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    LitCovid-PD-FMA-UBERON

    {"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T100","span":{"begin":174,"end":179},"obj":"Body_part"},{"id":"T101","span":{"begin":205,"end":212},"obj":"Body_part"},{"id":"T102","span":{"begin":364,"end":381},"obj":"Body_part"},{"id":"T103","span":{"begin":376,"end":381},"obj":"Body_part"},{"id":"T104","span":{"begin":467,"end":492},"obj":"Body_part"},{"id":"T105","span":{"begin":487,"end":492},"obj":"Body_part"},{"id":"T106","span":{"begin":525,"end":529},"obj":"Body_part"},{"id":"T107","span":{"begin":640,"end":644},"obj":"Body_part"},{"id":"T108","span":{"begin":656,"end":660},"obj":"Body_part"},{"id":"T109","span":{"begin":741,"end":753},"obj":"Body_part"},{"id":"T110","span":{"begin":778,"end":789},"obj":"Body_part"},{"id":"T111","span":{"begin":1668,"end":1673},"obj":"Body_part"},{"id":"T112","span":{"begin":1701,"end":1706},"obj":"Body_part"},{"id":"T113","span":{"begin":1838,"end":1843},"obj":"Body_part"},{"id":"T114","span":{"begin":2027,"end":2032},"obj":"Body_part"},{"id":"T115","span":{"begin":2043,"end":2048},"obj":"Body_part"},{"id":"T116","span":{"begin":2426,"end":2437},"obj":"Body_part"},{"id":"T117","span":{"begin":2469,"end":2481},"obj":"Body_part"},{"id":"T118","span":{"begin":2955,"end":2960},"obj":"Body_part"},{"id":"T119","span":{"begin":3618,"end":3623},"obj":"Body_part"},{"id":"T120","span":{"begin":4380,"end":4385},"obj":"Body_part"},{"id":"T121","span":{"begin":4467,"end":4472},"obj":"Body_part"},{"id":"T122","span":{"begin":4946,"end":4954},"obj":"Body_part"},{"id":"T123","span":{"begin":5111,"end":5116},"obj":"Body_part"},{"id":"T124","span":{"begin":5200,"end":5205},"obj":"Body_part"},{"id":"T125","span":{"begin":5220,"end":5225},"obj":"Body_part"},{"id":"T126","span":{"begin":5248,"end":5253},"obj":"Body_part"},{"id":"T127","span":{"begin":5328,"end":5333},"obj":"Body_part"},{"id":"T128","span":{"begin":5388,"end":5398},"obj":"Body_part"},{"id":"T129","span":{"begin":5585,"end":5604},"obj":"Body_part"},{"id":"T130","span":{"begin":5674,"end":5684},"obj":"Body_part"}],"attributes":[{"id":"A100","pred":"fma_id","subj":"T100","obj":"http://purl.org/sig/ont/fma/fma7197"},{"id":"A101","pred":"fma_id","subj":"T101","obj":"http://purl.org/sig/ont/fma/fma82749"},{"id":"A102","pred":"fma_id","subj":"T102","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A103","pred":"fma_id","subj":"T103","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A104","pred":"fma_id","subj":"T104","obj":"http://purl.org/sig/ont/fma/fma14515"},{"id":"A105","pred":"fma_id","subj":"T105","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A106","pred":"fma_id","subj":"T106","obj":"http://purl.org/sig/ont/fma/fma86583"},{"id":"A107","pred":"fma_id","subj":"T107","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A108","pred":"fma_id","subj":"T108","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A109","pred":"fma_id","subj":"T109","obj":"http://purl.org/sig/ont/fma/fma62861"},{"id":"A110","pred":"fma_id","subj":"T110","obj":"http://purl.org/sig/ont/fma/fma14515"},{"id":"A111","pred":"fma_id","subj":"T111","obj":"http://purl.org/sig/ont/fma/fma9576"},{"id":"A112","pred":"fma_id","subj":"T112","obj":"http://purl.org/sig/ont/fma/fma9576"},{"id":"A113","pred":"fma_id","subj":"T113","obj":"http://purl.org/sig/ont/fma/fma9576"},{"id":"A114","pred":"fma_id","subj":"T114","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A115","pred":"fma_id","subj":"T115","obj":"http://purl.org/sig/ont/fma/fma9576"},{"id":"A116","pred":"fma_id","subj":"T116","obj":"http://purl.org/sig/ont/fma/fma62863"},{"id":"A117","pred":"fma_id","subj":"T117","obj":"http://purl.org/sig/ont/fma/fma67328"},{"id":"A118","pred":"fma_id","subj":"T118","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A119","pred":"fma_id","subj":"T119","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A120","pred":"fma_id","subj":"T120","obj":"http://purl.org/sig/ont/fma/fma9576"},{"id":"A121","pred":"fma_id","subj":"T121","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A122","pred":"fma_id","subj":"T122","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A123","pred":"fma_id","subj":"T123","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A124","pred":"fma_id","subj":"T124","obj":"http://purl.org/sig/ont/fma/fma9670"},{"id":"A125","pred":"fma_id","subj":"T125","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A126","pred":"fma_id","subj":"T126","obj":"http://purl.org/sig/ont/fma/fma7088"},{"id":"A127","pred":"fma_id","subj":"T127","obj":"http://purl.org/sig/ont/fma/fma9576"},{"id":"A128","pred":"fma_id","subj":"T128","obj":"http://purl.org/sig/ont/fma/fma62293"},{"id":"A129","pred":"fma_id","subj":"T129","obj":"http://purl.org/sig/ont/fma/fma9486"},{"id":"A130","pred":"fma_id","subj":"T130","obj":"http://purl.org/sig/ont/fma/fma62340"}],"text":"SARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PD-UBERON

    {"project":"LitCovid-PD-UBERON","denotations":[{"id":"T62","span":{"begin":174,"end":179},"obj":"Body_part"},{"id":"T63","span":{"begin":1668,"end":1673},"obj":"Body_part"},{"id":"T64","span":{"begin":1701,"end":1706},"obj":"Body_part"},{"id":"T65","span":{"begin":1838,"end":1843},"obj":"Body_part"},{"id":"T66","span":{"begin":2027,"end":2032},"obj":"Body_part"},{"id":"T67","span":{"begin":2043,"end":2048},"obj":"Body_part"},{"id":"T68","span":{"begin":2415,"end":2422},"obj":"Body_part"},{"id":"T69","span":{"begin":2955,"end":2960},"obj":"Body_part"},{"id":"T70","span":{"begin":3618,"end":3623},"obj":"Body_part"},{"id":"T71","span":{"begin":4380,"end":4385},"obj":"Body_part"},{"id":"T72","span":{"begin":4467,"end":4472},"obj":"Body_part"},{"id":"T73","span":{"begin":5111,"end":5116},"obj":"Body_part"},{"id":"T74","span":{"begin":5200,"end":5205},"obj":"Body_part"},{"id":"T75","span":{"begin":5220,"end":5225},"obj":"Body_part"},{"id":"T76","span":{"begin":5248,"end":5253},"obj":"Body_part"},{"id":"T77","span":{"begin":5328,"end":5333},"obj":"Body_part"}],"attributes":[{"id":"A62","pred":"uberon_id","subj":"T62","obj":"http://purl.obolibrary.org/obo/UBERON_0002107"},{"id":"A63","pred":"uberon_id","subj":"T63","obj":"http://purl.obolibrary.org/obo/UBERON_0001443"},{"id":"A64","pred":"uberon_id","subj":"T64","obj":"http://purl.obolibrary.org/obo/UBERON_0001443"},{"id":"A65","pred":"uberon_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/UBERON_0001443"},{"id":"A66","pred":"uberon_id","subj":"T66","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A67","pred":"uberon_id","subj":"T67","obj":"http://purl.obolibrary.org/obo/UBERON_0001443"},{"id":"A68","pred":"uberon_id","subj":"T68","obj":"http://purl.obolibrary.org/obo/UBERON_0000055"},{"id":"A69","pred":"uberon_id","subj":"T69","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A70","pred":"uberon_id","subj":"T70","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A71","pred":"uberon_id","subj":"T71","obj":"http://purl.obolibrary.org/obo/UBERON_0001443"},{"id":"A72","pred":"uberon_id","subj":"T72","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A73","pred":"uberon_id","subj":"T73","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A74","pred":"uberon_id","subj":"T74","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A75","pred":"uberon_id","subj":"T75","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A76","pred":"uberon_id","subj":"T76","obj":"http://purl.obolibrary.org/obo/UBERON_0000948"},{"id":"A77","pred":"uberon_id","subj":"T77","obj":"http://purl.obolibrary.org/obo/UBERON_0001443"}],"text":"SARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PD-MONDO

    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in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PD-CLO

    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in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PD-CHEBI

    {"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T42","span":{"begin":205,"end":212},"obj":"Chemical"},{"id":"T43","span":{"begin":237,"end":246},"obj":"Chemical"},{"id":"T46","span":{"begin":525,"end":527},"obj":"Chemical"},{"id":"T48","span":{"begin":531,"end":533},"obj":"Chemical"},{"id":"T50","span":{"begin":540,"end":542},"obj":"Chemical"},{"id":"T52","span":{"begin":842,"end":852},"obj":"Chemical"},{"id":"T53","span":{"begin":1397,"end":1399},"obj":"Chemical"},{"id":"T54","span":{"begin":1812,"end":1814},"obj":"Chemical"},{"id":"T56","span":{"begin":1888,"end":1890},"obj":"Chemical"},{"id":"T57","span":{"begin":2119,"end":2121},"obj":"Chemical"},{"id":"T58","span":{"begin":2145,"end":2147},"obj":"Chemical"},{"id":"T59","span":{"begin":3455,"end":3458},"obj":"Chemical"},{"id":"T60","span":{"begin":3463,"end":3473},"obj":"Chemical"},{"id":"T61","span":{"begin":3496,"end":3498},"obj":"Chemical"},{"id":"T62","span":{"begin":4064,"end":4066},"obj":"Chemical"},{"id":"T63","span":{"begin":4638,"end":4640},"obj":"Chemical"},{"id":"T64","span":{"begin":4734,"end":4736},"obj":"Chemical"},{"id":"T65","span":{"begin":5163,"end":5166},"obj":"Chemical"},{"id":"T66","span":{"begin":5187,"end":5194},"obj":"Chemical"},{"id":"T67","span":{"begin":5196,"end":5198},"obj":"Chemical"},{"id":"T68","span":{"begin":5267,"end":5275},"obj":"Chemical"},{"id":"T70","span":{"begin":5290,"end":5298},"obj":"Chemical"},{"id":"T72","span":{"begin":5388,"end":5398},"obj":"Chemical"},{"id":"T73","span":{"begin":5431,"end":5438},"obj":"Chemical"},{"id":"T74","span":{"begin":5496,"end":5498},"obj":"Chemical"}],"attributes":[{"id":"A42","pred":"chebi_id","subj":"T42","obj":"http://purl.obolibrary.org/obo/CHEBI_16449"},{"id":"A43","pred":"chebi_id","subj":"T43","obj":"http://purl.obolibrary.org/obo/CHEBI_132943"},{"id":"A44","pred":"chebi_id","subj":"T43","obj":"http://purl.obolibrary.org/obo/CHEBI_29995"},{"id":"A45","pred":"chebi_id","subj":"T43","obj":"http://purl.obolibrary.org/obo/CHEBI_72314"},{"id":"A46","pred":"chebi_id","subj":"T46","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A47","pred":"chebi_id","subj":"T46","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A48","pred":"chebi_id","subj":"T48","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A49","pred":"chebi_id","subj":"T48","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A50","pred":"chebi_id","subj":"T50","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A51","pred":"chebi_id","subj":"T50","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A52","pred":"chebi_id","subj":"T52","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A53","pred":"chebi_id","subj":"T53","obj":"http://purl.obolibrary.org/obo/CHEBI_30145"},{"id":"A54","pred":"chebi_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/CHEBI_53620"},{"id":"A55","pred":"chebi_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/CHEBI_74704"},{"id":"A56","pred":"chebi_id","subj":"T56","obj":"http://purl.obolibrary.org/obo/CHEBI_29865"},{"id":"A57","pred":"chebi_id","subj":"T57","obj":"http://purl.obolibrary.org/obo/CHEBI_22984"},{"id":"A58","pred":"chebi_id","subj":"T58","obj":"http://purl.obolibrary.org/obo/CHEBI_25107"},{"id":"A59","pred":"chebi_id","subj":"T59","obj":"http://purl.obolibrary.org/obo/CHEBI_80234"},{"id":"A60","pred":"chebi_id","subj":"T60","obj":"http://purl.obolibrary.org/obo/CHEBI_16737"},{"id":"A61","pred":"chebi_id","subj":"T61","obj":"http://purl.obolibrary.org/obo/CHEBI_73579"},{"id":"A62","pred":"chebi_id","subj":"T62","obj":"http://purl.obolibrary.org/obo/CHEBI_29865"},{"id":"A63","pred":"chebi_id","subj":"T63","obj":"http://purl.obolibrary.org/obo/CHEBI_141393"},{"id":"A64","pred":"chebi_id","subj":"T64","obj":"http://purl.obolibrary.org/obo/CHEBI_29865"},{"id":"A65","pred":"chebi_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/CHEBI_80234"},{"id":"A66","pred":"chebi_id","subj":"T66","obj":"http://purl.obolibrary.org/obo/CHEBI_16670"},{"id":"A67","pred":"chebi_id","subj":"T67","obj":"http://purl.obolibrary.org/obo/CHEBI_29865"},{"id":"A68","pred":"chebi_id","subj":"T68","obj":"http://purl.obolibrary.org/obo/CHEBI_16919"},{"id":"A69","pred":"chebi_id","subj":"T68","obj":"http://purl.obolibrary.org/obo/CHEBI_57947"},{"id":"A70","pred":"chebi_id","subj":"T70","obj":"http://purl.obolibrary.org/obo/CHEBI_16919"},{"id":"A71","pred":"chebi_id","subj":"T70","obj":"http://purl.obolibrary.org/obo/CHEBI_57947"},{"id":"A72","pred":"chebi_id","subj":"T72","obj":"http://purl.obolibrary.org/obo/CHEBI_35143"},{"id":"A73","pred":"chebi_id","subj":"T73","obj":"http://purl.obolibrary.org/obo/CHEBI_24996"},{"id":"A74","pred":"chebi_id","subj":"T74","obj":"http://purl.obolibrary.org/obo/CHEBI_53620"},{"id":"A75","pred":"chebi_id","subj":"T74","obj":"http://purl.obolibrary.org/obo/CHEBI_74704"}],"text":"SARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PD-GO-BP

    {"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T16","span":{"begin":601,"end":628},"obj":"http://purl.obolibrary.org/obo/GO_0002526"},{"id":"T17","span":{"begin":607,"end":628},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T18","span":{"begin":656,"end":666},"obj":"http://purl.obolibrary.org/obo/GO_0007049"},{"id":"T19","span":{"begin":710,"end":719},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T20","span":{"begin":710,"end":719},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T21","span":{"begin":2300,"end":2304},"obj":"http://purl.obolibrary.org/obo/GO_0004111"},{"id":"T22","span":{"begin":2482,"end":2487},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T23","span":{"begin":4604,"end":4609},"obj":"http://purl.obolibrary.org/obo/GO_0004111"},{"id":"T24","span":{"begin":5284,"end":5288},"obj":"http://purl.obolibrary.org/obo/GO_0004111"}],"text":"SARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PD-HP

    {"project":"LitCovid-PD-HP","denotations":[{"id":"T131","span":{"begin":9,"end":18},"obj":"Phenotype"},{"id":"T132","span":{"begin":265,"end":280},"obj":"Phenotype"},{"id":"T133","span":{"begin":285,"end":303},"obj":"Phenotype"},{"id":"T134","span":{"begin":572,"end":581},"obj":"Phenotype"},{"id":"T135","span":{"begin":906,"end":915},"obj":"Phenotype"},{"id":"T136","span":{"begin":1079,"end":1092},"obj":"Phenotype"},{"id":"T137","span":{"begin":1668,"end":1678},"obj":"Phenotype"},{"id":"T138","span":{"begin":1701,"end":1711},"obj":"Phenotype"},{"id":"T139","span":{"begin":1721,"end":1724},"obj":"Phenotype"},{"id":"T140","span":{"begin":1763,"end":1766},"obj":"Phenotype"},{"id":"T141","span":{"begin":1782,"end":1803},"obj":"Phenotype"},{"id":"T142","span":{"begin":1819,"end":1829},"obj":"Phenotype"},{"id":"T143","span":{"begin":1838,"end":1848},"obj":"Phenotype"},{"id":"T144","span":{"begin":1993,"end":2005},"obj":"Phenotype"},{"id":"T145","span":{"begin":2027,"end":2040},"obj":"Phenotype"},{"id":"T146","span":{"begin":2067,"end":2079},"obj":"Phenotype"},{"id":"T147","span":{"begin":2391,"end":2396},"obj":"Phenotype"},{"id":"T148","span":{"begin":2759,"end":2768},"obj":"Phenotype"},{"id":"T149","span":{"begin":3005,"end":3013},"obj":"Phenotype"},{"id":"T150","span":{"begin":3107,"end":3118},"obj":"Phenotype"},{"id":"T151","span":{"begin":3147,"end":3165},"obj":"Phenotype"},{"id":"T152","span":{"begin":3383,"end":3386},"obj":"Phenotype"},{"id":"T153","span":{"begin":3399,"end":3411},"obj":"Phenotype"},{"id":"T154","span":{"begin":3526,"end":3537},"obj":"Phenotype"},{"id":"T155","span":{"begin":3596,"end":3607},"obj":"Phenotype"},{"id":"T156","span":{"begin":3618,"end":3631},"obj":"Phenotype"},{"id":"T157","span":{"begin":4320,"end":4330},"obj":"Phenotype"},{"id":"T158","span":{"begin":4365,"end":4377},"obj":"Phenotype"},{"id":"T159","span":{"begin":4380,"end":4395},"obj":"Phenotype"},{"id":"T160","span":{"begin":4467,"end":4480},"obj":"Phenotype"},{"id":"T161","span":{"begin":4483,"end":4500},"obj":"Phenotype"},{"id":"T162","span":{"begin":4638,"end":4659},"obj":"Phenotype"},{"id":"T163","span":{"begin":4823,"end":4835},"obj":"Phenotype"},{"id":"T164","span":{"begin":4845,"end":4856},"obj":"Phenotype"},{"id":"T165","span":{"begin":4946,"end":4960},"obj":"Phenotype"},{"id":"T166","span":{"begin":4963,"end":4972},"obj":"Phenotype"},{"id":"T167","span":{"begin":5020,"end":5039},"obj":"Phenotype"},{"id":"T168","span":{"begin":5232,"end":5235},"obj":"Phenotype"},{"id":"T169","span":{"begin":5237,"end":5261},"obj":"Phenotype"},{"id":"T170","span":{"begin":5500,"end":5521},"obj":"Phenotype"},{"id":"T171","span":{"begin":5585,"end":5610},"obj":"Phenotype"}],"attributes":[{"id":"A131","pred":"hp_id","subj":"T131","obj":"http://purl.obolibrary.org/obo/HP_0012115"},{"id":"A132","pred":"hp_id","subj":"T132","obj":"http://purl.obolibrary.org/obo/HP_0003073"},{"id":"A133","pred":"hp_id","subj":"T133","obj":"http://purl.obolibrary.org/obo/HP_0002904"},{"id":"A134","pred":"hp_id","subj":"T134","obj":"http://purl.obolibrary.org/obo/HP_0012115"},{"id":"A135","pred":"hp_id","subj":"T135","obj":"http://purl.obolibrary.org/obo/HP_0012115"},{"id":"A136","pred":"hp_id","subj":"T136","obj":"http://purl.obolibrary.org/obo/HP_0003074"},{"id":"A137","pred":"hp_id","subj":"T137","obj":"http://purl.obolibrary.org/obo/HP_0100749"},{"id":"A138","pred":"hp_id","subj":"T138","obj":"http://purl.obolibrary.org/obo/HP_0100749"},{"id":"A139","pred":"hp_id","subj":"T139","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A140","pred":"hp_id","subj":"T140","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A141","pred":"hp_id","subj":"T141","obj":"http://purl.obolibrary.org/obo/HP_0031628"},{"id":"A142","pred":"hp_id","subj":"T142","obj":"http://purl.obolibrary.org/obo/HP_0011675"},{"id":"A143","pred":"hp_id","subj":"T143","obj":"http://purl.obolibrary.org/obo/HP_0100749"},{"id":"A144","pred":"hp_id","subj":"T144","obj":"http://purl.obolibrary.org/obo/HP_0001640"},{"id":"A145","pred":"hp_id","subj":"T145","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A146","pred":"hp_id","subj":"T146","obj":"http://purl.obolibrary.org/obo/HP_0001962"},{"id":"A147","pred":"hp_id","subj":"T147","obj":"http://purl.obolibrary.org/obo/HP_0000969"},{"id":"A148","pred":"hp_id","subj":"T148","obj":"http://purl.obolibrary.org/obo/HP_0012418"},{"id":"A149","pred":"hp_id","subj":"T149","obj":"http://purl.obolibrary.org/obo/HP_0100614"},{"id":"A150","pred":"hp_id","subj":"T150","obj":"http://purl.obolibrary.org/obo/HP_0001649"},{"id":"A151","pred":"hp_id","subj":"T151","obj":"http://purl.obolibrary.org/obo/HP_0011675"},{"id":"A152","pred":"hp_id","subj":"T152","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A153","pred":"hp_id","subj":"T153","obj":"http://purl.obolibrary.org/obo/HP_0001701"},{"id":"A154","pred":"hp_id","subj":"T154","obj":"http://purl.obolibrary.org/obo/HP_0012819"},{"id":"A155","pred":"hp_id","subj":"T155","obj":"http://purl.obolibrary.org/obo/HP_0012819"},{"id":"A156","pred":"hp_id","subj":"T156","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A157","pred":"hp_id","subj":"T157","obj":"http://purl.obolibrary.org/obo/HP_0011675"},{"id":"A158","pred":"hp_id","subj":"T158","obj":"http://purl.obolibrary.org/obo/HP_0001962"},{"id":"A159","pred":"hp_id","subj":"T159","obj":"http://purl.obolibrary.org/obo/HP_0031352"},{"id":"A160","pred":"hp_id","subj":"T160","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A161","pred":"hp_id","subj":"T161","obj":"http://purl.obolibrary.org/obo/HP_0030149"},{"id":"A162","pred":"hp_id","subj":"T162","obj":"http://purl.obolibrary.org/obo/HP_0012251"},{"id":"A163","pred":"hp_id","subj":"T163","obj":"http://purl.obolibrary.org/obo/HP_0000822"},{"id":"A164","pred":"hp_id","subj":"T164","obj":"http://purl.obolibrary.org/obo/HP_0011675"},{"id":"A165","pred":"hp_id","subj":"T165","obj":"http://purl.obolibrary.org/obo/HP_0033041"},{"id":"A166","pred":"hp_id","subj":"T166","obj":"http://purl.obolibrary.org/obo/HP_0012418"},{"id":"A167","pred":"hp_id","subj":"T167","obj":"http://purl.obolibrary.org/obo/HP_0002878"},{"id":"A168","pred":"hp_id","subj":"T168","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A169","pred":"hp_id","subj":"T169","obj":"http://purl.obolibrary.org/obo/HP_0001635"},{"id":"A170","pred":"hp_id","subj":"T170","obj":"http://purl.obolibrary.org/obo/HP_0001658"},{"id":"A171","pred":"hp_id","subj":"T171","obj":"http://purl.obolibrary.org/obo/HP_0011712"}],"text":"SARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-sentences

    {"project":"LitCovid-sentences","denotations":[{"id":"T220","span":{"begin":0,"end":8},"obj":"Sentence"},{"id":"T221","span":{"begin":9,"end":113},"obj":"Sentence"},{"id":"T222","span":{"begin":114,"end":318},"obj":"Sentence"},{"id":"T223","span":{"begin":319,"end":1197},"obj":"Sentence"},{"id":"T224","span":{"begin":1198,"end":1271},"obj":"Sentence"},{"id":"T225","span":{"begin":1272,"end":1328},"obj":"Sentence"},{"id":"T226","span":{"begin":1329,"end":1647},"obj":"Sentence"},{"id":"T227","span":{"begin":1648,"end":1884},"obj":"Sentence"},{"id":"T228","span":{"begin":1885,"end":1979},"obj":"Sentence"},{"id":"T229","span":{"begin":1980,"end":2040},"obj":"Sentence"},{"id":"T230","span":{"begin":2041,"end":2064},"obj":"Sentence"},{"id":"T231","span":{"begin":2065,"end":2084},"obj":"Sentence"},{"id":"T232","span":{"begin":2085,"end":2129},"obj":"Sentence"},{"id":"T233","span":{"begin":2130,"end":2141},"obj":"Sentence"},{"id":"T234","span":{"begin":2142,"end":2155},"obj":"Sentence"},{"id":"T235","span":{"begin":2156,"end":2167},"obj":"Sentence"},{"id":"T236","span":{"begin":2168,"end":2188},"obj":"Sentence"},{"id":"T237","span":{"begin":2189,"end":2196},"obj":"Sentence"},{"id":"T238","span":{"begin":2197,"end":2202},"obj":"Sentence"},{"id":"T239","span":{"begin":2203,"end":2214},"obj":"Sentence"},{"id":"T240","span":{"begin":2215,"end":2272},"obj":"Sentence"},{"id":"T241","span":{"begin":2273,"end":2304},"obj":"Sentence"},{"id":"T242","span":{"begin":2305,"end":2312},"obj":"Sentence"},{"id":"T243","span":{"begin":2313,"end":2337},"obj":"Sentence"},{"id":"T244","span":{"begin":2338,"end":2342},"obj":"Sentence"},{"id":"T245","span":{"begin":2343,"end":2396},"obj":"Sentence"},{"id":"T246","span":{"begin":2397,"end":2437},"obj":"Sentence"},{"id":"T247","span":{"begin":2438,"end":2466},"obj":"Sentence"},{"id":"T248","span":{"begin":2467,"end":2491},"obj":"Sentence"},{"id":"T249","span":{"begin":2492,"end":2542},"obj":"Sentence"},{"id":"T250","span":{"begin":2543,"end":2578},"obj":"Sentence"},{"id":"T251","span":{"begin":2579,"end":2797},"obj":"Sentence"},{"id":"T252","span":{"begin":2798,"end":2830},"obj":"Sentence"},{"id":"T253","span":{"begin":2831,"end":2871},"obj":"Sentence"},{"id":"T254","span":{"begin":2872,"end":3039},"obj":"Sentence"},{"id":"T255","span":{"begin":3040,"end":3059},"obj":"Sentence"},{"id":"T256","span":{"begin":3060,"end":3104},"obj":"Sentence"},{"id":"T257","span":{"begin":3105,"end":3144},"obj":"Sentence"},{"id":"T258","span":{"begin":3145,"end":3177},"obj":"Sentence"},{"id":"T259","span":{"begin":3178,"end":3182},"obj":"Sentence"},{"id":"T260","span":{"begin":3183,"end":3364},"obj":"Sentence"},{"id":"T261","span":{"begin":3365,"end":3411},"obj":"Sentence"},{"id":"T262","span":{"begin":3412,"end":3450},"obj":"Sentence"},{"id":"T263","span":{"begin":3451,"end":3458},"obj":"Sentence"},{"id":"T264","span":{"begin":3459,"end":3473},"obj":"Sentence"},{"id":"T265","span":{"begin":3474,"end":3481},"obj":"Sentence"},{"id":"T266","span":{"begin":3482,"end":3510},"obj":"Sentence"},{"id":"T267","span":{"begin":3511,"end":3525},"obj":"Sentence"},{"id":"T268","span":{"begin":3526,"end":3545},"obj":"Sentence"},{"id":"T269","span":{"begin":3546,"end":3688},"obj":"Sentence"},{"id":"T270","span":{"begin":3689,"end":3763},"obj":"Sentence"},{"id":"T271","span":{"begin":3764,"end":3772},"obj":"Sentence"},{"id":"T272","span":{"begin":3773,"end":4042},"obj":"Sentence"},{"id":"T273","span":{"begin":4043,"end":4066},"obj":"Sentence"},{"id":"T274","span":{"begin":4067,"end":4206},"obj":"Sentence"},{"id":"T275","span":{"begin":4207,"end":4259},"obj":"Sentence"},{"id":"T276","span":{"begin":4260,"end":4317},"obj":"Sentence"},{"id":"T277","span":{"begin":4318,"end":4377},"obj":"Sentence"},{"id":"T278","span":{"begin":4378,"end":4407},"obj":"Sentence"},{"id":"T279","span":{"begin":4408,"end":4450},"obj":"Sentence"},{"id":"T280","span":{"begin":4451,"end":4480},"obj":"Sentence"},{"id":"T281","span":{"begin":4481,"end":4500},"obj":"Sentence"},{"id":"T282","span":{"begin":4501,"end":4599},"obj":"Sentence"},{"id":"T283","span":{"begin":4600,"end":4659},"obj":"Sentence"},{"id":"T284","span":{"begin":4660,"end":4686},"obj":"Sentence"},{"id":"T285","span":{"begin":4687,"end":4701},"obj":"Sentence"},{"id":"T286","span":{"begin":4702,"end":4943},"obj":"Sentence"},{"id":"T287","span":{"begin":4944,"end":4960},"obj":"Sentence"},{"id":"T288","span":{"begin":4961,"end":5072},"obj":"Sentence"},{"id":"T289","span":{"begin":5073,"end":5162},"obj":"Sentence"},{"id":"T290","span":{"begin":5163,"end":5685},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"SARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PMC-OGER-BB

    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in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    LitCovid-PubTator

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in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}

    2_test

    {"project":"2_test","denotations":[{"id":"32620220-14767982-2074089","span":{"begin":304,"end":306},"obj":"14767982"},{"id":"32620220-15141377-2074090","span":{"begin":382,"end":384},"obj":"15141377"},{"id":"32620220-14761595-2074091","span":{"begin":493,"end":495},"obj":"14761595"},{"id":"32620220-15141376-2074092","span":{"begin":498,"end":500},"obj":"15141376"},{"id":"32620220-32170806-2074093","span":{"begin":503,"end":505},"obj":"32170806"},{"id":"32620220-15268817-2074094","span":{"begin":629,"end":631},"obj":"15268817"},{"id":"32620220-31986264-2074095","span":{"begin":790,"end":792},"obj":"31986264"},{"id":"32620220-15730921-2074096","span":{"begin":942,"end":944},"obj":"15730921"},{"id":"32620220-19333547-2074097","span":{"begin":1042,"end":1044},"obj":"19333547"},{"id":"32620220-19333547-2074098","span":{"begin":1195,"end":1197},"obj":"19333547"}],"text":"SARS-CoV\nHepatitis in SARS-CoV is a well-recognized common complication, although it is a diagnosis of exclusion. Approximately 60% of patients with SARS-CoV had a degree of liver impairment with elevated alanine aminotransferase and/or aspartate aminotransferase, hypoalbuminemia and hyperbilirubinemia 53 (Table 2 ). ACE2 receptors are also found on the hepatic endothelial cells.54 On histopathology, SARS-CoV patients had a large number of virus particles in the hepatic parenchymal cells.38 , 39 , 55 Elevated levels of IL-1, IL-6 and IL-10 in patients with SARS-CoV hepatitis support coexisting acute inflammatory response.56 Hepatic cell damage and cell-cycle disruption was seen on hepatic biopsy with apoptosis, mitotic arrest with eosinophilic bodies and balloon-like hepatocytes.22 Unfortunately, hepatic damage potentially due to antivirals use complicates our understanding of the etiology of hepatitis in patients with SARS-CoV.57 Hepatic involvement may indicate a poor prognosis, particularly in patients with high LDH levels.58 Yang et al reported long-standing hyperglycemia (due to pancreatic injury) as an independent predictor for adverse outcomes in patients with SARS-CoV.58\nTable 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.\nSARS (only studies with large study population included)\nStudy Booth et al (2003)N = 144, confirmed casesRetrospective study Li et al (2003)N = 46, confirmed casesProspective study Pan et al (2003)N = 15, confirmed casesRetrospective study Ding et al (2004)N = 8 (4 confirmed cases, 4 control)Clinicopathologic study Yu et al (2006)N = 121, confirmed casesRetrospective study\nClinical features • Chest pain (10%)• ↑HR (46%) • No chest pain or overt CHF on admission• ↓HR (non-ICU) ↑HR (ICU)•CHF exacerbation • Sudden cardiac arrest (100%)• MI and arrhythmia (33%) • Chest pain • ↑HR (71.9%) (62.8%, 45.4%, 35.5%)\n• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)\n• Reversible cardiomegaly (10.7%), no clinical heart failure\n• Chest discomfort (7%)\n• Palpitations (4%)\nKey findings on investigations • ↓Ca++ (60%)\n• ↓K+ (26%)\n• ↓Mg++ (18%)\n• ↓P+ (27%)\n• ↑ LDH (87%) • ↑ CK\n• ↑ LDH\n• ↓Hb\n• EKG: RBBB\n• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK\n• ↑CK (26%) without TnI or CKMB\n• ↑ LDH\n• CXR or CT abnormality: 100%\nHistopathology N/A N/A N/A • Myocardial stromal edema\n• Infiltration of vessels by lymphocytes\n• Focal hyaline degeneration\n• Muscle fiber lysis N/A\nKey study findings and message • 20% ICU admission\n• 6.5% Case fatality rate (21 days)\n• Diabetes and other comorbidities independently associated with poor prognosis Possibly reversible subclinical diastolic impairment seen in SARS patients Proposed causes of SCD:• Hypoxemia leading to myocardial strain\n• Direct viral myocardial injury\n• Stress aggravates pre-existing disease\n• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal\n• 15% ICU admission\n• 18 (5) days mean duration of hospital stay\n• Tachycardia persists during follow up\n• Cardiac arrhythmia is uncommon\nMERS\nStudy Alhogbani (2016)N = 1 confirmed caseCase report Almekhlafi et al (2016)N = 31, confirmed casesRetrospective study Garout et al (2018)N = 52, confirmed casesRetrospective study\nClinical features CHF ↑HR (67.7%) Pericarditis\nKey findings on investigations • ↑ TnI\n• ↑ BNP\n• ↑ Creatinine\n• Echo: Severe global LV dysfunction\n• Cardiac MRI: Myocarditis N/A N/A\nKey study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)\n• 80.6% vasopressor support rate No association of ECMO need with outcomes\nCOVID-19\nStudy Huang et al (2020)N = 41, confirmed casesRetrospective study Wang et al (2020)N = 138, confirmed casesRetrospective study Zheng et al (2020)Review Bhatraju et al (2020)N = 24, confirmed casesRetrospective study Fried et al (2020)N = 4, confirmed casesCase reports\nClinical features • ↑BP\n• Acute cardiac injury (12%) more in ICU patients than non-ICU patients (31% vs. 4%) • Pre-existing HTN (31.2%) (58.3% in ICU, significant)\n• Pre-existing CVD (14.5%) (25% in ICU, significant)\n• Acute cardiac injury (7.2%) (22.2% in ICU, significant)\n• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations\n• Chest tightness • ↑HR (48%)\n• Vasopressor need (71%) • Myopericarditis\n• Decompensated heart failure\n• Cardiogenic Shock\nKey findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI\n• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations\n• Elevated cardiac enzymes\n• LVEF on echo\nKey Study findings and message ↑BP more common in ICU patients (P = 0.018) ICU patients more likely to have pre-existing hypertension, develop arrhythmias, acute cardiac injury (P \u003c 0.001) Proposed mechanism of cardiac injury:• ACE 2 related\n• Cytokine storm\n• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both\n• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients\nBNP, B-type natriuretic peptide; BP, blood pressure; HR, heart rate; CHF, congestive heart failure; CK, creatine kinase; CKMB, creatine kinase myocardial band; CXR; chest x-ray; ECMO, extracorporeal membrane oxygenation; Hb, hemoglobin; ICU, intensive care unit; LDH, lactate dehydrogenase; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MERS-CoV, middle east respiratory syndrome coronavirus; RBBB, right bundle branch block; SARS-COV, severe acute respiratory syndrome coronavirus; TnI, troponin-I."}