COVID-19-associated myocardial injury: Difference between revisions
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* A small number of patients have been reported to present primarily with [[COVID-19]] associated myocardial injury and minimal to no other [[pulmonary]]/systemic symptom | * A small number of patients have been reported to present primarily with [[COVID-19]] associated myocardial injury and minimal to no other [[pulmonary]]/systemic symptom | ||
**For [[chest pain]] differential diagnosis [[Chest pain differential diagnosis|Click here]] | **For [[chest pain]] differential diagnosis [[Chest pain differential diagnosis|Click here]] | ||
**For [[ | **For [[ACS]] differential diagnosis [[ACS|Click here]] | ||
**For [[Congestive heart failure|heart failure]] differential diagnosis [[Congestive heart failure|Click here]] | **For [[Congestive heart failure|heart failure]] differential diagnosis [[Congestive heart failure|Click here]] | ||
**For [[myocarditis]] differential diagnosis [[Myocarditis|Click here]] | **For [[myocarditis]] differential diagnosis [[Myocarditis|Click here]] | ||
Revision as of 17:42, 18 July 2020
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Main article: COVID-19
For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed rizvi, M.B.B.S[[2]]
Synonyms and Keywords: Novel coronavirus, COVID-19, Wuhan coronavirus, coronavirus disease-19, coronavirus disease 2019, SARS-CoV-2, COVID-19, COVID-19, 2019-nCoV, 2019 novel coronavirus, cardiovascular finding in COVID-19, myocardial injury in COVID-19, COVID-19-associated myocardial injury, SARS-CoV2-associated myocardial injury, COVID-19 myocardial injury.
Overview
Coronavirus disease 2019 (COVID-19) is a rapidly expanding global pandemic which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is associated with significant morbidity and mortality. It has been seen to cause myocardial injury, usually in patients requiring hospitalization with more severe SARS-CoV 2 infection. COVID-19 associated myocardial injury is a broad term that is used to describe any cause of myocardial tissue death induced by the SARS-CoV-2 virus. This includes acute coronary syndrome, cardiomyopathy and acute heart failure (with or without cardiogenic shock) and myocarditis. Diagnosis is largely based on elevated high sensitivity troponin I (hs-TnI) level of > 99th percentile of the upper limit of normal. The exact prevalence of COVID-19 associated myocardial injury is around 5000-38000 per 100,000 hospitalized individuals worldwide[1].
Historical Perspective
- COVID-19 (SARS-CoV-2) outbreak initiated and was discovered in December, 2019 in Wuhan, Hubei Province, China.
- January 30, 2020 - World Health Organization(WHO) declared the outbreak as a Public Health Emergency of International Concern.
- March 12, 2020 - WHO declared the COVID-19 outbreak a pandemic.
- January 2, 2020 - first observational study of 41 patients with COVID-19 pneumonia showed that 5 (12%) of the 41 patients had elevated hs-TnI ( high sensitivity troponin) level above the defined threshold (28 pg/ml) [2]
- To view the historical perspective of COVID-19, click here.
Classification
- There is no established system for the classification of Acute myocardial injury in COVID-19.
- To view the classification of COVID-19, click here.
A possible classification of COVID-19 associated myocardial injury is as follows:
- Vascular injury-induced myocardial death
- Macrovascular disease: Coronary artery thrombosis/plaque rupture
- Microvascular disease: microvascular thrombosis and hypercoagulability
- Direct myocardial tissue invasion associated injury
- Acute myocardial depression induced heart failure
- Myocarditis
Pathophysiology
The pathophysiology of COVID-19 acute myocardial injury depends on the underlying cause of myocardial tissue death. However, the overall trigger is an exaggerated inflammatory response (hyperinflammation) in response to viral infiltration into cells. SARS-CoV-2 virus gains entry via the ACE-2 (Angiotensin Converting Enzyme 2) receptor that is found abundantly in myocardial tissue and endothelium of blood vessels.
Proposed pathophysiological mechanisms of COVID-19 associated myocardial injury:
- SAQRS-CoV-2 down regulate ACE-2 expression and subsequent protective signaling pathways in cardiac myocytes
- Hyperinflammation and cytokine storm mediated through pathologic T-cells and monocytes leading to myocarditis[3]
- Respiratory failure and hypoxemia resulting in damage to cardiac myocytes[4]
- Hypercoagulability and development of coronary microvascular thrombosis[5]
- Diffuse endothelial injury and ‘endothelitis’ from direct cell invasion of SARS-CoV-2 and/or resulting from host inflammatory response.[6]
- Inflammation and/or stress causing coronary plaque rupture or supply-demand mismatch leading to myocardial ischemia/infarction.[7]
- Direct invasion of the cardiac tissue by COVID-19.[8]
Hyperinflammation and cytokine storm:
- Immune dysregulation, including T cell and immune signaling dysfunction, recognized as an important factor in the pathogenesis of vascular disease, may also adversely affect the body's response to SARS-CoV-2 infection[9]
- The role of CD4(+) CD25(+) FOXP3(+) regulatory T (TREG) cells in the modulation of inflammation and immunity has received increasing attention. Given the important role of TREG cells { T regulatory cells}) in the induction and maintenance of immune homeostasis and tolerance, dysregulation in the generation or function of TREG cells{ Regulatory T cells}) can trigger abnormal immune responses and lead to pathology.
- Evidence from experimental and clinical studies has indicated that TREG cells { Regulatory T cells})might have an important role in protecting against cardiovascular disease, in particular atherosclerosis and abdominal aortic aneurysm.
- The role of TREG cells is evident in the pathogenesis of a number of cardiovascular diseases, including atherosclerosis, hypertension, ischemic stroke, abdominal aortic aneurysm, Kawasaki disease, pulmonary arterial hypertension, myocardial infarction and remodelling, postischaemic neovascularization, myocarditis and dilated cardiomyopathy, and heart failure.[10]
Role of ACE-2 Receptor :
- ACE-2 is a membrane-bound aminopeptidate receptor expressed on the epithelial cells of the lungs, intestines, kidneys and blood vessels. It has important immune and cardiovascular roles. Angiotensin-converting enzyme (ACE) cleaves angiotensin I to generate angiotensin II (Ang II), which binds to and activates AT1R, thus promoting vasoconstriction.
- ACE-2 cleaves angiotensin II and generates angiotensin 1–7, a powerful vasodilator acting through Mas receptors
- SARS-CoV-2 has a spike protein receptor-binding domain, similar to SARS-CoV, which interacts with the ACE-2 receptor and acts as the primary functional receptor for pathogenicity and human-to-human transmission.[11] Furthermore, SARS-CoV-2 binding to ACE-2 leads to its down regulation and increases angiotensin II,a pro-inflammatory factor in the lung.
- This subsequently leads to lower amount of angiotensin 1–7. Thus loss of protective signaling pathway in cardiac myocytes. The detrimental effect of ACE-2 downregulation would impede cardioprotective effects of angiotensin 1–7 leading to increased TNFα production, other cytokines release that can result in acute respiratory distress syndrome, acute cardiac injury and multiorgan dysfunction.[12]
- To view the pathophysiology of COVID-19, click here
Causes
- Hypoxemia induced by Acute respiratory distress syndrome (ARDS)
- Hypercoagulability and plaque rupture
- Hyperinflammation and cytokine storm
- Direct invasion of the cardiac tissue by SARS-CoV-2
- Myocarditis and myocyte necrosis.
- To view causes of COVID-19, click here.
Differentiating COVID-19 associated Acute myocardial injury from other Diseases
- COVID-19 associated acute myocardial injury must be differentiated from other causes of myocardial injury not related to COVID-19 infection.
- The signs and symptoms of acute coronary syndrome, acute heart failure and myocarditis induced by COVID-19 cannot be differentiated from non-COVID-19 acute cardiac disease. Laboratory evaluation with hs-TnI, CK and LDH as well as EKG changes are similar and cannot differentiate between the two disease states
- All patients with COVID-19 induced myocardial injury must be PCR positive for SARS-CoV-2
- The majority of patients have other features of COVID-19, primarily fever, pneumonia and/or ARDS at initial presentation [13]
- A small number of patients have been reported to present primarily with COVID-19 associated myocardial injury and minimal to no other pulmonary/systemic symptom
- For chest pain differential diagnosis Click here
- For ACS differential diagnosis Click here
- For heart failure differential diagnosis Click here
- For myocarditis differential diagnosis Click here
- For the differential diagnosis of COVID-19, click here.
| COVID-19 associated AMI vs non COVID-19 AMI | ||
| Causes | Similar features | Features specific to COVID-19 |
| Acute coronary syndrome
- Type I & II MI |
Chest pain
Shortness of breath Elevated troponin I level Evidence of coronary occlusion by imaging/PCI |
Clinical evidence of SARS-CoV2 infection
- Fever - Cough - Dyspnea - Bilateral ground glass opacities on chest imaging (Patients may have nonspecific symptoms such as fatigue and malaise without specific symptoms of cardiac disease) |
| Acute Heart failure | Chest pain/pressure
Shortness of breath Elevated BNP Depressed ventricular function on echocardiography | |
| Myocarditis | Chest pain
Fatigue S3,S4 or summation gallop Elevated troponin I EKG abnormalities Absence of coronary occlusion | |
| AMI- acute myocardial injury; BNP – Brain Natriuretic peptide; MI – myocardial infarction; NSTEMI - non ST Elevation Myocardial Infarction; PCI – percutaneous intervention; STEMI - ST elevation Myocardial Infarction | ||
Epidemiology and Demographics
| Study | Site/
Location |
Sample size (n) | Age (years) | Pre-existing cardiac disease | Definition of myocardial injury used in study | Percent with myocardial injury |
| Huang et al [14] | Wuhan, China | 41 | Median 49.0 | 15% cardiovascular disease
15% hypertension |
Cardiac injury=troponin I above 99th percentile upper reference limit or new abnormalities on electrocardiography or echocardiography | 12 |
| Shi et al[15] | Wuhan, China | 416 | Median 64.0 (range 21.0–95.0) | 4% chronic heart failure
11% coronary heart disease 31% hypertension |
Cardiac injury=troponin I above 99th percentile upper reference limit, regardless of new abnormalities on electrocardiography or echocardiography | 19.7 |
| Zhou et al [16] | Wuhan, China | 191 | Median 56.0 | 8% coronary heart disease
30% hypertension |
Cardiac injury=high-sensitivity troponin I above 99th percentile upper reference limit or new abnormalities on electrocardiography or echocardiography | 17 |
| Guo et al[17] | Wuhan, China | 187 | Mean 58.5±14.7 | 4% cardiomyopathy
11% coronary heart disease 33% hypertension |
Myocardial injury=troponin T above 99th percentile upper reference limit | 27.8 |
| Wang et al [18] | Wuhan, China | 138 | Median 56.0 | 15% cardiovascular disease
31% hypertension |
Cardiac injury=troponin I above 99th percentile upper reference limit or new abnormalities on electrocardiography or echocardiography | 7.2 |
Incidence
- The incidence of COVID-19 associated myocardial injury has not been established yet.
Prevalence
- The prevalence of myocardial injury (as reflected by elevation in cardiac troponin levels) is variable among hospitalized patients with COVID-19 and its around 5000-38000 per 100,000 hospitalized individuals worldwide.[1]
- Reported frequencies of 5 to 38 percent [19] [20] [21]
- In a series of 416 patients with COVID-19 who were hospitalized in Wuhan, China, 19.7 percent had high-sensitivity troponin I (hs-TnI) above the 99th percentile upper reference limit on admission.[22]
Case-fatality rate/Mortality rate
- A summary of 44,672 COVID-19 cases documented by the Chinese Center for Disease Control and Prevention demonstrated a case fatality rate of 10.5% with comorbid CVD ( cardiovascular disease) compared to a 2.4% overall case fatality rate[23]
- The mortality rate was also higher in those with myocardial injury (51.2 versus 4.5 percent).[23]
Age
- Patients with this marker of myocardial injury were older and had more comorbidities (including chronic heart failure in 14.6 versus 1.5 percent), greater laboratory abnormalities (including higher levels of C-reactive protein, procalcitonin, and aspartate aminotransferase), more lung radiographic abnormalities, and more complications compared with those without myocardial injury.
Race
- As of June 12, 2020, age-adjusted hospitalization rates are highest among non-Hispanic American Indian or Alaska Native and non-Hispanic black persons, followed by Hispanic or Latino persons. CDC
- Non-Hispanic American Indian or Alaska Native persons have a rate approximately 5 times that of non-Hispanic white persons,
- non-Hispanic black persons have a rate approximately 5 times that of non-Hispanic white persons,
- Hispanic or Latino persons have a rate approximately 4 times that of non-Hispanic white persons
Gender
- .There is no data on gender predilection to acute myocardial injury in COVID-19.
Region
- COVID-19 is a pandemic.
Risk Factors
- A meta-analysis of 6 studies inclusive of 1,527 patients with COVID-19 examined the prevalence of cardiovascular disease (CVD) and reported the prevalence of hypertension, cardiac and cerebrovascular disease, and diabetes to be 17.1%, 16.4%, and 9.7%, respectively [24]
- To view the risk factors of COVID-19, click here.
Screening
- There is insufficient evidence to recommend routine screening for acute myocardial injury in COVID-19 patients.
- To view screening for COVID-19, click here.
Natural History, Complications, and Prognosis
Complications
- The disease also contributes to cardiovascular complications, including
Prognosis
- Prognosis of COVID-19 myocardial injury patients is generally poor.
- A retrospective analysis of the cause of death in Chinese patients infected with COVID-19 revealed that 40% of patients died at least in part because of myocardial injury and circulatory collapse.
- In another study, patients hospitalized for COVID-19 infection developed cardiac injury in roughly 20% of cases; thus leading to greater than 50% mortality.
- Older patients with preexisting cardiovascular comorbidities and diabetes are prone to develop a higher acuity of illness after contracting SARS-CoV-2 associated with higher risk of myocardial injury and a markedly higher short-term mortality rate.[25]
- To view natural history, complications, and prognosis of COVID-19, click here.
Diagnosis
| Initial evaluation of suspected acute myocardial injury in COVID-19 |
| History |
|
| Physical exam |
|
| EKG changes |
| Laboratory evaluation |
|
| Imaging studies |
For diagnosing of chest pain Click here
History and Symptoms
- Patients with COVID-19 present with the typical symptoms and signs of SARS-CoV-2 infection such as fever, cough, dyspnea. Acute myocardial injury in COVID-19 presents similar to non COVID-19 realted ACS and heart failure. [26] [27]
- For ACS sign and symptoms please Click here
- For Heart failure sign and symptoms please Click here
- To view the history and symptoms of COVID-19, click here.
Physical Examination
- To view the complete physical examination in COVID-19, click here.
- To view physical exam of ACS Click here
- To view physical exam of Heart failure Click here
Laboratory Findings
- Cardiac Biomarkers:
- The upper reference limit for the high-sensitivity troponin I (hs-TnI) test (0.04ng/mL), based on the 99th percentile of measurements reported in healthy population without the occlusion of coronary arteries.[28][29]
- In the recently published retrospective study of 191 COVID-19 patients from two separate hospitals in China, the incidence of elevation in high-sensitivity cardiac troponin I (cTnI) (>28 pg/ml) was 17%, and it was significantly higher among non-survivors (46% versus 1%, p<0.001).
- Furthermore, elevation of this biomarker was noted to be a predictor of in-hospital death (univariable OR 80.07, 95% CI [10.34–620.36], p<0.0001). The most abrupt increase in cTnI in non-survivors was noted beyond day 16 after the onset of disease. In the same study, the incidence of acute cardiac injury was 17% among all-comers, but significantly higher among non-survivors (59% versus 1%, p<0.0001).[30]
- CK-MB >2.2 ng/mL
- Guo et al11 provide additional novel insights that TnT levels are significantly associated with levels of C-reactive protein and N-terminal pro-B-type natriuretic peptide (NT-proBNP), thus linking myocardial injury to severity of inflammation and ventricular dysfunction[31]
Inflammatory biomarkers:
- Elevated levels of inflammatory markers including erythrocyte sedimentation rate, C reactive protein, and procalcitonin are usually seen in myocarditis but they are non-specific and do not confirm the diagnosis. Increases levels of Interleukin-6 (IL-6), d-dimer, serum ferritin, prothrombin time were seen in COVID-19 patients.
- To view the laboratory findings on COVID-19, click here.
Electrocardiogram
- The electrocardiogram (ECG) can demonstrate a range of findings
- In some cases mimicking acute coronary syndrome (ACS).
- The ECG abnormalities result from myocardial inflammation and include non-specific ST segment-T wave abnormalities.
- T wave inversion.
- PR segment and ST segment deviations (depression and elevation)
- The ECG can help to find previous cardiac abnormalities and triggering factors, such as acute myocardial infarction, and arrhythmias.
- To view the electrocardiogram findings of ACS Click here
- To view the electrocardiogram findings heart failure Click here
- To view the electrocardiogram findings on COVID-19, click here.
X-ray
- There are no specific X-ray findings in COVID-19 associated myocardial injury.
- To view the x-ray finidings on COVID-19, click here.
Ultrasound/Echocardiography
- There are no specific ultrasound/ echocardiographic findings related to COVID-19-associated acute myocardial injury
- To view the echocardiographic findings on COVID-19, click here.
CT Scan
- There are no specific CT scan findings related to COVID-19-associated acute myocardial injury.
- To view the CT scan findings on COVID-19, click here.
MRI
- There are no specific MRI findings related to COVID-19-associated acute myocardial injury.
- To view the MRI findings on COVID-19, click here.
Other Imaging Findings
- There are no other imaging findings related to COVID-19-associated acute myocardial injury.
- To view other imaging findings on COVID-19, click here.
Other Diagnostic Findings
- There are no other diagnostic studies related to COVID-19-associated acute myocardial injury.
- To view other diagnostic studies for COVID-19, click here.
Treatment
Medical Therapy
- There are no specific treatments, and treatment varies depending upon presentation, please click on the conditions to see the management.
- (COVID-19-associated myocarditis
- COVID-19-associated myocardial infarction
- COVID-19-associated heart failure
- COVID-19-associated arrhythmia and conduction system disease
- COVID-19-associated cardiogenic shock
- COVID-19-associated cardiac arrest
- COVID-19-associated pericarditis
- COVID-19-associated spontaneous coronary artery dissection
- To view medical treatment for COVID-19, click here.
Surgery
- There is no established surgical intervention for the treatment of COVID-19-associated acute myocardial injury.
Primary Prevention
- There are no available vaccines against COVID-19 and studies are going on for finding an effective vaccine.
- Other primary prevention strategies include measures to reduce the occurrence of myocardial injury among COVID-19 patients. Recent studies have suggested the use of medications improving microcirculation, especially for the high-risk group such as males, smokers, diabetic patients, and patients with established cardiovascular disease comorbidities.[32]
- For Risk factors associated with COVID-19 please click here
Secondary Prevention
- There are no established measures for the secondary prevention of COVID-19-associated myocardial injury.
References
- ↑ 1.0 1.1 Bavishi C, Bonow RO, Trivedi V, Abbott JD, Messerli FH, Bhatt DL (June 2020). "Acute myocardial injury in patients hospitalized with COVID-19 infection: A review". Prog Cardiovasc Dis. doi:10.1016/j.pcad.2020.05.013. PMC 7274977 Check
|pmc=value (help). PMID 32512122 Check|pmid=value (help). - ↑ Huang, Chaolin; Wang, Yeming; Li, Xingwang; Ren, Lili; Zhao, Jianping; Hu, Yi; Zhang, Li; Fan, Guohui; Xu, Jiuyang; Gu, Xiaoying; Cheng, Zhenshun; Yu, Ting; Xia, Jiaan; Wei, Yuan; Wu, Wenjuan; Xie, Xuelei; Yin, Wen; Li, Hui; Liu, Min; Xiao, Yan; Gao, Hong; Guo, Li; Xie, Jungang; Wang, Guangfa; Jiang, Rongmeng; Gao, Zhancheng; Jin, Qi; Wang, Jianwei; Cao, Bin (2020). "Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China". The Lancet. 395 (10223): 497–506. doi:10.1016/S0140-6736(20)30183-5. ISSN 0140-6736.
- ↑ Wei, Haiming; Xu, Xiaoling; Tian, Zhigang; Sun, Rui; Qi, Yingjie; Zhao, Changcheng; Wang, Dongsheng; Zheng, Xiaohu; Fu, Binqing; Zhou, Yonggang (2020). "Pathogenic T-cells and inflammatory monocytes incite inflammatory storms in severe COVID-19 patients". National Science Review. 7 (6): 998–1002. doi:10.1093/nsr/nwaa041. ISSN 2095-5138.
- ↑ Kubasiak, L. A.; Hernandez, O. M.; Bishopric, N. H.; Webster, K. A. (2002). "Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3". Proceedings of the National Academy of Sciences. 99 (20): 12825–12830. doi:10.1073/pnas.202474099. ISSN 0027-8424.
- ↑ Han, Huan; Yang, Lan; Liu, Rui; Liu, Fang; Wu, Kai-lang; Li, Jie; Liu, Xing-hui; Zhu, Cheng-liang (2020). "Prominent changes in blood coagulation of patients with SARS-CoV-2 infection". Clinical Chemistry and Laboratory Medicine (CCLM). 58 (7): 1116–1120. doi:10.1515/cclm-2020-0188. ISSN 1437-4331.
- ↑ Tavazzi, Guido; Pellegrini, Carlo; Maurelli, Marco; Belliato, Mirko; Sciutti, Fabio; Bottazzi, Andrea; Sepe, Paola Alessandra; Resasco, Tullia; Camporotondo, Rita; Bruno, Raffaele; Baldanti, Fausto; Paolucci, Stefania; Pelenghi, Stefano; Iotti, Giorgio Antonio; Mojoli, Francesco; Arbustini, Eloisa (2020). "Myocardial localization of coronavirus in COVID‐19 cardiogenic shock". European Journal of Heart Failure. 22 (5): 911–915. doi:10.1002/ejhf.1828. ISSN 1388-9842.
- ↑ Zhou, Fei; Yu, Ting; Du, Ronghui; Fan, Guohui; Liu, Ying; Liu, Zhibo; Xiang, Jie; Wang, Yeming; Song, Bin; Gu, Xiaoying; Guan, Lulu; Wei, Yuan; Li, Hui; Wu, Xudong; Xu, Jiuyang; Tu, Shengjin; Zhang, Yi; Chen, Hua; Cao, Bin (2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". The Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. ISSN 0140-6736.
- ↑ Tavazzi, Guido; Pellegrini, Carlo; Maurelli, Marco; Belliato, Mirko; Sciutti, Fabio; Bottazzi, Andrea; Sepe, Paola Alessandra; Resasco, Tullia; Camporotondo, Rita; Bruno, Raffaele; Baldanti, Fausto; Paolucci, Stefania; Pelenghi, Stefano; Iotti, Giorgio Antonio; Mojoli, Francesco; Arbustini, Eloisa (2020). "Myocardial localization of coronavirus in COVID‐19 cardiogenic shock". European Journal of Heart Failure. 22 (5): 911–915. doi:10.1002/ejhf.1828. ISSN 1388-9842.
- ↑ Meng, Xiao; Yang, Jianmin; Dong, Mei; Zhang, Kai; Tu, Eric; Gao, Qi; Chen, Wanjun; Zhang, Cheng; Zhang, Yun (2015). "Regulatory T cells in cardiovascular diseases". Nature Reviews Cardiology. 13 (3): 167–179. doi:10.1038/nrcardio.2015.169. ISSN 1759-5002.
- ↑ Meng, Xiao; Yang, Jianmin; Dong, Mei; Zhang, Kai; Tu, Eric; Gao, Qi; Chen, Wanjun; Zhang, Cheng; Zhang, Yun (2015). "Regulatory T cells in cardiovascular diseases". Nature Reviews Cardiology. 13 (3): 167–179. doi:10.1038/nrcardio.2015.169. ISSN 1759-5002.
- ↑ Wan, Yushun; Shang, Jian; Graham, Rachel; Baric, Ralph S.; Li, Fang; Gallagher, Tom (2020). "Receptor Recognition by the Novel Coronavirus from Wuhan: an Analysis Based on Decade-Long Structural Studies of SARS Coronavirus". Journal of Virology. 94 (7). doi:10.1128/JVI.00127-20. ISSN 0022-538X.
- ↑ Zhou, Peng; Yang, Xing-Lou; Wang, Xian-Guang; Hu, Ben; Zhang, Lei; Zhang, Wei; Si, Hao-Rui; Zhu, Yan; Li, Bei; Huang, Chao-Lin; Chen, Hui-Dong; Chen, Jing; Luo, Yun; Guo, Hua; Jiang, Ren-Di; Liu, Mei-Qin; Chen, Ying; Shen, Xu-Rui; Wang, Xi; Zheng, Xiao-Shuang; Zhao, Kai; Chen, Quan-Jiao; Deng, Fei; Liu, Lin-Lin; Yan, Bing; Zhan, Fa-Xian; Wang, Yan-Yi; Xiao, Geng-Fu; Shi, Zheng-Li (2020). "A pneumonia outbreak associated with a new coronavirus of probable bat origin". Nature. 579 (7798): 270–273. doi:10.1038/s41586-020-2012-7. ISSN 0028-0836.
- ↑ Zheng YY, Ma YT, Zhang JY, Xie X (May 2020). "COVID-19 and the cardiovascular system". Nat Rev Cardiol. 17 (5): 259–260. doi:10.1038/s41569-020-0360-5. PMC 7095524 Check
|pmc=value (help). PMID 32139904 Check|pmid=value (help). - ↑ Huang, Chaolin; Wang, Yeming; Li, Xingwang; Ren, Lili; Zhao, Jianping; Hu, Yi; Zhang, Li; Fan, Guohui; Xu, Jiuyang; Gu, Xiaoying; Cheng, Zhenshun; Yu, Ting; Xia, Jiaan; Wei, Yuan; Wu, Wenjuan; Xie, Xuelei; Yin, Wen; Li, Hui; Liu, Min; Xiao, Yan; Gao, Hong; Guo, Li; Xie, Jungang; Wang, Guangfa; Jiang, Rongmeng; Gao, Zhancheng; Jin, Qi; Wang, Jianwei; Cao, Bin (2020). "Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China". The Lancet. 395 (10223): 497–506. doi:10.1016/S0140-6736(20)30183-5. ISSN 0140-6736.
- ↑ Shi S, Qin M, Shen B, Cai Y, Liu T, Yang F, Gong W, Liu X, Liang J, Zhao Q, Huang H, Yang B, Huang C (March 2020). "Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China". JAMA Cardiol. doi:10.1001/jamacardio.2020.0950. PMC 7097841 Check
|pmc=value (help). PMID 32211816 Check|pmid=value (help). - ↑ Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z, Xiang J, Wang Y, Song B, Gu X, Guan L, Wei Y, Li H, Wu X, Xu J, Tu S, Zhang Y, Chen H, Cao B (March 2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. PMC 7270627 Check
|pmc=value (help). PMID 32171076 Check|pmid=value (help). - ↑ Guo, Tao; Fan, Yongzhen; Chen, Ming; Wu, Xiaoyan; Zhang, Lin; He, Tao; Wang, Hairong; Wan, Jing; Wang, Xinghuan; Lu, Zhibing (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiology. doi:10.1001/jamacardio.2020.1017. ISSN 2380-6583.
- ↑ Wang, Dawei; Hu, Bo; Hu, Chang; Zhu, Fangfang; Liu, Xing; Zhang, Jing; Wang, Binbin; Xiang, Hui; Cheng, Zhenshun; Xiong, Yong; Zhao, Yan; Li, Yirong; Wang, Xinghuan; Peng, Zhiyong (2020). "Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China". JAMA. 323 (11): 1061. doi:10.1001/jama.2020.1585. ISSN 0098-7484.
- ↑ Bavishi C, Bonow RO, Trivedi V, Abbott JD, Messerli FH, Bhatt DL (June 2020). "Acute myocardial injury in patients hospitalized with COVID-19 infection: A review". Prog Cardiovasc Dis. doi:10.1016/j.pcad.2020.05.013. PMC 7274977 Check
|pmc=value (help). PMID 32512122 Check|pmid=value (help). - ↑ Shi S, Qin M, Shen B, Cai Y, Liu T, Yang F, Gong W, Liu X, Liang J, Zhao Q, Huang H, Yang B, Huang C (March 2020). "Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China". JAMA Cardiol. doi:10.1001/jamacardio.2020.0950. PMC 7097841 Check
|pmc=value (help). PMID 32211816 Check|pmid=value (help). - ↑ Lippi G, Lavie CJ, Sanchis-Gomar F (March 2020). "Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): Evidence from a meta-analysis". Prog Cardiovasc Dis. doi:10.1016/j.pcad.2020.03.001. PMC 7127395 Check
|pmc=value (help). PMID 32169400 Check|pmid=value (help). - ↑ Shi S, Qin M, Shen B, Cai Y, Liu T, Yang F, Gong W, Liu X, Liang J, Zhao Q, Huang H, Yang B, Huang C (March 2020). "Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China". JAMA Cardiol. doi:10.1001/jamacardio.2020.0950. PMC 7097841 Check
|pmc=value (help). PMID 32211816 Check|pmid=value (help). - ↑ 23.0 23.1 Bodini G, Demarzo MG, Casagrande E, De Maria C, Kayali S, Ziola S, Giannini EG (May 2020). "Concerns related to COVID-19 pandemic among patients with inflammatory bowel disease and its influence on patient management". Eur. J. Clin. Invest. 50 (5): e13233. doi:10.1111/eci.13233. PMC 7235524 Check
|pmc=value (help). PMID 32294238 Check|pmid=value (help). - ↑ Li, Bo; Yang, Jing; Zhao, Faming; Zhi, Lili; Wang, Xiqian; Liu, Lin; Bi, Zhaohui; Zhao, Yunhe (2020). "Prevalence and impact of cardiovascular metabolic diseases on COVID-19 in China". Clinical Research in Cardiology. 109 (5): 531–538. doi:10.1007/s00392-020-01626-9. ISSN 1861-0684.
- ↑ Guo, Tao; Fan, Yongzhen; Chen, Ming; Wu, Xiaoyan; Zhang, Lin; He, Tao; Wang, Hairong; Wan, Jing; Wang, Xinghuan; Lu, Zhibing (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiology. doi:10.1001/jamacardio.2020.1017. ISSN 2380-6583.
- ↑ Wu, Zunyou; McGoogan, Jennifer M. (2020). "Characteristics of and Important Lessons From the Coronavirus Disease 2019 (COVID-19) Outbreak in China". JAMA. 323 (13): 1239. doi:10.1001/jama.2020.2648. ISSN 0098-7484.
- ↑ Ruan, Qiurong; Yang, Kun; Wang, Wenxia; Jiang, Lingyu; Song, Jianxin (2020). "Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China". Intensive Care Medicine. 46 (5): 846–848. doi:10.1007/s00134-020-05991-x. ISSN 0342-4642.
- ↑ Driggin, Elissa; Madhavan, Mahesh V.; Bikdeli, Behnood; Chuich, Taylor; Laracy, Justin; Biondi-Zoccai, Giuseppe; Brown, Tyler S.; Der Nigoghossian, Caroline; Zidar, David A.; Haythe, Jennifer; Brodie, Daniel; Beckman, Joshua A.; Kirtane, Ajay J.; Stone, Gregg W.; Krumholz, Harlan M.; Parikh, Sahil A. (2020). "Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the COVID-19 Pandemic". Journal of the American College of Cardiology. 75 (18): 2352–2371. doi:10.1016/j.jacc.2020.03.031. ISSN 0735-1097.
- ↑ Li, Dongze; Chen, You; Jia, Yu; Tong, Le; Tong, Jiale; Wang, Wei; Liu, Yanmei; Wan, Zhi; Cao, Yu; Zeng, Rui (2020). "SARS-CoV-2-Induced Immune Dysregulation and Myocardial Injury Risk in China: Insights from the ERS-COVID-19 Study". Circulation Research. doi:10.1161/CIRCRESAHA.120.317070. ISSN 0009-7330.
- ↑ Zhou, Fei; Yu, Ting; Du, Ronghui; Fan, Guohui; Liu, Ying; Liu, Zhibo; Xiang, Jie; Wang, Yeming; Song, Bin; Gu, Xiaoying; Guan, Lulu; Wei, Yuan; Li, Hui; Wu, Xudong; Xu, Jiuyang; Tu, Shengjin; Zhang, Yi; Chen, Hua; Cao, Bin (2020). "Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study". The Lancet. 395 (10229): 1054–1062. doi:10.1016/S0140-6736(20)30566-3. ISSN 0140-6736.
- ↑ Guo, Tao; Fan, Yongzhen; Chen, Ming; Wu, Xiaoyan; Zhang, Lin; He, Tao; Wang, Hairong; Wan, Jing; Wang, Xinghuan; Lu, Zhibing (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiology. doi:10.1001/jamacardio.2020.1017. ISSN 2380-6583.
- ↑ Montone, Rocco A; Iannaccone, Giulia; Meucci, Maria Chiara; Gurgoglione, Filippo; Niccoli, Giampaolo (2020). "Myocardial and Microvascular Injury Due to Coronavirus Disease 2019". European Cardiology Review. 15. doi:10.15420/ecr.2020.22. ISSN 1758-3764.
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