FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4207010309> ?p ?o ?g. }

• W4207010309 abstract "HomeCirculation: Cardiovascular ImagingVol. 13, No. 7COVID-19–Associated Stress (Takotsubo) Cardiomyopathy Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessCase ReportPDF/EPUBCOVID-19–Associated Stress (Takotsubo) Cardiomyopathy Connie W. Tsao, Jordan B. Strom, James D. Chang and Warren J. Manning Connie W. TsaoConnie W. Tsao Connie W. Tsao, MD, MPH, Cardiovascular Division, Beth Israel Deaconess Medical Center, 330 Brookline Ave, RW-453, Boston, MA 02215. Email E-mail Address: [email protected] Department of Medicine, Cardiovascular Division (C.W.T., J.B.S., J.D.C., W.J.M.), Beth Israel Deaconess Medical Center, Boston, MA. Harvard Medical School, Boston, MA (C.W.T., J.B.S., J.D.C., W.J.M.). Search for more papers by this author , Jordan B. StromJordan B. Strom Department of Medicine, Cardiovascular Division (C.W.T., J.B.S., J.D.C., W.J.M.), Beth Israel Deaconess Medical Center, Boston, MA. Richard A. and Susan F. Smith Center for Outcomes Research in Cardiology (J.B.S.), Beth Israel Deaconess Medical Center, Boston, MA. Harvard Medical School, Boston, MA (C.W.T., J.B.S., J.D.C., W.J.M.). Search for more papers by this author , James D. ChangJames D. Chang Department of Medicine, Cardiovascular Division (C.W.T., J.B.S., J.D.C., W.J.M.), Beth Israel Deaconess Medical Center, Boston, MA. Harvard Medical School, Boston, MA (C.W.T., J.B.S., J.D.C., W.J.M.). Search for more papers by this author and Warren J. ManningWarren J. Manning Department of Medicine, Cardiovascular Division (C.W.T., J.B.S., J.D.C., W.J.M.), Beth Israel Deaconess Medical Center, Boston, MA. Department of Radiology (W.J.M.), Beth Israel Deaconess Medical Center, Boston, MA. Harvard Medical School, Boston, MA (C.W.T., J.B.S., J.D.C., W.J.M.). Search for more papers by this author Originally published15 Jul 2020https://doi.org/10.1161/CIRCIMAGING.120.011222Circulation: Cardiovascular Imaging. 2020;13:e011222Coronavirus disease 2019 (COVID-19) infection has resulted in an unprecedented number of critical care hospitalizations and substantial mortality across the world. Emerging evidence suggests that severe acute respiratory syndrome coronavirus 2, responsible for the pandemic COVID-19, causes cardiac injury reflected by elevated biomarkers, hemodynamic instability, and cardiomyopathy.1 Cardiovascular dysfunction is hypothesized to relate to microvascular dysfunction, myocarditis, myocardial ischemia, or toxicity from elevated cytokines. A condition with cross-similarities, stress (Takotsubo) cardiomyopathy is a reversible but morbid condition thought to be triggered by physical, psychological, or metabolic stress, though dysfunction of the cardiac endothelium and microvasculature has been implicated.2 Stress cardiomyopathy associated with COVID-19 has not been well described. Here, we describe and discuss the case of a patient without a history of cardiovascular disease who developed and recovered from clinical stress cardiomyopathy in the setting of severe COVID-19 infection.A 59-year-old woman with obesity (body mass index, 33 kg/m2) but otherwise healthy presented to the emergency department of our tertiary care hospital with fevers, chills, fatigue, myalgias, and cough. Within 24 hours, she had an increasing oxygen requirement, necessitating transfer to the intensive care unit and mechanical ventilation. Chest radiograph demonstrated diffuse bilateral alveolar infiltrates without cephalization or prominent pulmonary vascular markings (Figure 1A). Severe acute respiratory syndrome coronavirus 2 reverse transcriptase polymerase chain reaction test performed on her nasopharyngeal swab specimen returned positive. Inflammatory markers were elevated with C-reactive protein, >300 mg/L (normal, ≤5 mg/L); D-dimer, 2184 ng/mL (normal, ≤500 ng/mL); ferritin, 2033 ng/mL (normal, ≤150 ng/mL); and IL (interleukin)-6, 724.38 pg/mL (normal, <5 pg/mL). On hospital day 3, the troponin T and creatine kinase myocardial band, normal on admission (<0.01 and 2 ng/mL, respectively), rose to 1.0 and 94 ng/mL. Twelve-lead ECG demonstrated slight ST-segment elevations diffusely with nonspecific T-wave inversions (Figure 1B). Transthoracic echocardiogram was performed for evaluation of left ventricular function in the setting of elevated cardiac biomarkers and abnormal ECG (Vivid S70 echocardiograph, analyzed using EchoPAC software, ViewPoint 6.11; General Electric Healthcare, Waukesha, WI). Transthoracic echocardiogram demonstrated severe hypokinesis of the mid-left ventricular cavity, with normal-to-hyperdynamic contractility of basal and apical left ventricular segments and a moderately reduced biplane ejection fraction of 36% (Figure 1C and 1D; Movies I through VII in the Data Supplement). The patient’s hospital course was notable for profound hypoxemic respiratory failure and vasodilatory shock requiring intravenous norepinephrine and vasopressin administration. Additionally, she was noted to have multiple episodes of monomorphic ventricular tachycardia responding to lidocaine. After several days of supportive care and receipt of sarilumab, the patient’s hemodynamic and respiratory status gradually improved. She no longer required vasopressor agents and was able to be extubated after 15 days of ventilator support. During this time, her cardiac and inflammatory biomarkers peaked and declined. On the day of extubation, repeat chest radiograph showed stable to slightly decreased bilateral airspace opacities and consolidations (Figure 2A), and ECG demonstrated resolution of diffuse ST-segment and T-wave abnormalities (Figure 2B). Repeat transthoracic echocardiogram the same day, 10 days after the initial transthoracic echocardiogram, revealed resolution of the stress cardiomyopathy, with normal biventricular systolic function (Figure 2C; Movies VIII through XII in the Data Supplement). She was ultimately discharged to a rehabilitation facility.Download figureDownload PowerPointFigure 1. Stress cardiomyopathy during coronavirus disease 2019 (COVID-19) infection.A, Chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. B, Twelve-lead ECG acquired within the hour of echocardiogram demonstrated slight ST-segment elevations. C, Transthoracic echocardiogram (TTE) demonstrated mid-wall hypokinesis of the left ventricle (LV) with normal contractility of the basal and apical segments and normal right ventricular systolic function (left to right: 4-chamber [4Ch], 3-chamber [3Ch], and 2-chamber [2Ch] images; top: end diastole; bottom: end systole). D, Short-axis TTE images demonstrate normal contractility of LV basal and apical segments and hypokinesis of the mid-ventricular segments (left to right: basal, mid, and apical images; top: end diastole; bottom: end systole). Yellow contours in C and D outline the LV endocardial borders.Download figureDownload PowerPointFigure 2. Recovery of stress cardiomyopathy during clinical improvement.A–C, Data obtained on the day of extubation, 10 d following data in Figure 1. A, Chest radiograph continued to demonstrate pulmonary infiltrates. B, ECG abnormalities had normalized compared with prior. C, Transthoracic echocardiogram demonstrated recovery of left ventricular (LV) systolic function with resolution of regional dysfunction (left to right: 4-chamber [4Ch] and short-axis basal, mid, and apical images; top: end diastole; bottom: end systole). Yellow contours outline the LV endocardial borders.The exact mechanisms of stress cardiomyopathy in COVID-19 are unknown. The cardiac tropism of the severe acute respiratory syndrome coronavirus 2 virus, in part, may be explained through viral entry via the angiotensin-converting enzyme 2 that is highly expressed in pulmonary and cardiac tissues, with associated endothelial dysfunction.1 While direct cellular infection has been evident in other viruses, thus far endomyocardial biopsy of suspected COVID-19 myocarditis has shown the presence of the virus within macrophages in the heart but not within cardiomyocytes per se, and a myocarditis-like syndrome may be distinct from that of stress cardiomyopathy. Alternatively, the pathogenesis of cardiac toxicity in COVID-19–associated stress cardiomyopathy may be primarily the result of indirect immune-mediated injury. The medical community has widely observed the cytokine storm of systemic inflammation and immune dysregulation that may occur with severe COVID-19 infection and multiorgan system dysfunction. This condition is marked by profound elevation of cytokines including IL-6 and inflammatory biomarkers including ferritin and D-dimer, as well as frequent modest elevations in cardiac biomarkers—all of which were notable findings in the patient described above. Supporting the immune response in myocardial injury, activation of lymphocytes resulting in cytokine release and inflammation previously has been demonstrated in non–COVID-19 viral myocarditis.3 Additionally, macrophage infiltrates and elevated cytokine levels have been demonstrated in noninfectious stress-induced cardiomyopathy.4 While the underlying trigger of noninfectious stress cardiomyopathy has centered on increased sympathetic tone, high catecholamines may in turn cause myocardial inflammation. Thus, while the pathophysiology of stress cardiomyopathy in COVID-19 remains to be defined, all of the above represent plausible pathogeneses that may occur in combination during the heightened stress and inflammatory milieu of severe infection. Additional assessment of the biochemical and histological profiles of the myocardium in individuals with COVID-19–associated stress cardiomyopathy may further shed light on its mechanisms. Further, in tandem with biomarkers and echocardiography, advanced cardiovascular imaging (eg, coronary computed tomography and cardiovascular magnetic resonance) may play important roles in analyses of coronary and myocardial structure, tissue characteristics, and mechanics to understand the conjoint roles of stress, inflammation, viral toxicity, and cellular damage contributing to the pathobiology of this disorder.In conclusion, reversible stress cardiomyopathy may occur in the setting of COVID-19 infection with elevated inflammatory and cardiac biomarkers and an abnormal ECG. The pathophysiology of COVID-19 stress cardiomyopathy may involve mechanisms shared between noninfectious stress cardiomyopathy and viral myocarditis including microvascular dysfunction, heightened sympathetic tone, and indirect immune-mediated injury with lymphocyte activation, cytokine release, and inflammation. Collaborative and longitudinal studies are needed to evaluate the underlying mechanisms and long-term outcomes of COVID-19–associated stress cardiomyopathy.Sources of FundingThis work was supported by research funding from the NHLBI (5R03HL145195 to Dr Tsao and 1K23HL144907 to Dr Strom).DisclosuresDr Tsao reports consulting fees from AstraZeneca and GlaxoSmithKline, and Dr Strom reports consulting fees from Philips Healthcare unrelated to the current work. The other authors report no conflicts.FootnotesThe Data Supplement is available at https://www.ahajournals.org/doi/suppl/10.1161/CIRCIMAGING.120.011222.Connie W. Tsao, MD, MPH, Cardiovascular Division, Beth Israel Deaconess Medical Center, 330 Brookline Ave, RW-453, Boston, MA 02215. Email ctsao1@bidmc.harvard.eduReferences1. Hendren NSDrazner MHBozkurt BCooper LT. Description and proposed management of the acute COVID-19 cardiovascular syndrome.Circulation. 2020; 141:1903–1914. doi: 10.1161/CIRCULATIONAHA.120.047349LinkGoogle Scholar2. Medina de Chazal HDel Buono MGKeyser-Marcus LMa LMoeller FGBerrocal DAbbate A. Stress cardiomyopathy diagnosis and treatment: JACC state-of-the-art review.J Am Coll Cardiol. 2018; 72:1955–1971. doi: 10.1016/j.jacc.2018.07.072CrossrefMedlineGoogle Scholar3. Matsumori AYamada TSuzuki HMatoba YSasayama S. Increased circulating cytokines in patients with myocarditis and cardiomyopathy.Br Heart J. 1994; 72:561–566. doi: 10.1136/hrt.72.6.561CrossrefMedlineGoogle Scholar4. Scally CAbbas HAhearn TSrinivasan JMezincescu ARudd ASpath NYucel-Finn AYuecel ROldroyd K, et al. Myocardial and systemic inflammation in acute stress-induced (Takotsubo) cardiomyopathy.Circulation. 2019; 139:1581–1592. doi: 10.1161/CIRCULATIONAHA.118.037975LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByBoulos P, Freeman S, Henry T, Mahmud E and Messenger J (2023) Interaction of COVID-19 With Common Cardiovascular Disorders, Circulation Research, 132:10, (1259-1271), Online publication date: 12-May-2023. Bashir H, Yildiz M, Cafardi J, Bhatia A, Garcia S, Henry T and Chung E (2023) A Review of Heart Failure in patients with COVID-19, Heart Failure Clinics, 10.1016/j.hfc.2023.03.002, Online publication date: 1-Mar-2023. Lopez A, Matusov Y, Pedraza I, Tapson V, Falk J and Chen P (2023) COVID‐19: Inpatient Management Coronavirus Disease 2019 (COVID‐19), 10.1002/9781119789741.ch10, (182-232), Online publication date: 6-Jan-2023. Ghasemi H, Kazemian S, Nejadghaderi S and Shafie M (2022) Takotsubo syndrome and COVID‐19: A systematic review, Health Science Reports, 10.1002/hsr2.972, 6:1, Online publication date: 1-Jan-2023. Shams Aldeen M, Logman Masaad M, Azhary A, Suliman A, Alziber M, MohammedAhmed M, Mohamed Aman F, Ismail S, Abuzeid N, Musa A, Mengistu S, Hamida M and Aga S (2022) The Presence of Antineutrophil Cytoplasmic Antibodies and Antiphospholipid Antibodies in Patients with Severe Acute Respiratory Syndrome Coronavirus 2: A Case-Control Study among Sudanese Patients, Interdisciplinary Perspectives on Infectious Diseases, 10.1155/2022/6511198, 2022, (1-11), Online publication date: 15-Dec-2022. Kodsi M and Bhat A (2022) Temporal trends in cardiovascular care: Insights from the COVID-19 pandemic, Frontiers in Cardiovascular Medicine, 10.3389/fcvm.2022.981023, 9 Chatzis D, Magounaki K, Pantazopoulos I and Bhaskar S (2022) COVID-19 and the cardiovascular system-current knowledge and future perspectives, World Journal of Clinical Cases, 10.12998/wjcc.v10.i27.9602, 10:27, (9602-9610), Online publication date: 26-Sep-2022. Sharma M, Jagirdhar G, Guntupalli K, Kashyap R and Surani S (2022) Heart failure in general and cardiac transplant patients with COVID-19, World Journal of Cardiology, 10.4330/wjc.v14.i7.392, 14:7, (392-402), Online publication date: 26-Jul-2022. Guglin M, Ballut K, Ilonze O, Jones M and Rao R (2021) Clinical variants of myocardial involvement in COVID-19-positive patients: a cumulative experience of 2020, Heart Failure Reviews, 10.1007/s10741-021-10129-2, 27:4, (1341-1353), Online publication date: 1-Jul-2022. Nakou E, De Garate E, Liang K, Williams M, Pennell D and Bucciarelli-Ducci C (2022) Imaging Findings of COVID-19–Related Cardiovascular Complications, Cardiac Electrophysiology Clinics, 10.1016/j.ccep.2021.10.008, 14:1, (79-93), Online publication date: 1-Mar-2022. Moady G and Atar S (2022) Stress-Induced Cardiomyopathy—Considerations for Diagnosis and Management during the COVID-19 Pandemic, Medicina, 10.3390/medicina58020192, 58:2, (192) Dhakal B, Sharma N, Pathak B, Simkhada N and limbu B (2022) Case Report: A case of Dilated Cardiomyopathy in COVID-19; A case report, F1000Research, 10.12688/f1000research.110063.1, 11, (567) Haussner W, DeRosa A, Haussner D, Tran J, Torres-Lavoro J, Kamler J and Shah K (2022) COVID-19 associated myocarditis: A systematic review, The American Journal of Emergency Medicine, 10.1016/j.ajem.2021.10.001, 51, (150-155), Online publication date: 1-Jan-2022. Techasatian W, Nishimura Y, Nagamine T, Ha G, Huang R, Shah P, Yeo J and Kanitsoraphan C (2022) Characteristics of Takotsubo cardiomyopathy in patients with COVID-19: Systematic scoping review, American Heart Journal Plus: Cardiology Research and Practice, 10.1016/j.ahjo.2022.100092, 13, (100092), Online publication date: 1-Jan-2022. Mallick U (2022) The Pathological Features of CoViD19 Cardiovascular Complications Cardiovascular Complications of COVID-19, 10.1007/978-3-030-90065-6_4, (47-62), . Madanchi N, Stingo F, Patrick K, Muthusamy S, Gupta N, Imran Fatani Y and Shah N Possible Association Between COVID-19 Infection and De Novo Antineutrophil Cytoplasmic Antibody-Associated Vasculitis, Cureus, 10.7759/cureus.20331 Ozdemir M, Ozdemir G and Guren O (2021) Classification of COVID-19 electrocardiograms by using hexaxial feature mapping and deep learning, BMC Medical Informatics and Decision Making, 10.1186/s12911-021-01521-x, 21:1, Online publication date: 1-Dec-2021. Attiq A, Yao L, Afzal S and Khan M (2021) The triumvirate of NF-κB, inflammation and cytokine storm in COVID-19, International Immunopharmacology, 10.1016/j.intimp.2021.108255, 101, (108255), Online publication date: 1-Dec-2021. Ramadan M, Bertolino L, Marrazzo T, Florio M, Durante-Mangoni E, Durante-Mangoni E, Iossa D, Bertolino L, Ursi M, D’Amico F, Karruli A, Ramadan M, Andini R, Zampino R, Bernardo M, Ruocco G, Dialetto G, Covino F, Manduca S, Corte A, De Feo M, De Vivo S, De Rimini M and Galdieri N (2021) Cardiac complications during the active phase of COVID-19: review of the current evidence, Internal and Emergency Medicine, 10.1007/s11739-021-02763-3, 16:8, (2051-2061), Online publication date: 1-Nov-2021. Wang W, Cao Q, Zhuo C, Mou Y, Pu Z and Zhou Y (2021) COVID-19 to Green Entrepreneurial Intention: Role of Green Entrepreneurial Self-Efficacy, Optimism, Ecological Values, Social Responsibility, and Green Entrepreneurial Motivation, Frontiers in Psychology, 10.3389/fpsyg.2021.732904, 12 Shah K, Hale Hammond M, Drakos S, Anderson J, Fang J, Knowlton K and Shaw R (2021) SARS-CoV-2 as an inflammatory cardiovascular disease: current knowledge and future challenges, Future Cardiology, 10.2217/fca-2020-0188, 17:7, (1277-1291), Online publication date: 1-Oct-2021. Doyen D, Dupland P, Morand L, Fourrier E, Saccheri C, Buscot M, Hyvernat H, Ferrari E, Bernardin G, Cariou A, Mira J, Jamme M, Dellamonica J and Jozwiak M (2021) Characteristics of Cardiac Injury in Critically Ill Patients With Coronavirus Disease 2019, Chest, 10.1016/j.chest.2020.10.056, 159:5, (1974-1985), Online publication date: 1-May-2021. Jin S and Hu W (2021) Severity of COVID-19 and Treatment Strategy for Patient With Diabetes, Frontiers in Endocrinology, 10.3389/fendo.2021.602735, 12 John K, Lal A and Mishra A (2021) A review of the presentation and outcome of Takotsubo cardiomyopathy in COVID-19, Monaldi Archives for Chest Disease, 10.4081/monaldi.2021.1710 Calabrese M, Garofano M, Palumbo R, Di Pietro P, Izzo C, Damato A, Venturini E, Iesu S, Virtuoso N, Strianese A, Ciccarelli M, Galasso G and Vecchione C (2021) Exercise Training and Cardiac Rehabilitation in COVID-19 Patients with Cardiovascular Complications: State of Art, Life, 10.3390/life11030259, 11:3, (259) Shah R, Shah M, Shah S, Li A and Jauhar S (2021) Takotsubo Syndrome and COVID-19: Associations and Implications, Current Problems in Cardiology, 10.1016/j.cpcardiol.2020.100763, 46:3, (100763), Online publication date: 1-Mar-2021. Finsterer J and Stöllberger C (2020) SARS‐CoV‐2 triggered Takotsubo in 38 patients, Journal of Medical Virology, 10.1002/jmv.26581, 93:3, (1236-1238), Online publication date: 1-Mar-2021. Kir D, Beer N and De Marchena E (2020) Takotsubo cardiomyopathy caused by emotional stressors in the coronavirus disease 2019 (COVID‐19) pandemic era, Journal of Cardiac Surgery, 10.1111/jocs.15251, 36:2, (764-769), Online publication date: 1-Feb-2021. Sharma K, Desai H, Patoliya J, Jadeja D and Gadhiya D (2021) Takotsubo Syndrome a Rare Entity in COVID-19: a Systemic Review—Focus on Biomarkers, Imaging, Treatment, and Outcome, SN Comprehensive Clinical Medicine, 10.1007/s42399-021-00743-4, 3:1, (62-72), Online publication date: 1-Jan-2021. Gopal R, Marinelli M and Alcorn J (2020) Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection, Frontiers in Immunology, 10.3389/fimmu.2020.570681, 11 Tsao C and Manning W (2020) Response by Tsao and Manning to Letter Regarding Article, “COVID-19-Associated Stress (Takotsubo) Cardiomyopathy”, Circulation: Cardiovascular Imaging, 13:10, Online publication date: 1-Oct-2020.Finsterer J (2020) Letter by Finsterer Regarding Article, “COVID-19-Associated Stress (Takotsubo) Cardiomyopathy”, Circulation: Cardiovascular Imaging, 13:10, Online publication date: 1-Oct-2020. July 2020Vol 13, Issue 7 Advertisement Article InformationMetrics © 2020 American Heart Association, Inc.https://doi.org/10.1161/CIRCIMAGING.120.011222PMID: 32673494 Originally publishedJuly 15, 2020 KeywordsechocardiographycoronavirusTakotsubo cardiomyopathystress cardiomyopathymorbidityPDF download Advertisement SubjectsEchocardiographyImaging" @default.
• W4207010309 created "2022-01-26" @default.
• W4207010309 creator A5002689169 @default.
• W4207010309 creator A5002927848 @default.
• W4207010309 creator A5065906325 @default.
• W4207010309 creator A5085159751 @default.
• W4207010309 date "2020-07-01" @default.
• W4207010309 modified "2023-10-03" @default.
• W4207010309 title "COVID-19–Associated Stress (Takotsubo) Cardiomyopathy" @default.
• W4207010309 cites W1985812804 @default.
• W4207010309 cites W2894551604 @default.
• W4207010309 cites W2900479021 @default.
• W4207010309 cites W3016959086 @default.
• W4207010309 doi "https://doi.org/10.1161/circimaging.120.011222" @default.
• W4207010309 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32673494" @default.
• W4207010309 hasPublicationYear "2020" @default.
• W4207010309 type Work @default.
• W4207010309 citedByCount "40" @default.
• W4207010309 countsByYear W42070103092020 @default.
• W4207010309 countsByYear W42070103092021 @default.
• W4207010309 countsByYear W42070103092022 @default.
• W4207010309 countsByYear W42070103092023 @default.
• W4207010309 crossrefType "journal-article" @default.
• W4207010309 hasAuthorship W4207010309A5002689169 @default.
• W4207010309 hasAuthorship W4207010309A5002927848 @default.
• W4207010309 hasAuthorship W4207010309A5065906325 @default.
• W4207010309 hasAuthorship W4207010309A5085159751 @default.
• W4207010309 hasBestOaLocation W42070103091 @default.
• W4207010309 hasConcept C116675565 @default.
• W4207010309 hasConcept C126322002 @default.
• W4207010309 hasConcept C138885662 @default.
• W4207010309 hasConcept C159047783 @default.
• W4207010309 hasConcept C164705383 @default.
• W4207010309 hasConcept C21036866 @default.
• W4207010309 hasConcept C2778198053 @default.
• W4207010309 hasConcept C2778797674 @default.
• W4207010309 hasConcept C2779134260 @default.
• W4207010309 hasConcept C2910792892 @default.
• W4207010309 hasConcept C3006700255 @default.
• W4207010309 hasConcept C3007834351 @default.
• W4207010309 hasConcept C3008058167 @default.
• W4207010309 hasConcept C41895202 @default.
• W4207010309 hasConcept C524204448 @default.
• W4207010309 hasConcept C71924100 @default.
• W4207010309 hasConceptScore W4207010309C116675565 @default.
• W4207010309 hasConceptScore W4207010309C126322002 @default.
• W4207010309 hasConceptScore W4207010309C138885662 @default.
• W4207010309 hasConceptScore W4207010309C159047783 @default.
• W4207010309 hasConceptScore W4207010309C164705383 @default.
• W4207010309 hasConceptScore W4207010309C21036866 @default.
• W4207010309 hasConceptScore W4207010309C2778198053 @default.
• W4207010309 hasConceptScore W4207010309C2778797674 @default.
• W4207010309 hasConceptScore W4207010309C2779134260 @default.
• W4207010309 hasConceptScore W4207010309C2910792892 @default.
• W4207010309 hasConceptScore W4207010309C3006700255 @default.
• W4207010309 hasConceptScore W4207010309C3007834351 @default.
• W4207010309 hasConceptScore W4207010309C3008058167 @default.
• W4207010309 hasConceptScore W4207010309C41895202 @default.
• W4207010309 hasConceptScore W4207010309C524204448 @default.
• W4207010309 hasConceptScore W4207010309C71924100 @default.
• W4207010309 hasIssue "7" @default.
• W4207010309 hasLocation W42070103091 @default.
• W4207010309 hasLocation W42070103092 @default.
• W4207010309 hasLocation W42070103093 @default.
• W4207010309 hasOpenAccess W4207010309 @default.
• W4207010309 hasPrimaryLocation W42070103091 @default.
• W4207010309 hasRelatedWork W3009669391 @default.
• W4207010309 hasRelatedWork W3036314732 @default.
• W4207010309 hasRelatedWork W3113664224 @default.
• W4207010309 hasRelatedWork W3176864053 @default.
• W4207010309 hasRelatedWork W3198183218 @default.
• W4207010309 hasRelatedWork W4200329650 @default.
• W4207010309 hasRelatedWork W4205317059 @default.
• W4207010309 hasRelatedWork W4206669628 @default.
• W4207010309 hasRelatedWork W4382894326 @default.
• W4207010309 hasRelatedWork W3127156785 @default.
• W4207010309 hasVolume "13" @default.
• W4207010309 isParatext "false" @default.
• W4207010309 isRetracted "false" @default.
• W4207010309 workType "article" @default.