115, no. 4 (April 1988): 768–76. http://dx.doi.org/10.1016/0002-8703(88)90877-0.

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O’Brien, Caitlin E., John D. Coulson, Priya Sekar, Jon R. Resar, and Kristen Nelson McMillan. "Non-rheumatic streptococcal myocarditis mimicking acute myocardial infarction in an adolescent male." Cardiology in the Young 28, no. 3 (January 8, 2018): 454–57. http://dx.doi.org/10.1017/s1047951117001524.

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AbstractAn adolescent male with a recent history of streptococcal pharyngitis presented with severe substernal chest pain, troponin leak, and ST-segment elevation, which are suggestive of acute inferolateral myocardial infarction. The coronary angiogram was normal. The patient was subsequently diagnosed with non-rheumatic streptococcal myocarditis. He was treated with amoxicillin and had excellent recovery. Non-rheumatic streptococcal myocarditis is an important mimic of acute myocardial infarction in young adults.

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Izmozherova, N. V., A. A. Popov, A. I. Tsvetkov, M. A. Shambatov, I. P. Antropova, L. I. Kadnikov, and V. E. Ispavsky. "Acute myocardial damage in new coronavirus infection (COVID-19)." Ural Medical Journal 20, no. 5 (December 5, 2021): 98–104. http://dx.doi.org/10.52420/2071-5943-2021-20-5-98-104.

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Introduction. Acute respiratory distress syndrome (ARDS) and cardiovascular events, acute myocardial injury being the most frequent of the latter, are among the leading causes of death in COVID-19 patients. The lack of consensus on acute myocardial injury pathogenesis mechanisms, the patients management, treatment an rehabilitation logistics, the anticoagulant treatment in identified SARS-CoV-2 or suspected COVID-19 patients setting indicates the need to assess, analyze and summarize the available data on the issue.Materials and methods. Scientific publications search was carried out in PubMed, Google Scholar databases for the period from December 2019 to September 2021.Results and Discussion. Cardiospecific troponin I increase beyond reference limits is reported to occur in at least every tenth patient with identified SARS-CoV-2, the elevated troponin detection rate increasing among persons with moderate to severe course of the infection. The mechanisms of acute myocardial injury in patients with COVID-19 are poorly understood. By September 2021, there are several pathogenesis theories. A high frequency viral myocarditis direct cardiomyocytes damage is explained by the high SARS-CoV-2 affinity to ACE2 expressed in the myocardium. The cytokine storm related myocardial damage is reported a multiple organ failure consequence. Coagulopathy may also trigger myocardial microvessels damage. Up to every third death of SARS-CoV-2 infected persons is related to the acute myocardial injury. At the same time, due to the high incidence of the acute myocardial injury, it is rather difficult to assess the true incidence of acute myocardial infarction in patients with COVID-19. In the pandemic setting, the waiting time for medical care increases, the population, trying to reduce social contacts, is less likely to seek medical help. In this regard, in order to provide effective medical care to patients with acute myocardial infarction, it is necessary to develop algorithms for providing care adapted to the current epidemiological situation.Conclusion. The treatment of patients with probable development of acute myocardial damage against the background of new coronavirus infection should be performed in accordance with the current clinical guidelines. Anticoagulant therapy should be administered in a prophylactic dose under control of hemostasis parameters and a wide range of biochemical parameters.

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Markousis-Mavrogenis, George, Loukia Koutsogeorgopoulou, Gikas Katsifis, Theodoros Dimitroulas, Genovefa Kolovou, George D. Kitas, Petros P. Sfikakis, and Sophie I. Mavrogeni. "The Double-Edged Sword of T1-Mapping in Systemic Sclerosis—A Comparison with Infectious Myocarditis Using Cardiovascular Magnetic Resonance." Diagnostics 10, no. 5 (May 24, 2020): 335. http://dx.doi.org/10.3390/diagnostics10050335.

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Aims: T1-mapping is considered a surrogate marker of acute myocardial inflammation. However, in diffuse cutaneous systemic sclerosis (dcSSc) this might be confounded by coexisting myocardial fibrosis. We hypothesized that T1-based indices should not by themselves be considered as indicators of myocardial inflammation in dcSSc patients. Methods/Results: A cohort of 59 dcSSc and 34 infectious myocarditis patients was prospectively evaluated using a 1.5-Tesla system for an indication of suspected myocardial inflammation and was compared with 31 healthy controls. Collectively, 33 (97%) and 57 (98%) of myocarditis and dcSSc patients respectively had ≥1 pathologic T2-based index. However, 33 (97%) and 45 (76%) of myocarditis and dcSSc patients respectively had ≥1 pathologic T2-based index. T2-signal ratio was significantly higher in myocarditis patients compared with dcSSc patients (2.5 (0.6) vs. 2.1 (0.4), p < 0.001). Early gadolinium enhancement, late gadolinium enhancement and T2-mapping did not differ significantly between groups. However, both native T1-mapping and extracellular volume fraction were significantly lower in myocarditis compared with dcSSc patients (1051.0 (1027.0, 1099.0) vs. 1120.0 (1065.0, 1170.0), p < 0.001 and 28.0 (26.0, 30.0) vs. 31.5 (30.0, 33.0), p < 0.001, respectively). The original Lake Louise criteria (LLc) were positive in 34 (100%) myocarditis and 40 (69%) dcSSc patients, while the updated LLc were positive in 32 (94%) and 44 (76%) patients, respectively. Both criteria had good agreement with greater but nonsignificant discordance in dcSSc patients. Conclusions: ~25% of dcSSc patients with suspected myocardial inflammation had no CMR evidence of acute inflammatory processes. T1-based indices should not be used by themselves as surrogates of acute myocardial inflammation in dcSSc patients.

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Valletta, Enrico. "Screening per rilevare il maltrattamento in un ambiente ospedaliero pediatrico." PAGINE ELETTRONICHE DI QUADERNI ACP 29, no. 2 (2022): 1. http://dx.doi.org/10.53141/peqacp.2022.2.am1.

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Old and new myocarditis This month’s article allows us to revisit a topic - myocarditis - that has recently come to the attention of pediatricians during the SARS-CoV-2 pandemic, both in its form with acute myocardial damage and as part of the post-Covid systemic inflammatory manifestations that identify MIS-C (multisystem inflammatory syndrome in children). It is also an opportunity to analyze the most frequent viral causes of acute myocarditis in children, the distinctive elements with myocarditis related to SARS-CoV-2 infection and how MIS-C may represent a possible link between acute myocarditis and Kawasaki disease.

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Zhong, Ze, Jia-qing Hu, Xin-dong Wu, Yong Sun, and Jun Jiang. "Anti-apoptotic effects of myocardin-related transcription factor-A on rat cardiomyocytes following hypoxia-induced injury." Canadian Journal of Physiology and Pharmacology 94, no. 4 (April 2016): 379–87. http://dx.doi.org/10.1139/cjpp-2014-0461.

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Myocardin-related transcription factor-A (MRTF-A) can transduce both biomechanical and humoral signals, which can positively modulate cardiac damage induced by acute myocardial infarction. However, the molecular mechanism that underlies the contribution that MRTF-A provides to the myocardium is not completely understood. The objective of this study was to investigate the effects of MRTF-A on myocardium apoptosis and its mechanisms. Our experiment results showed that MRTF-A expression increased and Bcl-2 expression reduced during myocardial ischemia–reperfusion in rat. Meanwhile, primary cardiomyocytes were pretreated with wild-type MRTF-A or siRNA of MRTF-A before exposure to hypoxia. We found that overexpression of MRTF-A in myocardial cells inhibited apoptosis and the release of cytochrome c. MRTF-A enhanced Bcl-2, which contributes to MRTF-A interaction with Bcl-2 in the nuclei of cardiomyocytes. MRTF-A upregulation expression of Bcl-2 in cardiomyocytes induced by hypoxia was inhibited by PD98059, an ERK1/2 inhibitor. In conclusions, MRTF-A improved myocardial cell survival in a cardiomyocyte model of hypoxia-induced injury; this effect was correlated with the upregulation of anti-apoptotic gene Bcl-2 through the activation of ERK1/2.

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Narula, Jagat, Ban An Khaw, G. William Dec, Igor F. Palacios, James F. Southern, John T. Fallon, H. William Strauss, Edgar Haber, and Tsunehiro Yasuda. "Recognition of Acute Myocarditis Masquerading as Acute Myocardial Infarction." New England Journal of Medicine 328, no. 2 (January 14, 1993): 100–104. http://dx.doi.org/10.1056/nejm199301143280205.

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Arslan, Z., M. Tavlaşoglu, M. Unlu, M. Aparci, and S. Demirkol. "PP-253 ACUTE MYOCARDITIS MIMICKING ACUTE INFERIOR MYOCARDIAL INFARCTION." International Journal of Cardiology 163, no. 3 (March 2013): S181. http://dx.doi.org/10.1016/s0167-5273(13)70457-1.

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Raev, Dimitar. "Acute Staphylococcal myocarditis masquerading as an acute myocardial infarction." International Journal of Cardiology 60, no. 1 (June 1997): 95–98. http://dx.doi.org/10.1016/s0167-5273(97)02962-8.

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Si-Mohamed, Salim Aymeric, Lauria Marie Restier, Arthur Branchu, Sara Boccalini, Anaelle Congi, Arthur Ziegler, Danka Tomasevic, Thomas Bochaton, Loic Boussel, and Philippe Charles Douek. "Diagnostic Performance of Extracellular Volume Quantified by Dual-Layer Dual-Energy CT for Detection of Acute Myocarditis." Journal of Clinical Medicine 10, no. 15 (July 26, 2021): 3286. http://dx.doi.org/10.3390/jcm10153286.

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Background: Myocardial extracellular volume (ECV) is a marker of the myocarditis inflammation burden and can be used for acute myocarditis diagnosis. Dual-energy computed tomography (DECT) enables its quantification with high concordance with cardiac magnetic resonance (CMR). Purpose: To investigate the diagnostic performance of myocardial ECV quantified on a cardiac dual-layer DECT in a population of patients with suspected myocarditis, in comparison to CMR. Methods: 78 patients were included in this retrospective monocenter study, 60 were diagnosed with acute myocarditis and 18 patients were considered as a control population, based on the 2009 Lake and Louise criteria. All subjects underwent a cardiac DECT in acute phase consisted in an arterial phase followed by a late iodine enhancement phase at 10 min after injection (1.2 mL/kg, iodinated contrast agent). ECV was calculated using the hematocrit level measured the day of DECT examinations. Non-parametric analyses have been used to test the differences between groups and the correlations between the variables. A ROC curve has been used to identify the optimal ECV cut-off discriminating value allowing the detection of acute myocarditis cases. A p value < 0.05 has been considered as significant. Results: The mean ECV was significantly higher (p < 0.001) for the myocarditis group compared to the control (34.18 ± 0.43 vs. 30.04 ± 0.53%). A cut-off value of ECV = 31.60% (ROC AUC = 0.835, p < 0.001) allows to discriminate the myocarditis with a sensitivity of 80% and a specificity of 78% (positive predictive value = 92.3%, negative predictive value = 53.8% and accuracy = 79.5%). Conclusion: Myocardial ECV enabled by DECT allows to diagnose the acute myocarditis with a cut-off at 31.60% for a sensitivity of 80% and specificity of 78%.

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Pommier, Thibaut, Thibault Leclercq, Charles Guenancia, Simon Tisserand, Céline Lairet, Max Carré, Alain Lalande, et al. "More than 50% of Persistent Myocardial Scarring at One Year in “Infarct-like” Acute Myocarditis Evaluated by CMR." Journal of Clinical Medicine 10, no. 20 (October 13, 2021): 4677. http://dx.doi.org/10.3390/jcm10204677.

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Background: Cardiac magnetic resonance (CMR) has emerged as a reference tool for the non-invasive diagnosis of myocarditis. However, its role in follow-up (FU) after the acute event is unclear. The objectives were to assess the evolution of CMR parameters between the acute phase of infarct-like myocarditis and 12 months thereafter and to identify the predictive factors of persistent myocardial scarring at one year. Methods: All patients with infarct-like acute myocarditis confirmed by CMR were included. CMR was performed within 8 days following symptom onset, at 3 months and at one year. One-year FU included ECG, a cardiac stress test, Holter recording, biological assessments, medical history and a quality-of-life questionnaire. Patients were classified according to the presence or absence of complete recovery at one year based on the CMR evaluation. Results: A total of 174 patients were included, and 147 patients had three CMR. At one year, 79 patients (54%) exhibited persistent myocardial scarring on CMR. A multivariate analysis showed that high peak troponin at the acute phase (OR: 3.0—95%CI: 1.16–7.96—p = 0.024) and the initial extent of late gadolinium enhancement (LGE) (OR: 1.1—95%CI: 1.03–1.19—p = 0.006) were independent predictors of persistent myocardial scarring. Moreover, patients with myocardial scarring on the FU CMR were more likely to have premature ventricular contractions during the cardiac stress test (25% versus 9%, p = 0.008). Conclusion: Less than 50% of patients with infarct-like acute myocarditis showed complete recovery at one year. Although major adverse cardiac events were rare, ventricular dysrhythmias at one year were more frequent in patients with persistent myocardial scarring.

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DRAGOI GALRIHNO, Ruxandra, Anca BALINISTEANU, Vladimir BRATU, Andrea CIOBANU, Laura MITREA, Alina NICULA, and Dragos VINEREANU. "On the Precipice of Disaster – Fulminant Acute Myocarditis Mimicking ST-Elevation Myocardial Infarction in a Young Patient." Romanian Journal of Cardiology 31, no. 2 (July 2, 2021): 361–65. http://dx.doi.org/10.47803/rjc.2021.31.2.361.

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Although acute myocarditis and coronary vasospasm are common differential diagnoses in the case of young patients with persistent ST elevation, the association of coronary vasospasm and acute fulminant myocarditis is a rare situation. We present the case of a 21 year-old male who presented with chest pain, ECG changes and biomarker levels initially interpreted as ST elevation myocardial infarction (STEMI), in which severe coronary vasospasm was identifi ed. Shortly after, he developed cardiogenic shock and fulminant acute myocarditis was suspected.

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Ismail, Tevfik F., Alina Hua, Sven Plein, David P. D’Cruz, Michelle M. A. Fernando, Matthias G. Friedrich, Michael J. Zellweger, Assuero Giorgetti, Federico Caobelli, and Philip Haaf. "The role of cardiovascular magnetic resonance in the evaluation of acute myocarditis and inflammatory cardiomyopathies in clinical practice — a comprehensive review." European Heart Journal - Cardiovascular Imaging 23, no. 4 (February 15, 2022): 450–64. http://dx.doi.org/10.1093/ehjci/jeac021.

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Abstract Inflammatory cardiomyopathy (I-CMP) is defined as myocarditis in association with cardiac dysfunction and/or ventricular remodelling. It is characterized by inflammatory cell infiltration into the myocardium and has heterogeneous infectious and non-infectious aetiologies. A complex interplay of genetic, autoimmune, and environmental factors contributes to the substantial risk of deteriorating cardiac function, acute heart failure, and arrhythmia as well as chronic dilated cardiomyopathy and its sequelae. Multi-parametric cardiovascular magnetic resonance (CMR) imaging is sensitive to many tissue changes that occur during myocardial inflammation, regardless of its aetiology. In this review, we summarize the various aetiologies of I-CMP and illustrate how CMR contributes to non-invasive diagnosis.

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Mavrogeni, Sophie, Dimitris Apostolou, Panayiotis Argyriou, Stella Velitsista, Lilika Papa, Stelios Efentakis, Evangelos Vernardos, Mikela Kanoupaki, George Kanoupakis, and Athanassios Manginas. "T1 and T2 Mapping in Cardiology: “Mapping the Obscure Object of Desire”." Cardiology 138, no. 4 (2017): 207–17. http://dx.doi.org/10.1159/000478901.

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Abstract:

The increasing use of cardiovascular magnetic resonance (CMR) is based on its capability to perform biventricular function assessment and tissue characterization without radiation and with high reproducibility. The use of late gadolinium enhancement (LGE) gave the potential of non-invasive biopsy for fibrosis quantification. However, LGE is unable to detect diffuse myocardial disease. Native T1 mapping and extracellular volume fraction (ECV) provide knowledge about pathologies affecting both the myocardium and interstitium that is otherwise difficult to identify. Changes of myocardial native T1 reflect cardiac diseases (acute coronary syndromes, infarction, myocarditis, and diffuse fibrosis, all with high T1) and systemic diseases such as cardiac amyloid (high T1), Anderson-Fabry disease (low T1), and siderosis (low T1). The ECV, an index generated by native and post-contrast T1 mapping, measures the cellular and extracellular interstitial matrix (ECM) compartments. This myocyte-ECM dichotomy has important implications for identifying specific therapeutic targets of great value for heart failure treatment. On the other hand, T2 mapping is superior compared with myocardial T1 and ECM for assessing the activity of myocarditis in recent-onset heart failure. Although these indices can significantly affect the clinical decision making, multicentre studies and a community-wide approach (including MRI vendors, funding, software, contrast agent manufacturers, and clinicians) are still missing.

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V.N., Priyanka, Anil Kumar V.R., and Nagamalesh U.M. "Acute Myocardial Infarction Presenting with Atypical Symptoms." Indian Journal of Emergency Medicine 4, no. 3 (2018): 161–64. http://dx.doi.org/10.21088/ijem.2395.311x.4318.8.

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Journal articles on the topic 'Acute myocarditi'

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