scholarly journals Case report of acute myocarditis after administration of COVID-19 vaccine in Japan

2022 ◽  
Author(s):  
Masato Ohnishi ◽  
Yasunori Tanaka ◽  
Sakiya Nishida ◽  
Toshiro Sugimoto
Keyword(s):  
Troponin I ◽  
Case Reports ◽  
Acute Myocarditis ◽  
The United States ◽  
Temporal Association ◽  
Reactive Protein ◽  
Coronary Syndrome ◽  
Contrast Enhanced ◽  
St Elevation ◽  
Magnetic Resonance Imaging Mri

Abstract Background The worldwide spread of Coronavirus disease 2019 (COVID-19) is still not under control and vaccination in Japan started in February 2021, albeit later than in Europe and the United States of America. The COVID-19 vaccination frequently leads to minor adverse reactions, that may be more intense after the second dose. The number of case reports of myocarditis following COVID-19 vaccination have been recently increased. Case Summary We report a case of a 26-year-old healthy man who presented to our hospital with chest pain on May 24 2021, 4 days after his second COVID-19 vaccination. The electrocardiogram showed ST elevation with upward concavity in I, II, aVL, aVF, V4 to V6, and small Q wave in II, III, aVF. Laboratory studies revealed elevation of troponin-I, creatine kinase, C-reactive protein and negative viral serologies. Acute aortic dissection and pulmonary thromboembolism were ruled out by contrast-enhanced thoracoabdominal computed tomography (CT). An urgent coronary angiogram was performed because an acute coronary syndrome was suspected, but no significant stenosis was found. Cardiac magnetic resonance imaging (MRI) demonstrated oedema and late gadolinium enhancement of the left ventricle in a midmyocardial and epicardial distribution. Discussion Although the temporal association does not prove causation, the very short span between the second vaccination and the onset of myocarditis suggests that this acute myocarditis seemed to be an adverse reaction to COVID-19 vaccine. To the best of our knowledge, this is the first published case of acute myocarditis following COVID-19 vaccine in Asia.

scholarly journals Paraoxonase-1 55 LL Genotype Is Associated with No ST-Elevation Myocardial Infarction and with High Levels of Myoglobin

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Francesca Marchegiani ◽  
Liana Spazzafumo ◽  
Maurizio Cardelli ◽  
Mauro Provinciali ◽  
Francesco Lescai ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Troponin I ◽  
Paraoxonase 1 ◽  
Ischemic Damage ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Serum Paraoxonase

It is well known that serum paraoxonase (PON1) plays an important role in the protection of LDL from oxidation. PON1 55 polymorphism is currently investigated for its possible involvement in cardiovascular diseases. The objective of our study is to verify if PON1 55 polymorphism is associated with risk of acute coronary syndrome (ACS) and with biochemical myocardial ischemia markers, such as troponin I, creatine kinase (CK)-MB, myoglobin, and C-reactive protein. We analysed PON1 55 polymorphism in a total of 440 elderly patients who underwent an ACS episode: 98 patients affected by unstable angina (UA), 207 AMI (acute myocardial infarction) patients affected by STEMI (ST elevation), and 135 AMI patients affected by NSTEMI (no ST elevation). We found that individuals carrying PON1 55 LL genotype are significantly more represented among AMI patients affected by NSTEMI; moreover, the patients carrying LL genotype showed significantly higher levels of myoglobin in comparison to LM + MM carriers patients. Our study suggests that PON1 55 polymorphism could play a role in the pathogenesis of cardiac ischemic damage. In particular, the significant association between PON1 55 LL genotype and the occurrence of a NSTEMI may contribute to improve the stratification of the cardiovascular risk within a population.

scholarly journals Free vs Total Pregnancy-Associated Plasma Protein A (PAPP-A) as a Predictor of 1-Year Outcome in Patients Presenting with Non–ST-Elevation Acute Coronary Syndrome

2010 ◽  
Vol 56 (7) ◽  
pp. 1158-1165 ◽  
Author(s):  
Juha Lund ◽  
Saara Wittfooth ◽  
Qiu-Ping Qin ◽  
Tuomo Ilva ◽  
Pekka Porela ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Coronary Syndrome ◽  
Plasma Protein ◽  
Troponin I ◽  
Protein A ◽  
Free Fraction ◽  
Prognostic Information ◽  
Reactive Protein ◽  
Coronary Syndrome ◽  
St Elevation

Abstract Background: The free fraction of pregnancy-associated plasma protein A (FPAPP-A) was found to be the PAPP-A form released to the circulation in acute coronary syndrome (ACS). We estimated the prognostic value of FPAPP-A vs total PAPP-A (TPAPP-A) concentrations in forecasting death and nonfatal myocardial infarction (combined endpoint) in patients with non–ST-elevation ACS. Methods: We recruited 267 patients hospitalized for symptoms consistent with non–ST-elevation ACS and followed them for 12 months. FPAPP-A, TPAPP-A, C-reactive protein (CRP), and cardiac troponin I (cTnI) were measured at admission; cTnI was also measured at 6–12 h and 24 h. Because of the recently shown interaction between PAPP-A and heparin, we excluded patients treated with any heparin preparations before the admission blood sampling. Results: During the follow-up, 57 (21.3%) patients met the endpoint (22 deaths and 35 nonfatal myocardial infarctions). According to FPAPP-A (<1.27, 1.27–1.74, >1.74 mIU/L) and TPAPP-A (<1.98, 1.98–2.99, >2.99 mIU/L) tertiles, this endpoint was met by 12 (13.5%), 18 (20.2%), 27 (30.3%) (P = 0.02), and 17 (19.1%), 17 (19.1%), 23 (25.8%) (P = 0.54) patients, respectively. After adjusting for age, sex, diabetes, previous myocardial infarction, and ischemic electrocardiogram (ECG) findings, FPAPP-A >1.74 mIU/L [risk ratio (RR) 2.0; 95% CI 1.0–4.1, P = 0.053), increased cTnI, and CRP ≥2.0 mg/L were independent predictors of an endpoint. The prognostic performance of TPAPP-A was inferior to that of FPAPP-A. Conclusions: FPAPP-A seems to be superior as a prognostic marker compared to TPAPP-A, giving independent and additive prognostic information when measured at the time of admission in patients hospitalized for non–ST-elevation ACS.

scholarly journals Active Duty Personnel With ST Elevation Myocardial Infarctions Are Deployment Ineligible Despite Receiving Standard Management

2020 ◽  
Vol 185 (5-6) ◽  
pp. e638-e642 ◽  
Author(s):  
Andrew S Wilson ◽  
James A Watts ◽  
Kelvin N V Bush
Keyword(s):  
United States ◽  
Vascular Complications ◽  
Quality Measures ◽  
The United States ◽  
Active Duty ◽  
Cardiac Biomarkers ◽  
Atherosclerotic Cardiovascular Disease ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Door To Balloon

Abstract Introduction ST elevation myocardial infarction (STEMI) is a high acuity diagnosis that requires prompt recognition and developed system responses to reduce morbidity and mortality. There is a paucity of literature describing active duty (AD) military personnel with STEMI syndromes at military treatment facilities (MTFs). This study aims to describe AD military members with STEMI diagnoses, military treatment facility management, and subsequent military dispositions observed. Materials and Methods We performed a single-center, retrospective review of all STEMI diagnoses at San Antonio Military Medical Center (SAMMC) from January 2008 to June 2018. Patients met inclusion in the analysis if they were (1) AD personnel in the United States Air Force (USAF) or United States Army (USA) and (2) presented with electrocardiogram findings and cardiac biomarkers diagnostic of a STEMI diagnosis. ASCVD and STEMI diagnoses were confirmed by board certified interventional cardiologists with coronary angiography. The 2017 American College of Cardiology (ACC) STEMI clinical performance and quality measures were used as the standard of care metrics for our case reviews. Results A total of 236 patients were treated for STEMI at SAMMC during the study period. Eight (3.4%) of these cases met inclusion criteria of being AD status at the time of diagnosis. Five (63%) of the AD STEMI diagnoses were USA members, three (37%) were USAF members, 50% were Caucasian, and 100% were male sex. The average age and body mass index were 46.3 ± 5.5 years old and 28.5 ± 3.1 kg/m 2, respectively. Preexisting cardiovascular risk factors were present in six (75%) of the individuals with hypertension being most common (63%). The eight patients had a baseline average low-density lipoprotein cholesterol of 110 ± 39 mg/dL, total cholesterol of 180 ± 49 mg/dL and calculated 10-year risk of atherosclerotic cardiovascular disease (ASCVD) 3.9 ± 1.6%. 100% of patients underwent primary percutaneous coronary intervention (PCI) within 90 minutes of presentation (average door-to-balloon time 59.3 ± 24 min). Single-vessel disease was found in all eight patients and seven of them underwent drug-eluting stent placement (average number of stents 2 ± 1.5). Performance and quality measures were met in all applicable categories including door-to-balloon times, discharge medical therapies, and cardiac rehabilitation enrollments for 100% AD personnel. Reported adverse events included two stent thromboses and two vascular complications. Three of eight individuals (37.5%) were diagnosed with behavioral health disorders secondary to their acute coronary syndrome. Medical retirement secondary to STEMI diagnosis occurred in 87.5% of subjects and all study personnel medically retired within 24 months (average 12.8 ± 7.9 months). Conclusions AD personnel represent a small minority of MTF STEMI diagnoses and present with lower risk cardiovascular profiles. AD personnel received standard STEMI management compared to national performance measures, and were deployment ineligible after STEMI diagnoses. Further studies are needed to definitively explore the appropriate military dispositions for members with STEMI diagnoses and acute coronary syndromes.

scholarly journals Autoantibodies to Cardiac Troponin Associate with Higher Initial Concentrations and Longer Release of Troponin I in Acute Coronary Syndrome Patients

2009 ◽  
Vol 55 (5) ◽  
pp. 938-945 ◽  
Author(s):  
Kim Pettersson ◽  
Susann Eriksson ◽  
Saara Wittfooth ◽  
Emilia Engström ◽  
Markku Nieminen ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Myocardial Damage ◽  
Prognostic Impact ◽  
Serum Samples ◽  
Igg Antibody ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Autoantibody Formation

Abstract Background: Cardiac troponin (cTn) is an established marker of myocardial infarction. Pronounced heterogeneity and the minute amounts released into the circulation constitute significant challenges for cTn detection. Recently, autoantibody formation to cTn was shown to be common and to interfere with immunoassay performance. In this study, we investigated cTn autoantibodies and cardiac troponin I (cTnI) in acute coronary syndrome (ACS) patients over a 1-year period after the index event. Methods: We used a second-generation cTnI assay designed to reduce the interference of cTn autoantibodies. The assay for cTn autoantibodies used 2 anti-cTnI antibodies to capture the ternary cTnI-complex, enabling unrestricted binding of the autoantibodies, which were detected with a labeled antihuman IgG antibody. We analyzed serum samples from 81 non–ST-elevation ACS patients taken at admission and after 1 week and 3 and 12 months. Results: We found 14 cTn autoantibody–positive patients (21%) among the 67 cTnI-positive and none among the 14 cTnI-negative patients. Nine were autoantibody-positive at admission, and 5 became positive at 1 week. Autoantibody signals significantly increased in the 1-week and 3-month samples. At all time points, cTnI was significantly increased in the autoantibody-positive group relative to the negative group. Persistent cTnI elevations at 3 and 12 months were seen in the patients already autoantibody positive at admission. Conclusions: During ACS, patients with cTn autoantibodies have higher cTnI release and therefore larger myocardial damage than patients without autoantibodies. Their cTnI release also lasts longer, at least months. The possible prognostic impact of these observations must be evaluated in larger clinical cohorts.

scholarly journals Utility of Ischemia Modified Albumin as an Early Marker for Diagnosis of Acute Coronary Syndrome

2018 ◽  
Vol 16 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Bijaya Mishra ◽  
Sunil Pandey ◽  
Surya Raj Niraula ◽  
Bijendra Kumar Rai ◽  
Prahlad Karki ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Creatine Kinase ◽  
Diagnostic Performance ◽  
Operating Characteristic ◽  
Troponin I ◽  
Characteristic Curve ◽  
Ischemia Modified Albumin ◽  
Coronary Syndrome ◽  
Creatine Kinase Mb ◽  
St Elevation

Background: The diagnosis of acute coronary syndrome remains challenging, as cardiac troponins and creatine kinase-MB do not detect myocardial ischemia. Ischemia modified albumin is biomarker positive within 6-10 minutes following ischemic onset, where oxygen free radicals leads to reduction in binding capacity of human serum albumin to transitional metal-cobalt. The objective of this study was to compare ischemia modified albumin between acute coronary syndrome patients and healthy controls, and evaluate diagnostic performance of ischemia modified albumin compared to cardiac troponins, creatine kinase-MB and electrocardiogram in acute coronary syndrome patients.Methods: Fifty ACS patients and 50 healthy controls were enrolled in this cross-sectional study. Ischemia modified albumin was measured after addition of known amount of cobalt to human serum albumin, followed by spectrophotometric determination of unbound cobalt fraction at 470 nm using dithiothreitol as coloring agent. Independent student t-test and One-way ANOVA to compare differences of mean between groups; diagnostic sensitivity and specificity of ischemia modified albumin was determined by receiver operating characteristic curve; McNemar-test was used to assess diagnostic performance of entire test parameters, when used alone and in combinations.Results: Ischemia modified albumin was significantly higher in acute coronary syndrome patients compared to controls (0.823±0.191 vs 0.410±0.081)(p<0.001). Receiver operating characteristic curve derived optimal cutoff of 0.475 Absorbance unit had sensitivity and specificity of 92% and 82% respectively (area under curve- 0.96). However, no significant differences in mean ischemia modified albumin values between three categories of acute coronary syndrome were seen. Sensitivity of ischemia modified albumin assay (92%) was significantly higher compared to electrocardiogram (72%), cardiac troponin I (18%), and creatine kinase-MB(42%).Conclusions: Ischemia modified albumin is elevated in acute coronary syndrome patients with better diagnostic performance compared to electrocardiogram, cardiac troponin I, and creatine kinase-MB for early diagnosis, however, with limited ability to discriminate between ST-elevation myocardial infarction, non-ST-elevation myocardial infarction and unstable angina.

scholarly journals Sandwich Immunoassay for Soluble Glycoprotein VI in Patients with Symptomatic Coronary Artery Disease

2011 ◽  
Vol 57 (6) ◽  
pp. 898-904 ◽  
Author(s):  
Boris Bigalke ◽  
Oliver Pötz ◽  
Elisabeth Kremmer ◽  
Tobias Geisler ◽  
Peter Seizer ◽  
...  
Keyword(s):  
Subgroup Analysis ◽  
Troponin I ◽  
Early Stage ◽  
Surface Expression ◽  
Sandwich Immunoassay ◽  
Platelet Glycoprotein ◽  
Glycoprotein Vi ◽  
Coronary Syndrome ◽  
St Elevation ◽  
Artery Disease

BACKGROUND Platelet glycoprotein VI (pGPVI) expression is increased in acute coronary syndrome (ACS), reflecting platelet activation. There is no reliable method available to measure pGPVI. Our aim was to develop a bead-based sandwich immunoassay to measure soluble GPVI (sGPVI). METHODS Based on antibodies for sGPVI developed earlier, we established and validated a bead-based sandwich immunoassay in 2438 consecutive patients with stable angina pectoris (SAP; n = 1371), non–ST-elevation myocardial infarction (NSTEMI; n = 724), and ST-elevation MI (STEMI; n = 343). In a subgroup (n = 1011), we measured surface expression of pGPVI using flow cytometry. RESULTS The assay revealed a working range of 8–500 ng/L. Intra- and interassay imprecision was &lt;7% and &lt;14%, respectively. Patients with NSTEMI and STEMI showed significantly lower mean sGPVI concentrations than patients with SAP [mean (SD), 8.4 (3.6) μg/L and 8.6 (4.1) μg/L vs 9.8 (4.8) μg/L; P = 0.002], whereas subgroup analysis revealed significantly enhanced pGPVI in NSTEMI (n = 276) and STEMI (n = 80) patients compared with SAP (n = 655) [mean fluorescence intensity (SD), 21.2 (8.1) and 19.8 (6.8) vs 18.5 (7.7); P = 0.002 and P = 0.018]. pGPVI and sGPVI were inversely correlated (r = −0.076; P = 0.023). Area under the ROC curve was 0.716, 95% CI 0.681–0.751, for sGPVI, distinguishing patients with SAP from those with ACS, and was superior (P = 0.044) to the curve of subgroup analysis for pGPVI (0.624, 95% CI 0.586–0.662). sGPVI (P = 0.023) and pGPVI (P = 0.028) had better association with the development of ACS than troponin I (P = 0.055) in the very early stage of disease, based on logistic regression analysis. CONCLUSIONS This sandwich immunoassay reliably measures sGPVI and may help to identify patients with ACS earlier than other laboratory markers.

scholarly journals Decitabine Induced Transient Cardiomyopathy: A Case Report

2012 ◽  
Vol 6 ◽  
pp. CMO.S8598 ◽  
Author(s):  
Chitradeep De ◽  
Jaya Phookan ◽  
Valay Parikh ◽  
Tarun Nagrani ◽  
Mayur Lakhani ◽  
...  
Keyword(s):  
Case Report ◽  
Chest Pain ◽  
Troponin I ◽  
Acute Myocarditis ◽  
Coronary Vessels ◽  
Left Ventricular ◽  
Ventricular Rate ◽  
Heart Catheterization ◽  
Exertional Dyspnea ◽  
Coronary Syndrome

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.

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