scholarly journals A 23-Year-Old Man With Multisystem Inflammatory Syndrome After Mild COVID-19

2020 ◽  
Vol 8 ◽  
pp. 232470962097420
Author(s):  
Alexander C. Razavi ◽  
Jonathan L. Chang ◽  
Aimee Sutherland ◽  
Anjali Niyogi ◽  
Geraldine E. Ménard

We present the case of a young obese patient with recent COVID-19 (coronavirus disease 2019) who developed multisystem inflammatory syndrome (MIS) 1 month after spontaneous resolution. A 23-year-old African American man was admitted with a 1-week history of worsening fatigue, myalgias, headache, and dyspnea. Nasopharyngeal swab for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was negative by polymerase chain reaction; however, the patient was febrile and had leukocytosis, elevated troponin I, transaminitis, and acute kidney injury. Bedside echocardiogram showed decreased left ventricular ejection fraction (40% to 45%) and global hypokinesis in the setting of a type II non-ST segment myocardial infarction. Despite being on broad spectrum antibiotic therapy, the patient’s clinical condition continued to worsen. The patient was then empirically treated for MIS with intravenous immunoglobulin and methylprednisolone, which led to a rapid resolution of fever and laboratory abnormalities. This case highlights that MIS associated with COVID-19 may present in patients above the age of 21 years and can occur with a delayed onset after mild illness in those with no previous oxygen requirement or hospitalization during SARS-CoV-2 infection.

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Yucheng Zhong ◽  
Kunwu Yu ◽  
Xiang Wang ◽  
Xiaoya Wang ◽  
Qingwei Ji ◽  
...  

Objective.Recent studies suggest that IL-38 is associated with autoimmune diseases. Furthermore, IL-38 is expressed in human atheromatous plaque. However, the plasma levels of IL-38 in patients with ST-segment elevation myocardial infarction (STEMI) have not yet to be investigated.Methods.On admission, at 24 h, at 48 h, and at 7 days, plasma IL-38, C-reactive protein (CRP), cardiac troponin I (cTNI), and N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) levels were measured and IL-38 gene in peripheral blood mononuclear cells (PBMCs) was detected in STEMI patients.Results.The results showed that plasma IL-38 levels and IL-38 gene expression in PBMCs were significantly increased in STEMI patients compared with control group and were time dependent, peaked at 24 h. In addition, plasma IL-38 levels were dramatically reduced in patients with reperfusion treatment compared with control group. Similar results were also demonstrated with CRP, cTNI, and NT-proBNP levels. Furthermore, IL-38 levels were found to be positively correlated with CRP, cTNI, and NT-proBNP and be weakly negatively correlated with left ventricular ejection fraction (LVEF) in STEMI patients.Conclusions.The results indicate that circulating IL-38 is a potentially novel biomarker for patients with STEMI and IL-38 might be a new target for MI study.


2017 ◽  
Vol 22 (6) ◽  
pp. 538-545 ◽  
Author(s):  
Daniel Medeiros Moreira ◽  
Maria Emilia Lueneberg ◽  
Roberto Leo da Silva ◽  
Tammuz Fattah ◽  
Carlos Antonio Mascia Gottschall

Purpose: Methotrexate is an anti-inflammatory drug that has been shown to have anti-ischemic effects. Our aim was to evaluate if methotrexate could reduce infarct size in patients with ST-segment elevation myocardial infarction (STEMI). Methods: We randomly assigned patients with STEMI to receive either methotrexate or placebo. Primary outcome was infarct size determined by calculating the area under the curve (AUC) for creatine kinase (CK) release. Secondary outcomes were AUC of CK MB (CK-MB) and AUC of troponin I; peak CK, peak CK-MB, and troponin I; B-type natriuretic peptide (BNP) level, high-sensitivity C-reactive protein (hsCRP) result, and erythrocyte sedimentation rate (ESR); left ventricular ejection fraction (LVEF); thrombolysis in myocardial infarction (TIMI) frame count; Killip score; mortality and reinfarction incidence; and incidence of adverse reactions. Results: We included 84 patients. Median AUC of CK was 78 861.0 in the methotrexate group and 68 088.0 in the placebo group ( P = .10). Patients given methotrexate and placebo exhibited, respectively, median AUC for CK-MB of 9803.4 and 8037.0 ( P = .42); median AUC for troponin of 3691.1 and 2132.6 ( P = .09); peak CK of 2806.0 and 2147.0 ( P = .05); peak CK-MB of 516.0 and 462.3 ( P = .25); and peak troponin of 121.0 and 85.1 ( P = .06). At 3 months, LVEF was lower in patients who received methotrexate (49.0% ± 14.1%) than in patients given placebo (56.4% ± 10.0%; P = .01). There were no differences in hsCRP, ESR, BNP, Killip scores, TIMI frame count, reinfarction, and mortality rates. There was a higher median serum glutamic–pyruvic transaminase levels in the methotrexate group. Conclusion: Methotrexate did not reduce infarction size and worsened LVEF at 3 months ( Clinicaltrials.gov identifier NCT01741558).


Angiology ◽  
2016 ◽  
Vol 68 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Harun Kundi ◽  
Ahmet Balun ◽  
Hulya Cicekcioglu ◽  
Orhan Karayigit ◽  
Canan Topcuoglu ◽  
...  

We assessed the prognostic role of serum endocan level in patients with ST-segment elevation myocardial infarction (STEMI) and compared the results with a normal coronary angiography group. A total of 133 patients were included in the study (88 patients with STEMI and 45 patients with normal coronary arteries). The SYNTAX score was determined based on the baseline coronary angiogram. Multivariate logistic regression analysis indicated that endocan independently correlated with the presence of STEMI. Moreover, high-sensitivity C-reactive protein (hsCRP), peak troponin I, and left ventricular ejection fraction (LVEF) were found to be independently associated with STEMI. Endocan level correlated significantly with hsCRP and SYNTAX score. We analyzed the discriminatory capability of endocan level for the presence of STEMI using a receiver–operating characteristics curve. A cutoff endocan level of 1.7 (ng/mL) predicted the presence of STEMI with a sensitivity of 76.1% and specificity of 73.6%. In conclusion, a high endocan level on hospital admission is an independent predictor of a worse cardiovascular outcome and a high SYNTAX score in patients with STEMI.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Shibata ◽  
S Nohara ◽  
K Nagafuji ◽  
Y Fukumoto

Abstract Background Multiple myeloma (MM) is a plasma cell dyscrasia accounting for approximately 13% of hematologic malignancies. Patients with MM have an increased risk of cardiovascular adverse events (CAEs) due to disease burden and/or anti-myeloma treatment-related risk factors. However, little is known about the incidence of cardiovascular toxicity of patients with MM. Methods We analyzed 42 consecutive patients (Male/Female 22/20, age 67±10 years old) who received anti-MM therapies between October 2016 and September 2018 from our University Cardio-REnal Oncology (CREO) registry. We examined the incidence of CAEs through January 2019 including congestive heart failure and cardiomyopathy (CHF/CM), ischemic cardiac event, newly symptomatic arrhythmias included atrial fibrillation or flutter requiring treatment, and venous thromboembolism (VTE). Results Within the 408-day median follow-up period (range 15–844 days), CAEs occurred in 23.8% (n=10); CHF/CM in 11.9%, newly diagnosed atrial fibrillation in 4.8%, VTE in 4.8%, vasospastic angina in 2.4%, and death in 28.6%. There were no significant differences between CAEs group and non-CAEs group in terms of sex, body mass index (BMI), incidence of hypertension, ischemic heart disease, prior history of heart failure, cardiovascular medications, left ventricular ejection fraction, serum high-sensitivity troponin-I, estimated glomerular filtration rate, blood urea nitrogen and N-terminal pro-brain natriuretic peptide levels at the time of enrollment. The use of various types of proteasome inhibitors and immunomodulatory drugs were not associated with the increased risk of CAEs. By multivariate analysis, a history of prior anti-myeloma therapies was identified as an independent risk factor for CAEs. Conclusion CAEs were significantly associated with the recurrent MM in Japanese MM patients.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Daniel M Moreira ◽  
Roberto L da Silva ◽  
Maria E Lueneberg ◽  
Tammuz Fattah ◽  
Carlos A Gottschall

Introduction: Acute myocardial infarction provokes inflammatory activation. Methotrexate is one drug that has been shown to have anti-ischemic effects in experimental studies. Hypothesis: Methotrexate could reduce inflammation and the ischemia area in acute myocardial infarction Methods: We randomly assigned patients with myocardial infarction with ST-segment elevation to receive either methotrexate (0.05 mg/kg bolus followed by 0.05 mg/kg/h for 6 h) or matching placebo (riboflavin sodium phosphate 0.1%, in order to preserve double-blinding) at a ratio of 1:1. Patients in both groups were given a 5mg single dose of folic acid. The primary endpoint was infarct size, determined by the area under the curve (AUC) for creatine kinase (CK) release. Secondary endpoints were AUC of CK-MB and AUC of troponin I; peak CK, peak CK-MB and troponin I; B-type natriuretic peptide (BNP) level, high-sensitivity C-reactive protein (hsCRP) result and erythrocyte sedimentation rate (ESR); left ventricular ejection fraction (LVEF); TIMI frame count; Killip score; mortality and reinfarction incidence. The safety endpoint was the incidence of adverse reactions. Results: We included 84 patients. The AUC of CK was 78,861.00 in the methotrexate group and 68,088.00 in the placebo group (P=0.10). Patients given methotrexate and placebo exhibited, respectively, AUC for CK-MB of 9,803.40 and 8,037.00 (P=0.42); AUC for troponin I of 3,691.11 and 2,132.63 (P=0.09); peak CK of 2,806.00 and 2,147.00 (P=0.05), peak CK-MB of 516.00 and 462.25 (P=0.25) and peak troponin I of 121.00 and 85.05 (P=0,06). At 3 months, LVEF was lower in patients who received methotrexate (48.97±14.09%) than in patients given placebo (56.37±9.97%) (P=0.01). There were no differences in hsCRP, ESR, BNP, Killip scores or TIMI frame count. There were also no differences in reinfarction or mortality rates or in incidence of side effects, with the exception of higher median serum glutamic-pyruvic transaminase (SGPT) levels in the methotrexate group. Conclusions: Methotrexate did not reduce infarction size and worsened LVEF at 3 months.


2020 ◽  
Vol 72 (1) ◽  
Author(s):  
Ahmed Ayuna ◽  
Nik Abidin

Abstract Background Anthracycline-induced cardiotoxicity has been classified based on its onset into acute, early, and late. It may have a significant burden on the quality and quantity of life of those exposed to this class of medication. Currently, there are several ongoing debates on the role of different measures in the primary prevention of cardiotoxicity in cancer survivors. Our article aims to focus on the role of neurohormonal blockers in the primary prevention of anthracycline-induced cardiotoxicity, whether it is acute, early, or late onset. Main body of the abstract PubMed and Google Scholar database were searched for the relevant articles; we reviewed and appraised 15 RCTs, and we found that angiotensin-converting enzyme inhibitors (ACEI) and B-blockers were the most commonly used agents. Angiotensin II receptor blockers (ARBs) and mineralocorticoid receptor antagonists (MRAs) were used in a few other trials. The follow-up period was on the range of 1–156 weeks (mode 26 weeks). Left ventricular ejection fraction (LVEF), left ventricular diameters, and diastolic function were assessed by either echocardiogram or occasionally by cardiac magnetic resonance imaging (MRI). The occurrence of myocardial injury was assessed by troponin I. It was obvious that neurohormonal blockers reduced the occurrence of LVEF and myocardial injury in 14/15 RCTs. Short conclusion Beta-blockers, especially carvedilol and ACEI, especially enalapril, should be considered for the primary prevention of acute- and early-onset cardiotoxicity. ARB and MRA are suitable alternatives when patients are intolerant to ACE-I and B-blockers. We recommend further studies to explore and establish the role of neurohormonal blockers in the primary prevention of the acute-, early-, and late-onset cardiotoxicity.


2021 ◽  
Author(s):  
Julian Müller ◽  
Michael Behnes ◽  
Tobias Schupp ◽  
Dominik Ellguth ◽  
Gabriel Taton ◽  
...  

AbstractBoth acute myocardial infarction complicated by ventricular tachyarrhythmias (AMI–VTA) and electrical storm (ES) represent life-threatening clinical conditions. However, a direct comparison of both sub-groups regarding prognostic endpoints has never been investigated. All consecutive implantable cardioverter-defibrillator (ICD) recipients were included retrospectively from 2002 to 2016. Patients with ES apart from AMI (ES) were compared to patients with AMI accompanied by ventricular tachyarrhythmias (AMI–VTA). The primary endpoint was all-cause mortality at 3 years, secondary endpoints were in-hospital mortality, rehospitalization rates and major adverse cardiac event (MACE) at 3 years. A total of 198 consecutive ICD recipients were included (AMI–VTA: 56%; ST-segment elevation myocardial infarction (STEMI): 22%; non-ST-segment myocardial infarction (NSTEMI) 78%; ES: 44%). ES patients were older and had higher rates of severely reduced left ventricular ejection fraction (LVEF) < 35%. ES was associated with increased all-cause mortality at 3 years (37% vs. 19%; p = 0.001; hazard ratio [HR] = 2.242; 95% CI 2.291–3.894; p = 0.004) and with increased risk of first cardiac rehospitalization (44% vs. 12%; p = 0.001; HR = 4.694; 95% CI 2.498–8.823; p = 0.001). This worse prognosis of ES compared to AMI–VTA was still evident after multivariable adjustment (long-term all-cause mortality: HR = 2.504; 95% CI 1.093–5.739; p = 0.030; first cardiac rehospitalization: HR = 2.887; 95% CI 1.240–6.720; p = 0.014). In contrast, the rates of MACE (40% vs. 32%; p = 0.326) were comparable in both groups. At long-term follow-up of 3 years, ES was associated with higher rates of all-cause mortality and rehospitalization compared to patients with AMI–VTA.


2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
E Marcusohn ◽  
O Kobo ◽  
M Postnikov ◽  
D Epstein ◽  
Y Agmon ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Background  The diagnosis of atrial fibrillation (AF) induced cardiomyopathy can be challenging. It relies on ruling out other causes of dilated cardiomyopathy, upon recovery of left ventricular ejection fraction (LVEF) following return to sinus rhythm (SR). Aim  The aim of this study was to identify clinical and echocardiographic predictors for developing new dilated cardiomyopathy in patients with AF or atrial flutter (AFL). Methods  This is a retrospective study conducted in a large tertiary care center. Patients that suffered deterioration of LVEF under 50% during AF demonstrated by pre-cardioversion trans-esophageal echocardiography (TEE) were compared to those with preserved LV function during AF. All patients had documented preserved LVEF at baseline (EF &gt;50%) while in SR. Patients with a previous history of reduced LVEF during SR were excluded. Results From a total of 482 patients included in the final analysis, 80 (17%) patients had reduced LV function and 402 (83%) had preserved LV function during the pre-cardioversion TEE. Patients with reduced LVEF were more likely to be male and with a more rapid ventricular response during AF/AFL. A history of prosthetic valves was also identified as a risk factor for reduced LVEF. Patients with reduced LVEF also had higher incidence of TR and RV dysfunction. Conclusion In "real world" experience, male patients with rapid ventricular response during AF or AFL are more prone to LVEF reduction. Patients with prosthetic valves are also at risk for LVEF reduction during AF/AFL. Lastly, TR and RV dysfunction may indicate relatively long-standing AF with an associated reduction in LVEF.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shuai Meng ◽  
Yong Zhu ◽  
Kesen Liu ◽  
Ruofei Jia ◽  
Jing Nan ◽  
...  

Abstract Background Left ventricular negative remodelling after ST-segment elevation myocardial infarction (STEMI) is considered as the major cause for the poor prognosis. But the predisposing factors and potential mechanisms of left ventricular negative remodelling after STEMI remain not fully understood. The present research mainly assessed the association between the stress hyperglycaemia ratio (SHR) and left ventricular negative remodelling. Methods We recruited 127 first-time, anterior, and acute STEMI patients in the present study. All enrolled patients were divided into 2 subgroups equally according to the median value of SHR level (1.191). Echocardiography was conducted within 24 h after admission and 6 months post-STEMI to measure left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), and left ventricular end-systolic diameter (LVESD). Changes in echocardiography parameters (δLVEF, δLVEDD, δLVESD) were calculated as LVEF, LVEDD, and LVESD at 6 months after infarction minus baseline LVEF, LVEDD and LVESD, respectively. Results In the present study, the mean SHR was 1.22 ± 0.25 and there was significant difference in SHR between the 2 subgroups (1.05 (0.95, 1.11) vs 1.39 (1.28, 1.50), p < 0.0001). The global LVEF at 6 months post-STEMI was significantly higher in the low SHR group than the high SHR group (59.37 ± 7.33 vs 54.03 ± 9.64, p  = 0.001). Additionally, the global LVEDD (49.84 ± 5.10 vs 51.81 ± 5.60, p  = 0.040) and LVESD (33.27 ± 5.03 vs 35.38 ± 6.05, p  = 0.035) at 6 months after STEMI were lower in the low SHR group. Most importantly, after adjusting through multivariable linear regression analysis, SHR remained associated with δLVEF (beta = −9.825, 95% CI −15.168 to −4.481, p  < 0.0001), δLVEDD (beta = 4.879, 95% CI 1.725 to 8.069, p  = 0.003), and δLVESD (beta = 5.079, 95% CI 1.421 to 8.738, p  = 0.007). Conclusions In the present research, we demonstrated for the first time that SHR is significantly correlated with left ventricular negative remodelling after STEMI.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Osokina ◽  
V.N Karetnikova ◽  
O.M Polikutina ◽  
Y.S Slepynina ◽  
T.P Artemova ◽  
...  

Abstract Objective To investigate the correlation between Procollagen I C-Terminal Propeptide (PICP), Procollagen III N-Terminal Propeptide (PIIINP), indices of echocardiography and anamnestic data in patients with ST segment elevation myocardial infarction (STEMI) and preserved myocardial contractility. Materials and methods 60 men and 23 women diagnosed with STEMI were examined. Echocardiographic studies were performed using SONOS 2500 Cardiac – Vascular Ultrasound (Hewlett Packard, USA). Myocardial contractility was considered to be preserved with left ventricular ejection fraction (LVEF) ≥50%. In addition to standard indices of echocardiography, mitral flow propagation velocity (FPV) was evaluated to diagnose diastolic dysfunction. Coronary angiography was performed using INNOVA 3100 Cardiovascular Imaging System (USA). All patients, during the first twelve hours of the disease, underwent percutaneous coronary intervention (PCI) with stenting of the occluded culprit infarct-related artery. On the 1st and 12th days of hospitalization, the concentrations of PICP and PIIINP were determined for all patients by enzyme-linked immunosorbent assay (ELISA) using laboratory BCM Diagnostics kits (USA). All patients at the hospital received standard therapy. Results The following marker values were obtained: 1st day: PICP 609 (583; 635) ng/ml, PIIINP 26 (18.9; 34.9) ng/ml; 12th day: PICP 588 (580; 561) ng/ml, PIIINP 24.2 (18.6; 30.3) ng/ml. The following significant correlations were revealed: PICP 1st day / isovolumic contraction time – IVCT (m/s) 12th day, r=−0.68, p=0.042; PICP 1st day / Tei Index 12th day, r=−0.72, p=0.028; PICP 1st day / diastolic rigidity 12th day, r=−0.74, p=0.021; PIIINP 1st day/age, r=0.55, p=0.016; PIIINP 1st day/ body mass index (BMI), r=−0.59, p=0.009; PIIINP 1st day / E (cm/s) 1st day, r=0.72, p=0.018; PIIINP 1st day / Em /FPV 1st day, r=0.78, p=0.007; PIIINP 12th day / Em / FPV 1st day, r=0.65, p=0.041; PIIINP 12th day / E (cm/s) 1st day, r=0.67, p=0.033; PIIINP 12th day / E / Em) 12th day, r=0.70, p=0.023; PIIINP 12th day / Em/FPV 12th day, r=0.73, p=0.014. Conclusions The data obtained indicates the correlation between serum markers of myocardial fibrosis and the indices of echocardiography, as well as age. We conclude that, all the markers listed above, are able to represent myocardial remodeling in patients with STEMI. Funding Acknowledgement Type of funding source: None


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