Clinical and Genetic Characteristics of Thymoma Patients With Autoimmune Hepatitis and Myocarditis

BackgroundOur study investigated a special series of thymoma with autoimmune hepatitis and myocarditis and tried to reveal the gene expression profiles of this series of thymoma.MethodsFrom 2011 to 2019, a total of 13 special thymoma patients presented with autoimmune hepatitis and myocarditis, accounting for about 1.26% of thymoma patients undergoing surgery in Beijing TongRen Hospital. Clinical data were retrospectively collected. All samples were harvested during surgical procedures, and analyzed to identify changes in gene expression using the CapitalBio mRNA microarray analysis, the Whole exome sequencing analysis (WES), qPCR and immunohistochemistry (IHC) tools.ResultsAfter surgery, patient symptoms were relieved gradually. Levels of lactate dehydrogenase (LDH), creatine kinase MB (CK-MB), aspartate transaminase (AST), and alanine amiotransferase (ALT) increased to some extent within 1 to 3 months after surgery, and fluctuated, and then, gradually decreased close to normal within 6 months after surgery. Enrichment analysis of Kyoto Genome and Genome Encyclopedia (KEGG) pathway was performed and enrichment results were visualized. It indicated that gene expression of 5 signaling pathways, including cell cycle and p53 signaling pathway, were generally abnormal. P53 expression was up-regulated in all tumor tissues. However, IHC and qPCR analysis showed that there was no significant difference in p21 expression between normal and tumor tissue. Results of WES showed that only one driver gene-MDM4 amplified 4 fold in 53.2% thymoma cells. Further qPCR and IHC analysis confirmed the up-regulation of the expression of p53 and mdm4 in 13 thymoma patients with autoimmune hepatitis and myocarditis.ConclusionOur study reveals the clinical and genetic characteristics of thymoma patients with autoimmune hepatitis and myocarditis. For this special category of thymoma, the up-regulation of p53 and mdm4 plays an important role in the occurrence of thymoma and autoimmune hepatitis/myocarditis.

Perbandingan Oedema Paru Akut Yang Disebabkan Oleh Tingkat Kardiogenik dan Non Kardiogenik Dengan Mortalitas Dan Morbiditas Pasien

Latar Belakang: Prognosis jangka panjang edema paru akut (APE) tetap tidak jelas. Metode dan Hasil: Kami mengevaluasi data demografis, ekokardiografi, dan angiographic dari 806 pasien berturut-turut dengan APE dengan (CAD) dan tanpa penyakit arteri koroner (non-CAD) yang diterima dari tahun 2000 hingga 2010. Perbedaan antara rumah sakit dan kematian jangka panjang dan prediktornya juga dinilai. Pasien CAD (n = 638) lebih tua dan memiliki insiden diabetes dan penyakit vaskular perifer yang lebih tinggi daripada non-CAD (n = 168), dan fraksi ejeksi yang lebih rendah. Kematian di rumah sakit serupa pada kedua kelompok (26,5% vs 31,5%; P = 0,169) tetapi kekambuhan KERA lebih tinggi pada pasien CAD (17,3% vs 6,5%; P<0.001). Usia, masuk tekanan darah sistolik, kekambuhan APE, dan kebutuhan inotropics atau intubasi endotrakcheal adalah prediktor independen utama kematian di rumah sakit. Sebaliknya, kematian secara keseluruhan (70,0% vs 57,1%; P = 0,002) dan penerimaan kembali untuk gagal jantung nonfatal setelah tindak lanjut 45 bulan (10-140; 17,3% vs 7,6%; P = 0,009) lebih tinggi pada CAD daripada pasien non-CAD. Usia, penyakit vaskular perifer, dan puncak creatine kinase MB selama rawat inap indeks, tetapi bukan fraksi ejeksi, adalah prediktor independen utama dari kematian secara keseluruhan, sedangkan revaskularisasi koroner atau operasi valvular bersifat protektif. Intervensi ini sebagian besar dilakukan selama indeks rawat inap (294 dari 307; 96%) dan tidak pasien yang diintervensi menunjukkan profil risiko yang lebih tinggi. Kesimpulan: Kematian jangka panjang di APE tinggi dan lebih tinggi pada CAD daripada pada pasien non-CAD. Mengingat prediktor kematian di rumah sakit dan jangka panjang yang berbeda di sini dijelaskan, yang tidak selalu melibatkan fungsi sistolik, dapat dibayangkan bahwa program intervensi yang lebih agresif dapat meningkatkan kelangsungan hidup pada pasien berisiko tinggi.

Case Report: Abnormal ECG in a Patient With Acute Pancreatitis

Background: Both acute pancreatitis and acute myocardial infarction (AMI) are rapidly progressive and frequently fatal diseases that can be interrelated and lead to a vicious cycle for further problems. The concomitant occurrence of AMI and acute pancreatitis is rare but critical, and efficient diagnosis and treatment of such patients are challenging.Case Summary: We reported an uncommon case of abnormal ECG findings in a 63-year-old woman with acute pancreatitis. The patient exhibited increased biomarkers of myocardial injury, such as creatine kinase-MB (CK-MB) and troponin T, as well as ST segment elevation in inferior leads II, III, and aVF. Both of these have been previously observed in patients with acute abdomen in the absence of ST-segment elevation myocardial infarction (STEMI), including pancreatitis. In addition, lacking complaints of chest pain or tightness was also supportive of this idea. Echocardiography indicated abnormalities in the functioning of the left inferior posterior wall segments and decreased overall systolic function of the left ventricle with a 51% ejection fraction. Eventually, AMI was diagnosed after coronary computed tomography angiography (CCTA) showing critical stenosis of the right coronary artery and left anterior descending artery segments. The patient was urgently transferred to intensive care unit and was treated with anticoagulation, antiplatelet aggregation, lipid-lowering and other palliative drugs.Conclusion: Concomitant acute pancreatitis and AMI are often considered to be critical conditions with a poor prognosis. Therefore, it is important to rapidly identify this condition and consider transferring patients for multidisciplinary supportive care.

Laboratory features of cardiovascular injury in COVID-19 and other acute respiratory viral infections

The article presents data from a study of specific cardiac markers in patients with acute respiratory viral infection (ARVI) or coronavirus disease 2019 (COVID-19). COVID-19 caused by severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) is characterized by cardiovascular injury. However, with other ARVIs, the prevalence of heart involvement is also high and, according to the literature data, is about 20%. At the same time, laboratory characteristics of these lesions have significant differences in ARVI and COVID-19, which necessitates different approaches to therapy.Aim. To determine the most significant markers for the diagnosis of cardiovascular involvement in patients with COVID-19.Material and methods. A total of 60 patients were included in the study: main group (n=30), COVID-19 was laboratory confirmed; comparison group (n=30), other ARVI pathogens were verified. The groups were completely comparable in sex, age and severity of disease course. The average values of troponin, creatine kinase MB, N-terminal pro-brain natriuretic peptide (NT-proBNP) and D-dimer were compared in patients of both groups in the acute disease phase, corresponding from 1 to 8 days from the symptoms’ onset. Data analysis was performed using a two-sided independent samples t-test using SPSS Statistics version 23.Results. The higher levels of troponin-I and D-dimer were significantly more common in the main group. The mean value of creatine kinase MB did not exceed the upper limits of reference values. There were no significant differences in NTproBnP levels between the groups. At the same time, in both groups, its level significantly exceeded the age reference values.Conclusion. The most effective markers of cardiovascular complications in COVID-19 patients should be considered troponin-I, D-dimer and NT-proBNP. Early diagnosis and laboratory monitoring in dynamics is important for the timely detection of cardiac pathology and alteration of therapy regimen.

Regulatory T Cell as Predictor of Intramyocardial Hemorrhage in STEMI Patients After Primary PCI

Background: Intramyocardial hemorrhage (IMH) is a result of ischemia-reperfusion injury in ST-segment elevation myocardial infarction(STEMI) after primary percutaneous coronary intervention (PPCI). Despite patients with IMH show poorer prognoses, studies investigating predictors of IMH occurrence are scarce. This study firstly investigated the effectiveness of regulatory T cell (Treg), peak value of Creatine Kinase MB (pCKMB), high-sensitivity C-reactive protein (hsCRP), and left ventricular end-systolic diameter (LVESD) as predictors for IMH in STEMI patients received PPCI.Methods: A prospective observational cohort study was performed in STEMI patients with cardiac magnetic resonance examination 6.3±2.3 days after PPCI. Logistic regression analysis was used to screen the risk factors for IMH. The predictive ability of risk factors for IMH were determined by Receiver operating characteristic curves, net reclassification improvement (NRI), integrated discrimination improvement (IDI) and C-index.Results: Of the 182 patients, 80 patients (44.0%) developed IMH. On multivariable analysis, all 4 biomarkers were independent predictors of IMH [odds radio (OR) and 95% confidence interval (CI): 0.350(0.202-0.606) for Treg, 1.004(1.001-1.006) for pCKMB, 1.060(1.022-1.100) for hsCRP, and 3.329(1.346-8.236) for LVESD]. After propensity score matching, the biomarkers individually and together significantly predicted IMH with areas under the curve of 0.750 for Treg, 0.721 for pCKMB, 0.656 for hsCRP, 0.633 for LVESD, and 0.821 for the integrated 4-marker panel. The addition of integrated 4-marker panel to a baseline risk model had an incremental effect on the predictive value for IMH [NRI: 0.197 (0.039 to 0.356); IDI: 0.200 (0.142 to 0.259); C-index: 0.806 (0.744 to 0.869), all p < 0.05].Conclusions: Treg individually or in combination with pCKMB, hsCRP, and LVESD can effectively predict the existence of IMH in STEMI patients received PPCI.Name of the registry: ClinicalTrials. govTrial registration number: NCT03939338Date of registration: 6 May 2019URL of trial registry record: https://clinicaltrials.gov/ct2/show/NCT03939338?term=03939338&cntry=CN&draw=2&rank=1

Transient Myocardial Ischemia in a Case Post Intra-Muscular Adrenaline

Background: Anaphylaxis is a medical emergency and requires immediate medical attention. Kounis syndrome is myocardial infarction or injury occurring in the setting of anaphylaxis and can also be due to the effects of epinephrine. Adrenaline is a common drug in the management of anaphylaxis but the electrocardiographic consequences of its administration post an attack are seldomly seen. Vasospasm is generally the cause for myocardial injury in an acute setting following the administration of epinephrine. Case Presentation: A 21-year- old female developed sudden onset breathlessness and giddiness post vaccination with the oxford –AstraZeneca COVID -19 vaccine. She was administered 0.5 ml adrenaline (1:1000) intramuscularly on the lateral aspect of the left thigh, following which she complained of chest tightness and palpitations. This was accompanied by hypotension and global ST segment depression on her Electrocardiogram. The second electrocardiogram, done after 30 minutes showed a relative resolution in ST segment depressions with sinus rhythm in the one done at 16:00 hours. Creatine Kinase- MB and Troponin I were within normal limits and the patient experienced symptomatic improvement with normalization of blood pressure post fluid challenge. Conclusion: This case report highlights the case of a young female with no comorbidities who developed transient myocardial ischemia after administration of intramuscular adrenalin in therapeutic dose in view of an anaphylactic reaction. The probable action is alpha mediated coronary vasospasm. The potential adverse effects in an acute setting are hence outlined in this case report without discouraging its use given the potential benefits outweigh the risks.

Utility of S100A12 as an Early Biomarker in Patients With ST-Segment Elevation Myocardial Infarction

Importance: S100A12 is a calcium binding protein which is involved in inflammation and progression of atherosclerosis.Objective: We sought to investigate the utility of S100A12 as a biomarker for the early diagnosis and prognostication of patients presenting with ST-segment elevation myocardial infarction (STEMI).Design, Setting, and Participants: S100A12 was measured in 1023 patients presenting to the emergency department with acute chest pain between June 2012 and November 2015. An independent cohort of 398 patients enrolled at 3 different hospitals served as a validation cohort.Main Outcomes and Measures: The primary clinical endpoint of interest was major adverse cardiac and cerebral events (MACCE) defined as a composite of all-cause death, MI, stroke, or hospitalization for heart failure.Results: A total of 438/1023 patients (42.8%) in the diagnosis cohort were adjudicated as STEMI, among whom plasma S100A12 levels increased within 30 min and peaked 1–2 h after symptom onset. Compared with high-sensitivity cardiac troponin T and creatine kinase-MB isoenzyme, S100A12 more accurately identified STEMI, especially within the first 2 h after symptom onset (area under the curve 0.963 compared with 0.860 for hscTnT and 0.711 for CK-MB, both P &lt; 0.05). These results were consistent in the 243-patient validation cohort. The 1-year rate of MACCE was greatest in patients in the highest peak S100A12 tertile, intermediate in the middle tertile and least in the lowest tertile (9.3 vs. 5.7 vs. 3.0% respectively, Ptrend = 0.0006). By multivariable analysis the peak plasma concentration of S100A12 was an independent predictor of MACCE within 1 year after STEMI (HR, 1.001, 95%CI, 1.000–1.002; P = 0.0104).Conclusions and Relevance: S100A12 rapidly identified patients with STEMI, more accurately than other cardiac biomarkers, especially within the first 2 h after symptom onset. The peak plasma S100A12 level was a strong predictor of 1-year prognosis after STEMI.

Frequency of Cardiovascular Complications and Its Association with Prognosis of COVID-19 Patients

Coronavirus disease 2019 (COVID-19) may lead to acute respiratory disease; cardiovascular, gastrointestinal, and coagulation complications; and even death. One of the major complications is cardiovascular disorders, including arrhythmias, myocarditis, pericarditis, and acute coronary artery disease. The aim of this study was to evaluate the frequency of cardiovascular complications and to determine its association with the prognosis of COVID-19 patients. In a prospective analytic study, 137 hospitalized COVID-19 patients were enrolled. During hospitalization, an electrocardiogram (ECG) was performed every other day, and laboratory tests such as cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) were done 0, 6, and 12 hours after admission. These tests were repeated for patients with chest pain or ECG changes. Patients were categorized into three groups (improved, complicated, and expired patients) and assessed for the rate and type of arrhythmias, cardiac complications, lab tests, and outcomes of treatments. There was no significant relationship among the three groups related to primary arrhythmia and arrhythmias during treatment. The most common arrhythmia during hospitalization and after treatment was ST-T fragment changes. There was a significant age difference between the three groups ( P = 0.001 ). There was a significant difference among the three groups for some underlying diseases, including diabetes mellitus ( P = 0.003 ) and hyperlipidemia ( P = 0.004 ). In our study, different types of arrhythmias had no association with patients’ outcomes but age over 60 years, diabetes mellitus, and hyperlipidemia played an important role in the prognosis of COVID-19 cases.

The Value of Admission Serological Indicators for Predicting 28-Day Mortality in Intensive Care Patients With Acute Heart Failure: Construction and Validation of a Nomogram

Background: Acute heart failure (AHF) is a severe clinical syndrome characterized as rapid onset or worsening of symptoms of chronic heart failure (CHF). Risk stratification for patients with AHF in the intensive care unit (ICU) may help clinicians to predict the 28-day mortality risk in this subpopulation and further raise the quality of care.Methods: We retrospectively reviewed and analyzed the demographic characteristics and serological indicators of patients with AHF in the Medical Information Mart for Intensive Care III (MIMIC III) (version 1.4) between June 2001 and October 2012 and our medical center between January 2019 and April 2021. The chi-squared test and the Fisher's exact test were used for comparison of qualitative variables among the AHF death group and non-death group. The clinical variables were selected by using the least absolute shrinkage and selection operator (LASSO) regression. A clinical nomogram for predicting the 28-day mortality was constructed based on the multivariate Cox proportional hazard regression analysis and further validated by the internal and external cohorts.Results: Age &gt; 65 years [hazard ratio (HR) = 2.47], the high Sequential Organ Failure Assessment (SOFA) score (≥3 and ≤8, HR = 2.21; ≥9 and ≤20, HR = 3.29), lactic acid (Lac) (&gt;2 mmol/l, HR = 1.40), bicarbonate (HCO3-) (&gt;28 mmol/l, HR = 1.59), blood urea nitrogen (BUN) (&gt;21 mg/dl, HR = 1.75), albumin (&lt;3.5 g/dl, HR = 2.02), troponin T (TnT) (&gt;0.04 ng/ml, HR = 4.02), and creatine kinase-MB (CK-MB) (&gt;5 ng/ml, HR = 1.64) were the independent risk factors for predicting 28-day mortality of intensive care patients with AHF (p &lt; 0.05). The novel nomogram was developed and validated with a promising C-index of 0.814 (95% CI: 0.754–0.882), 0.820 (95% CI: 0.721–0.897), and 0.828 (95% CI: 0.743–0.917), respectively.Conclusion: This study provides a new insight in early predicting the risk of 28-day mortality in intensive care patients with AHF. The age, the SOFA score, and serum TnT level are the leading three predictors in evaluating the short-term outcome of intensive care patients with AHF. Based on the nomogram, clinicians could better stratify patients with AHF at high risk and make adequate treatment plans.

First manifestation and evolution of early left ventricular dysfunction in children with Duchenne muscular dystrophy

Background: Standard pediatric cardiology examinations and echocardiography fail to discover when the cardiomyopathy will occur in patient with Duchenne muscular dystrophy (DMD). Noninvasive markers are needed to fill this gap. Material and methods: This cohort study included a total number of 30 children (21 children (70%) with DMD and 9 (30%) healthy children. Blood samples were used for biochemical (level of creatine kinase, creatine kinase-MB, lactate dehydrogenase) and miRNA (presence of miR133a 3p, miR133b 3p, miR206 3p, miR208a 3p, miR208b 3p) analysis. All patients underwent partial conventional echocardiography ECOCG and Speckle Tracking. Results: The children in the working group presented compared to healthy children: FCC values increased by 15 (71%) vs 2 (22%), high levels of CK, CK-MB, LDH, which is characteristic for the disease and reflects its stage. Also, there is a decrease in systolic function indicators in the working group: mean FE 59 ± 3.8 %, and GLS: -16.2 ± 3.1%. MiRNA analyses confirmed the presence of miR133a 3p, miR133b 3p, miR206 3p, miR208a 3p, miR208b 3p in both working and control group. Conclusions: For the first time in the Republic of Moldova, we developed and adapted protocols for RNA extraction from human blood, performing screening of specific miRNA in the serum of patients with DMD and healthy children. Also, altered LV strain notwithstanding a normal or mildly modified LVEF represents an essential viewpoint for prospective pediatric drug trials in DMD-related cardiomyopathy prevention.