scholarly journals 740 A case of acute Campylobacter COLI myocarditis post-mRNA anti-SARS-CoV-2 vaccine. Was vaccination an innocent bystander or a determining factor?

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Costantina Catalano ◽  
Damiano Fedele ◽  
Andrea Impellizzeri ◽  
Lorenzo Bartoli ◽  
Francesco Fallani ◽  
...  

Abstract A 24-year-old healthy man, smoker (2 pack-years), was admitted to the Cardiology Unit for chest pain and fever occurred 2 days after anti-SARS-CoV-2 vaccination. There were no pathological findings at physical examination. The electrocardiogram showed diffuse ST elevation. Laboratory tests showed a significant increment of Troponin I levels (4697 ng/l → 6236 ng/l after 3 h), White Blood Cells (17 610/mmc) and C-Reactive Protein (8.36 mg/dl). Echocardiography showed normal left ventricular systolic function with no evidence of pericarditis. These findings were consistent with a probable case of acute myocarditis. Cardiac magnetic imaging demonstrated myocardial oedema of the posterior wall of the left ventricle at T2-weighted images, with patchy areas of subepicardial late gadolinium enhancement. Based on Centers for Disease Control and Prevention myocarditis diagnostic criteria, a diagnosis of acute myocarditis was made and treatment with Non-Steroidal Anti-Inflammatory Drugs was started. Regarding etiology agent determination, in the COVID19 era, the first suspect was anti-SARS-CoV-2 mRNA-vaccine-induced myocarditis. Several case series and analyses of a large national health care organization database helped to identify features linked to these types of myocarditis. The highest incidence was observed among male juvenile subjects, usually 48–72 h after the second dose of vaccination, with elevated levels of spike antibody for SARS-CoV-2. Nevertheless, in the presented clinical case, the patient had received the first dose of BNT162b2 vaccination two days before hospital admission and showed negative serology tests for SARS-CoV-2. In recent medical history, two days before the onset of fever and chest pain, the patient had episodes of diarrhea which persisted during the first week of hospitalization. All immunological and microbiological tests result negative, except for a stool culture positive for Campylobacter coli. Interestingly a revision of literature showed several cases of myocarditis linked to Campylobacter species. In particular, of 13 reported cases, 12 (92%) were male with a mean age of 26 ± 8.8 years, and cardiac symptoms present generally 2–4 days after diarrhea. In this particular setting, the first and more obvious hypothesis was strongly questioned because of an unexpected finding in the stool culture. In fact, Campylobacter spp. related myocarditis is an extremely rare condition, even if this pathogen is associated with important immunological interferences, as shown by its relationship with the Guillain-Barre syndrome. Further, myocarditis related to mRNA anti-SARS-CoV-2 vaccine is considered a rare complication. We hypothesized that the association of the two components could have acted synergistically to produce an immune system activation against cardiac muscle. Additional investigations are required to clarify the link between vaccination and possible improper immune response. In conclusion, this case represents a typical example in which the cause of the disease should be well investigated because the initial etiological theory is not definitive, especially in the SARS-CoV-2 era.

2012 ◽  
Vol 6 ◽  
pp. CMO.S8598 ◽  
Author(s):  
Chitradeep De ◽  
Jaya Phookan ◽  
Valay Parikh ◽  
Tarun Nagrani ◽  
Mayur Lakhani ◽  
...  

Case Report A 75-yr-old gentleman, with a past medical history of diabetes mellitus and Acute Myeloid Leukemia presented to our emergency department with a chief complaint of exertional dyspnea and chest pain. A week prior to this visit, he had recieved a cycle of decitabine chemotherapy at 20 mg/metered square for ten days. This was his second cycle of decitabine. His out patient medications included megesterol, omeprazole, morphine sulfate and insulin glargine. The patient was admitted to the Coronary Care Unit for Acute Coronary Syndrome. His cardiac enzymes were elevated (peak troponin 30 ng/mL, CKMB 67.4 ng/mL). His 12 lead EKG revealed sinus tachycardia with a ventricular rate of 113, but without acute ST–T wave changes. The BNP was 259 pg/mL. A 2D echo revealed moderate diffuse hypokinesis with an EF of 35%. He subsequently underwent a left heart catheterization, which showed non-obstructive CAD. In our patient, the elevated troponins (peak troponin 30 ng/mL) and BNP were seen concomitant with the onset of cardiogenic shock. Two months ago, his 2 D echocardiogram revealed an ejection fraction of about 55%–65% with slightly increased left ventricular (LV) wall thickness. Discussion The most common adverse effects of decitabine include cytopenia, nausea, pain and erythema/nodules at the injection site. To date, there has been only one reported case of a hypomethylating agent inducing acute myocarditis. We a present a case of reversible, non-ischemic cardiomyopathy secondary to decitabine chemotherapy, which resolved after the drug was discontinued. Trials involving decitabine for the treatment of MDS reported no myocarditis. In our case, the diagnosis of transient cardiomyopathy was highly probable since the patient's troponins and echocardiogram returned to baseline after discontinuation of treatment. Also, the patient never had any further chest pain at his 6 month follow up. In this case, we believe that the elevated Troponin I levels, along with a cardiac catheterization revealing patent coronary vessels, favor our hypothesis that our patient suffered from acute myocarditis as a result of direct toxicity from decitabine chemotherapy. We doubt that there was an underlying infectious etiology, since the patient had three negative blood cultures, two negative urine cultures and a negative viral serology. Our case demonstrates that chest pains in a patient treated with hypomethylating agents should be further explored in order to rule out acute myocarditis.


2016 ◽  
Vol 62 (3) ◽  
pp. 363-367
Author(s):  
Pintilie Irina ◽  
Scridon Alina ◽  
Șerban Răzvan Constantin

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.


2019 ◽  
Vol 12 (1) ◽  
pp. 24-29
Author(s):  
Mohammad Jakir Hossain ◽  
Khondoker Asaduzzaman ◽  
Solaiman Hossain ◽  
Muhammad Badrul Alam ◽  
Nur Hossain

Background: In the diagnosis of acute coronary syndrome, cardiac troponin I is highly reliable and widely available biomarker. Serum level of cardiac troponin I is related to amount of myocardial damage and also closely relates to infarct size. Our aim of the study is to find out the relationship between cardiac troponin I and left ventricular systolic function after acute coronary syndrome. Methods: Total of 132 acute coronary syndrome patients were included in this study after admission in coronary care unit of Sir Salimullah Medical College, Mitford Hospital. Troponin I level was measured at admission and left ventricular ejection fraction (LVEF) was measured by echocardiography between 12-48 hours of onset of chest pain. Results: There was negative correlation between Troponin I at 12 to 48 hours of chest pain with LVEF in these study patients. With a cutoff value of troponin I e”6.8 ng/ml in STEMI patients there is a significant negative relation between 12 to 48 hrs troponin I and LVEF (p<0.001). Sensitivity of troponin I e” 6.8 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% in STEMI was 93.75% and specificity was 77.78%. In NSTEMI sensitivity of troponin I e” 4.5 ng/ml between 12 to 48 hours of chest pain in predicting LVEF <50% was 65% and specificity was 54.05%. Conclusion: Serum troponin I level had a strong negative correlation with left ventricular ejection fraction after acute coronary syndrome and hence can be used to predict the LVEF in this setting. Cardiovasc. j. 2019; 12(1): 24-29


2020 ◽  
Vol 2020 ◽  
pp. 1-4 ◽  
Author(s):  
Sunny Patel ◽  
Sepideh Nabatian ◽  
Michael Goyfman

A 66-year-old female was brought to the emergency department for acute-onset left-sided chest pain. Prior to arrival, she was at an outpatient appointment with a vascular surgeon for elective sclerotherapy treatment of her lower extremity varicose veins. After receiving an IV injection of polidocanol, she developed severe chest pain with left arm and jaw numbness for the first time in her life. Upon arrival to the ED, the patient reported that her symptoms had resolved. Electrocardiogram (ECG) on presentation was significant for T-wave inversions in leads V1-V3. An initial set of cardiac enzymes showed a troponin I level of 0.62 ng/mL, which subsequently increased to 2.26 ng/mL. Her echocardiogram was significant for mild left ventricular systolic dysfunction with apical hypokinesis (ejection fraction 50%). A repeat ECG showed new T-wave inversions compared to that from the time of admission. The patient eventually agreed to cardiac catheterization, which revealed patent vessels without coronary artery disease, supporting our diagnosis of Takotsubo syndrome and what is the first reported case of likely polidocanol-induced Takotsubo syndrome in the United States.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Anne Munch ◽  
Jens Sundbøll ◽  
Søren Høyer ◽  
Manan Pareek

A 22-year-old woman recently diagnosed with granulomatosis with polyangiitis (GPA) was admitted to the department of cardiology due to chest pain and shortness of breath. The ECG showed widespread mild PR-segment depression, upwardly convex ST-segment elevation, and T-wave inversion. The troponin T level was elevated at 550 ng/L. Transthoracic echocardiography showed basal inferoseptal thinning and hypokinesis, mild pericardial effusion, and an overall preserved left ventricular ejection fraction of 55%. Global longitudinal strain, however, was clearly reduced. Cardiac magnetic resonance imaging (MRI) showed findings consistent with myocarditis but the etiology of the apical hypokinesis could not be determined with certainty and may well have been due to a myocardial infarction, a notion supported by a coronary angiogram displaying slow flow in the territory of the left anterior descending artery. Finally, an endomyocardial biopsy confirmed the diagnosis of myocarditis. The cardiac symptoms subsided upon treatment with high-dose prednisolone and rituximab.


2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Han-Ping Wu ◽  
Mao-Jen Lin ◽  
Wen-Chieh Yang ◽  
Kang-Hsi Wu ◽  
Chun-Yu Chen

The clinical presentation of acute myocarditis in children may range from asymptomatic to sudden cardiac arrest. This study analyzed the clinical spectrum of acute myocarditis in children to identify factors that could aid primary care physicians to predict the need for extracorporeal membrane oxygenation (ECMO) earlier and consult the pediatric cardiologist promptly. Between October 2011 and September 2016, we retrospectively analyzed 60 patients aged 18 years or younger who were admitted to our pediatric emergency department with a definite diagnosis of acute myocarditis. Data on demographics, presentation, laboratory tests, electrocardiogram and echocardiography findings, treatment modalities, complications, and long-term outcomes were obtained. During the study period, 60 patients (32 male, 28 female; mean age, 8.8±6.32 years) were diagnosed with acute myocarditis. Fever, cough, and chest pain were the most common symptoms (68.3%, 56.7%, and 53.3%, resp.). Arrhythmia and left ventricular ejection fraction (LVEF) < 60%, vomiting, weakness, and seizure were more common in the ECMO group than in the non-ECMO group, with statistical significance (P<0.05). Female sex, vomiting, weakness, seizure, arrhythmia, and echocardiography showing LVEF < 60% may predict the need for ECMO. Initial serum troponin-I cutoff values greater than 14.21 ng/mL may also indicate the need for ECMO support for children with acute myocarditis.


2018 ◽  
Vol 71 (11) ◽  
pp. A984
Author(s):  
Kaoru Hirose ◽  
Aitoshi Isotani ◽  
Kyohei Yamaji ◽  
Takashi Morinaga ◽  
Takenori Domei ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Lujin Wu ◽  
Wei Wang ◽  
Qianru Leng ◽  
Nana Tang ◽  
Ning Zhou ◽  
...  

The manifestations of hyperthyroidism-related myocardial damage are multitudinous, including arrhythmia, dilated cardiomyopathy, valvular diseases, and even cardiogenic shock. Acute myocarditis induced by thyrotoxicosis had been reported in a few studies. However, attention on its prevalence and underlying mechanisms is sorely lacking. Its long-term harm is often ignored, and it may eventually develop into dilated cardiomyopathy and heart failure. We report a case of Graves' disease with a progressive elevation of hypersensitive cardiac troponin-I at several days after discontinuation of the patient's anti-thyroid drugs. Cardiac magnetic resonance imaging (CMRI) showed inflammatory edema of some cardiomyocytes (stranded enhanced signals under T2 mapping), myocardial necrosis (scattered enhanced signals under T1 late gadolinium enhancement) in the medial and inferior epicardial wall, with a decreased left ventricular systolic function (48%), which implied a possibility of acute myocarditis induced by thyrotoxicosis. The patient was then given a transient glucocorticoid (GC) treatment and achieved a good curative effect. Inspired by this case, we aim to systematically elaborate the pathogenesis, diagnosis, and treatment of hyperthyroidism-induced autoimmune myocarditis. Additionally, we emphasize the importance of CMRI and GC therapy in the diagnosis and treatment of hyperthyroidism-related myocarditis.


2021 ◽  
Vol 8 ◽  
Author(s):  
Radu Tanacli ◽  
Patrick Doeblin ◽  
Collin Götze ◽  
Victoria Zieschang ◽  
Alessandro Faragli ◽  
...  

Background: Despite the ongoing global pandemic, the impact of COVID-19 on cardiac structure and function is still not completely understood. Myocarditis is a rare but potentially serious complication of other viral infections with variable recovery, and is, in some cases, associated with long-term cardiac remodeling and functional impairment.Aim: To assess myocardial injury in patients who recently recovered from an acute SARS-CoV-2 infection with advanced cardiac magnetic resonance imaging (CMR) and endomyocardial biopsy (EMB).Methods: In total, 32 patients with persistent cardiac symptoms after a COVID-19 infection, 22 patients with acute classic myocarditis not related to COVID-19, and 16 healthy volunteers were included in this study and underwent a comprehensive baseline CMR scan. Of these, 10 patients post COVID-19 and 13 with non-COVID-19 myocarditis underwent a follow-up scan. In 10 of the post-COVID-19 and 15 of the non-COVID-19 patients with myocarditis endomyocardial biopsy (EMB) with histological, immunohistological, and molecular analysis was performed.Results: In total, 10 (31%) patients with COVID-19 showed evidence of myocardial injury, eight (25%) presented with myocardial oedema, eight (25%) exhibited global or regional systolic left ventricular (LV) dysfunction, and nine (28%) exhibited impaired right ventricular (RV) function. However, only three (9%) of COVID-19 patients fulfilled updated CMR–Lake Louise criteria (LLC) for acute myocarditis. Regarding EMB, none of the COVID-19 patients but 87% of the non-COVID-19 patients with myocarditis presented histological findings in keeping with acute or chronic inflammation. COVID-19 patients with severe disease on the WHO scale presented with reduced biventricular longitudinal function, increased RV mass, and longer native T1 times compared with those with only mild or moderate disease.Conclusions: In our cohort, CMR and EMB findings revealed that SARS-CoV-2 infection was associated with relatively mild but variable cardiac involvement. More symptomatic COVID-19 patients and those with higher clinical care demands were more likely to exhibit chronic inflammation and impaired cardiac function compared to patients with milder forms of the disease.


Author(s):  
Jia Hui Zeng ◽  
Ying-Xia Liu ◽  
Jing Yuan ◽  
Fu-Xiang Wang ◽  
Wei-Bo Wu ◽  
...  

Background: The Coronavirus Disease 2019 (COVID-19) has been demonstrated as the cause of pneumonia. Nevertheless, it has not been reported as the cause of acute myocarditis or fulminant myocarditis. Case Presentation: A 63-year-old male was admitted with pneumonia and cardiac symptoms. He was genetically confirmed as COVID-19 by testing sputum on the first day of admission. He also had an elevated troponin-I (Trop I) level and diffuse myocardial dyskinesia along with decreased left ventricular ejection fraction (LVEF) on echocardiography. The highest level of Interleukin 6 was 272.40pg/ml. Bedside chest radiograph had typical ground-glass changes of viral pneumonia. The laboratory test results of virus that can cause myocarditis are all negative. The patient conformed to the diagnostic criteria of Chinese expert consensus statement for fulminant myocarditis. After receiving antiviral therapy and mechanical life support, the Trop I reduced to 0.10 g/L, and Interleukin 6 was 7.63 pg/ml. Meanwhile the LVEF of the patient gradually recovered to 68%. Conclusion: COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure, and this is the first case of COVID-19 infection complicated with fulminant myocarditis. The mechanism of cardiac pathology caused by COVID-19 needs further study.


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