SARS-CoV
Hepatitis 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
Table 2 Cardiovascular manifestations of SARS-CoV, MERS-CoV and COVID-19.
SARS (only studies with large study population included)
Study 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
Clinical 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%)
• ↓BP (50.4%) (28.1%, 21.5%, 14.8% during the first, second, third week)↓HR, transient (14.9%)
• Reversible cardiomegaly (10.7%), no clinical heart failure
• Chest discomfort (7%)
• Palpitations (4%)
Key findings on investigations • ↓Ca++ (60%)
• ↓K+ (26%)
• ↓Mg++ (18%)
• ↓P+ (27%)
• ↑ LDH (87%) • ↑ CK
• ↑ LDH
• ↓Hb
• EKG: RBBB
• Echo: ↓LVEF • Abnormal cardiac enzymes (66%) N/A • ↑ CK
• ↑CK (26%) without TnI or CKMB
• ↑ LDH
• CXR or CT abnormality: 100%
Histopathology N/A N/A N/A • Myocardial stromal edema
• Infiltration of vessels by lymphocytes
• Focal hyaline degeneration
• Muscle fiber lysis N/A
Key study findings and message • 20% ICU admission
• 6.5% Case fatality rate (21 days)
• 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
• Direct viral myocardial injury
• Stress aggravates pre-existing disease
• Sympathetic response causing electrical myocardial instability ACE2 expressed in heart, but virus not detected • ↑CK likely due to myositis as cardiac enzymes normal
• 15% ICU admission
• 18 (5) days mean duration of hospital stay
• Tachycardia persists during follow up
• Cardiac arrhythmia is uncommon
MERS
Study 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
Clinical features CHF ↑HR (67.7%) Pericarditis
Key findings on investigations • ↑ TnI
• ↑ BNP
• ↑ Creatinine
• Echo: Severe global LV dysfunction
• Cardiac MRI: Myocarditis N/A N/A
Key study findings and message MERS-CoV may cause myocarditis and acute heart failure • Vasopressor need is a risk factor for death (P = 0.04)
• 80.6% vasopressor support rate No association of ECMO need with outcomes
COVID-19
Study 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
Clinical features • ↑BP
• 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)
• Pre-existing CVD (14.5%) (25% in ICU, significant)
• Acute cardiac injury (7.2%) (22.2% in ICU, significant)
• Arrhythmia (16.7%) (44.4% in ICU patients) • Palpitations
• Chest tightness • ↑HR (48%)
• Vasopressor need (71%) • Myopericarditis
• Decompensated heart failure
• Cardiogenic Shock
Key findings on investigations • ↑ TnI (12%) (31% in ICU patients, 4% in non-ICU patients) • ↑ TnI
• ↑ CK-MB N/A • ↑ TnI (15%) • Diffuse ST segment elevations
• Elevated cardiac enzymes
• LVEF on echo
Key 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 < 0.001) Proposed mechanism of cardiac injury:• ACE 2 related
• Cytokine storm
• Hypoxemia • ICU admission most commonly due to hypoxemic respiratory failure, vasopressor requirement or both
• 50% mortality • Similar symptoms in heart transplant patients as nontransplant patients
BNP, 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.