Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Ver. Summary Created by Modification Content Size Created at Operation
1 + 2016 word(s) 2016 2021-09-18 10:28:29 |
2 format correct Meta information modification 2016 2021-09-23 02:33:06 |

Video Upload Options

Do you have a full video?


Are you sure to Delete?
If you have any further questions, please contact Encyclopedia Editorial Office.
Reiss, A.B.; Dayaramani, C.; De Leon, J. Cardiovascular Disease Complicating COVID-19. Encyclopedia. Available online: (accessed on 05 December 2023).
Reiss AB, Dayaramani C, De Leon J. Cardiovascular Disease Complicating COVID-19. Encyclopedia. Available at: Accessed December 05, 2023.
Reiss, Allison B., Christopher Dayaramani, Joshua De Leon. "Cardiovascular Disease Complicating COVID-19" Encyclopedia, (accessed December 05, 2023).
Reiss, A.B., Dayaramani, C., & De Leon, J.(2021, September 22). Cardiovascular Disease Complicating COVID-19. In Encyclopedia.
Reiss, Allison B., et al. "Cardiovascular Disease Complicating COVID-19." Encyclopedia. Web. 22 September, 2021.
Cardiovascular Disease Complicating COVID-19

Cardiovascular disease (CVD) is the leading cause of death worldwide. Its incidence increases sharply with age, and the elderly bear a disproportionate burden of CVD morbidity and mortality. Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2), has also caused significant mortality, specifically amongst the elderly, who are the most likely patient population to be hospitalized and die from the infection. Pre-existing CVD is a known risk factor for poor outcome in Covid-19 patients and, in our efforts to preserve life, attention must be paid to the adverse impact of the virus on the cardiovascular system. The emergence of novel SARS-CoV-2 pathogenic variants with greater transmissibility is prolonging the pandemic and sustaining the threat to life and health. An understanding of the pathogenic mechanisms that underlie the CVD-Covid-19 interaction can lead to improved treatment and reduced sequelae in the midst of this global health crisis.

COVID-19 atherosclerosis cardiovascular disease hypertension inflammation cytokines

1. Introduction

Cardiovascular disease (CVD) is the leading cause of death worldwide [1][2]. Its incidence increases sharply with age, and the elderly bear a disproportionate burden of CVD morbidity and mortality [3][4][5]. Severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2), the causal agent of Coronavirus disease 2019 (COVID-19), has a single-stranded RNA genome. It is able to invade cells through attachment of the spike (S) protein to the angiotensin-converting enzyme 2 (ACE2) receptor. This highly infectious virus has spread globally, causing significant mortality. A poor prognosis is observed amongst the elderly who are the most likely patient population to be hospitalized and die from the infection [6][7][8].

Factors that likely contribute to a complicated course and higher death rate in COVID-19 patients with underlying CVD are the hypercoagulable state that can result from COVID-19 infection, as well as polypharmacy (an indicator of comorbidities) [9][10][11][12]. Furthermore, the pandemic can disrupt lifestyle, leading to poorer diet and inactivity [13]. Another obstacle for older CVD patients is the avoidance of medical care from fear of contracting COVID-19. Hypertension, diabetes, and obesity, which often accompany CVD, are themselves established risk factors for severe COVID-19 that require careful management [14]. There is also a higher prevalence of cancer within the elderly population [15]. In addition to being immunocompromised from the cancer itself, cancer patients are frequently treated with immunosuppressants and cardiotoxic chemotherapies, making them especially susceptible to both viral illnesses and secondary cardiovascular complications. A particularly high risk of poor outcome is seen in those who have undergone recent bone marrow or stem cell transplantation and those exposed to poly ADP ribose polymerase (PARP) inhibitors [16][17]. The aforementioned conditions are more prevalent in those over age 65 and extremely common in those over age 85. Low vitamin D levels, common in the obese state, may add further risk [18].

Excess production of cytokines and cytokine storms are central to many of the sequelae of COVID-19, including damage to the cardiovascular system via pathways that involve direct cardiotoxicity and through inflammation-induced myocarditis and pericarditis [19][20]. The effects of cytokines, particularly of interleukin (IL)-6, will be discussed in the sections to follow.

Since persons with CVD are susceptible to poor COVID-19 outcomes, targeted treatment and removal of barriers to care are crucial for this population [21]. These may include the use of telemedicine, adjusting antihypertensive regimens, and online activity tracking.

2. Coagulopathy in COVID-19: Mechanisms, Manifestations, and Treatment

A state of hypercoagulability frequently accompanies COVID-19, especially in severe disease [22][23]. Coagulopathy leaves patients vulnerable to thrombotic complications, including venous thromboembolism, pulmonary embolism, and disseminated intravascular coagulation [24][25][26][27][28].
Pro-inflammatory mediators produced during COVID-19 infection cause the release of tissue factor, an initiator of blood coagulation, from mononuclear cells [29][30]. IL-6, a key mediator elevated in the COVID-19 setting, can raise tissue factor levels and may also stimulate platelet production in bone marrow and lungs [31][32][33]. The panoply of inflammatory factors also activates endothelial cells, increasing their expression of adhesion molecules and leading to the release of the von Willebrand factor, thus promoting a procoagulant endothelial phenotype, excessive activity in the coagulation cascade, and multiple thrombotic complications.
Coagulation abnormalities are detected in laboratory tests as increased serum concentrations of the procoagulants fibrinogen and D-dimers as well as decreased antithrombin and prolonged prothrombin time (Table 1) [34][35].
Table 1. Early Markers Associated with Poor Outcomes in COVID-19 Patients.
Marker Mean Level Time of Measurement Definition of Poor Outcome Reference
IL-6 7.39 pg/mL On admission ARDS [20]
Fibrinogen 5.16 g/L On admission Death [26]
D-dimer ≥1 µg/mL Outpatient Death [32]
LDH 445 µg/mL On admission Ventilation [34]
CAC score ≥400 During hospitalization Death [36]
CRP >40 mg/L On admission Death/ARDS [37]
Ferritin >950 ng/L On admission ARDS [38]
ARDS: acute respiratory distress syndrome; CAC: coronary artery calcium; CRP: C-reactive protein; LDH: lactate dehydrogenase; IL-6: interleukin-6.
As a result of vascular injury, the propeptide fibrinogen is cleaved to fibrin, and high circulating fibrin levels are common in the early phase of COVID-19 infection. Either hyper- or hypofibrinolysis can occur in the setting of COVID-19, with hyperfibrinolysis causing susceptibility to bleeding and hypofibrinolysis creating susceptibility to thrombus formation [39]. The hypofibrinolytic state may be attributed to the elevated production of plasminogen activator inhibitor 1 (PAI-1) by epithelial and endothelial cells in the inflamed lung [40]. D-dimers, produced during the degradation of crosslinked fibrin, are below 0.5 μg/mL under normal physiologic conditions. An increase in fibrinogen and D-dimers is associated with the risk of microthrombus formation in COVID-19 patients and subsequent emboli and/or organ failure [41][42]. Fibrinogen levels were, on average, higher in patients who developed severe versus less severe illness (5.16 vs. 4.51 g/L) [43]. D-dimer levels over 1 μg/mL can identify patients with poorer prognoses early in the course of disease and may signal the need for admission to critical care. Elevated D-dimer appears to be an independent risk factor for death [43][44]. In evaluating D-dimer levels, the implementation of age adjustment instead of a fixed cutoff may increase the accuracy of clinical assessment [45].
Sepsis-induced coagulopathy due to COVID-19 infection can lead to thrombotic stroke and myocardial infarction (MI) [46][47][48][49]. Losartan, previously mentioned for its ability to normalize levels of ACE2, is believed to be protective against strokes, offering another reason for its use in place of ACEIs [50].
Addressing the hypercoagulability risk at all levels of COVID-19 severity and in different age groups is challenging. Hypercoagulability may worsen in the setting of this pandemic via decreased activity, decreased exercise, and less movement in general under quarantine restrictions. Particularly affected are the elderly, with more limited movement capability due to age and co-morbidities. Venous stasis that accompanies inactivity, combined with hypercoagulability, sets the stage for two of three predisposing factors described in Virchow’s triad for vascular thrombosis (blood flow alterations, endothelial injury, and hypercoagulability) [51]. Hypertension predisposes to endothelial injury, the last remaining factor in Virchow’s triad. As discussed above, ACEIs should be used cautiously in COVID-19 patients. Anti-inflammatory drugs, cytokine inhibitors, and statins may be considered to protect the endothelium while simultaneously working against viral replication. Thromboprophylaxis with low molecular weight heparin could decrease D-dimer levels, and heparin can decrease fibrosis in those suffering from COVID-19-induced ARDS [43]. At this time, there are different approaches to coagulopathy in the field, with the evaluation of efficacy still ongoing. We await the results of major clinical trials regarding the dosage, class, and timeline of the use of anticoagulation therapy [52].

3. Myocardial Injury: Subclinical Atherosclerosis and Acute Coronary Syndrome

COVID-19 cardiac manifestations may include myocarditis, cardiac arrhythmias, and new or worsening heart failure, which may be particularly damaging to patients with a history of CVD [53][54]. The mechanisms underlying cardiac injury may be multifactorial ( Figure 1 ). Inflammation and thrombosis are known culprits [55]. Infection increases overall metabolic demand and heart rate. This intensifies oxygen expenditure while shortening the filling time in the diastole and limiting coronary perfusion. Infection-mediated vasoconstriction and ventilation/perfusion mismatch negatively affecting blood oxygenation can exacerbate the oxygen deficit, leading to myocardial ischemia [56][57]. Internalized virus loads within cardiomyocytes may directly damage the heart.

Figure 1. Factors contributing to cardiovascular damage in COVID-19. The white text in blue bubbles represents some of the pathologies that are associated with CVD in patients with COVID-19. Arrows are drawn from each factor to the central image of the heart and associated vasculature to emphasize their effect on the cardiovascular system specifically. CAC—Coronary Artery Calcium score; IL-6: interleukin-6; CVD: cardiovascular disease.

Immune-inflammatory-mediated injury to the heart from COVID-19 is more likely in severe cases and in those with high blood pressure and can be monitored via the release of certain injury biomarkers, including cardiac-specific troponin and creatine kinase-MB [58][59][60][61]. Elevated lactate dehydrogenase (LDH) may be of cardiac origin but is nonspecific and can result from damage to other organs [62]. In COVID-19, LDH may be released from the lung since this is a key site for inflammatory processes [63]. LDH levels above 445 μg/mL on admission can be predictive of more severe COVID-19 [46][64][65][66]. An analysis of 353 COVID-19 patients, 79 (22.4%) of whom presented with myocardial injury, revealed more frequent elevations in LDH (mean level: 244 U/L (without MI) vs. 655 U/L (with MI) and creatinine (71 μmol/L (without MI) vs. 155 μmol/L (with MI) in the MI group during their hospitalization [67]. In addition to acute MI, differential diagnoses for increased serum cardiac biomarkers include stress-induced cardiomyopathy as well as myocarditis [68][69][70].

Evidence is accumulating that cardiac injury combined with COVID-19 infection, whether the myocardial injury is pre-existing or occurs during the infection, is associated with poorer outcomes [71][72][73]. A prospective, multicenter cohort study in Spain found that in patients with acute MI, COVID-19 is an independent risk factor for in-hospital mortality [74]. A small study of 77 COVID-19 patients who died in Wuhan, China, in early 2020 found that heart disease was present in 32%, and heart disease patients were more likely to be in the short-term survival group and to die within 14 days of COVID-19 onset [66].

Subclinical atherosclerosis can impact the course of COVID-19. Coronary artery calcification (CAC), a specific imaging marker of coronary atherosclerosis that correlates with the plaque burden, can reveal previously undiagnosed CVD in COVID-19 patients [75]. In a cross-sectional study of 209 consecutively admitted COVID-19 patients without known CVD, assessed for CAC, CAC was detected in 106 (Table 1) (50.7%). Half of those positive patients required mechanical ventilation, extracorporeal membrane oxygenation, or died, whereas only 17.5% of patients negative for CAC had such poor outcomes [76]. A separate study by Nai Fovino et al. from Italy also found that high CAC as a surrogate for subclinical atherosclerosis was a marker for worse outcomes [77]. In this study, 75% of patients with high CAC either died or were admitted to the ICU, in contrast with only 20% of the group with lower CAC scores. Patients with a high score were also more likely to experience an MI.

4. Summary and Conclusions

There is frequent involvement of the cardiovascular system in COVID-19 and this presents a particular danger in the elderly who are likely to have multiple heart-related comorbidities such as diabetes, hypertension and hyperlipidemia [1][2]. The cardiovascular manifestations most commonly associated with COVID-19 infection are thromboembolic events, sepsis-related coagulopathy, cardiac arrhythmias, myocardial infarction, heart failure and sudden death. A meta-analysis of 38 studies covering 19 countries found that, early in the pandemic, in-hospital mortality of ST-segment elevation myocardial infarction (STEMI) patients with COVID-19 was significantly higher than that of non-COVID-19 STEMI patients [3]. Excessive inflammation and oxidative stress from COVID-19 sepsis may cause hypoxia, tissue injury and heart damage[4]. COVID-19 incites endothelial dysfunction upon entry into endothelial cells which occurs via the high level of ACE2 receptors on the surface of this cell type. Endothelial damage from invading viral particles likely plays a role in the procoagulant state [5]. COVID-19 can also enter cardiomyocytes [6][7]. All of these mechanisms likely play a role in the pathophysiology of the cardiac manifestations which are part of the Post-acute Covid-19 syndrome as well [8]. In addition to treatment of the underlying CVD and related conditions (diabetes, hypertension), anti-coagulation may be introduced and statins are being studied as a way to reduce inflammation and improve endothelial  dysfunction [9][10][11] The role of viral load is also being explored and a small study from Detroit Medical Center USA found that there was no relationship between viral load measured via PCR from a nasopharyngeal swab and incidence of myocardial injury (defined by high sensitivity cardiac troponin I above 100 ng/L) . However, high viral load accompanying myocardial injury was associated with decreased survival versus myocardial injury alone or high viral load alone [12].


  1. Benjamin, E.J.; Muntner, P.; Alonso, A.; Bittencourt, M.S.; Callaway, C.W.; Carson, A.P.; Chamberlain, A.M.; Chang, A.R.; Cheng, S.; Das, S.R.; et al. American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2019 update: A report from the American Heart Association. Circulation 2019, 139, e56–e528.
  2. GBD 2015 Mortality and Causes of Death Collaborators. Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: A systematic analysis for the Global Burden of Disease Study 2015. Lancet 2016, 388, 1459–1544.
  3. Go, A.S.; Mozaffarian, D.; Roger, V.L.; Benjamin, E.J.; Berry, J.D.; Blaha, M.J.; Dai, S.; Ford, E.S.; Fox, C.S.; Franco, S.; et al. Heart Disease and Stroke Statistics-2014 update. Circulation 2014, 129, e28–e292.
  4. Savji, N.; Rockman, C.B.; Skolnick, A.H.; Guo, Y.; Adelman, M.A.; Riles, T.; Berger, J.S. Association between advanced age and vascular disease in different arterial territories: A population database of over 3.6 million subjects. J. Am. Coll. Cardiol. 2013, 61, 1736–1743.
  5. Rodgers, J.L.; Jones, J.; Bolleddu, S.I.; Vanthenapalli, S.; Rodgers, L.E.; Shah, K.; Karia, K.; Panguluri, S.K. Cardiovascular Risks Associated with Gender and Aging. J. Cardiovasc. Dev. Dis. 2019, 6, 19.
  6. Wu, Z.; McGoogan, J.M. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72,314 cases from the Chinese Center for Disease Control and Prevention. JAMA 2020, 323, 1239–1242.
  7. Neumann-Podczaska, A.; Chojnicki, M.; Karbowski, L.M.; Al-Saad, S.R.; Hashmi, A.A.; Chudek, J.; Tobis, S.; Kropinska, S.; Mozer-Lisewska, I.; Suwalska, A.; et al. Clinical characteristics and survival analysis in a small sample of older COVID-19 patients with defined 60-day outcome. Int. J. Environ. Res. Public Health 2020, 17, E8362.
  8. Grasselli, G.; Zangrillo, A.; Zanella, A.; Antonelli, M.; Cabrini, L.; Castelli, A.; Cereda, D.; Coluccello, A.; Foti, G.; Fumagalli, R.; et al. Baseline characteristics and outcomes of 1591 patients infected with SARS-CoV-2 admitted to ICUs of the Lombardy region, Italy. JAMA 2020, 323, 1574–1581.
  9. Yang, C.; Liu, F.; Liu, W.; Cao, G.; Liu, J.; Huang, S.; Zhu, M.; Tu, C.; Wang, J.; Xiong, B. Myocardial injury and risk factors for mortality in patients with COVID-19 pneumonia. Int. J. Cardiol. 2021, 326, 230–236.
  10. Nadkarni, G.N.; Lala, A.; Bagiella, E.; Chang, H.L.; Moreno, P.R.; Pujadas, E.; Arvind, V.; Bose, S.; Charney, A.W.; Chen, M.D.; et al. Anticoagulation, bleeding, mortality, and pathology in hospitalized patients with COVID-19. J. Am. Coll. Cardiol. 2020, 76, 1815–1826.
  11. Awortwe, C.; Cascorbi, I. Meta-analysis on outcome-worsening comorbidities of COVID-19 and related potential drug-drug interactions. Pharmacol. Res. 2020, 161, 105250.
  12. McQueenie, R.; Foster, H.M.E.; Jani, B.D.; Katikireddi, S.V.; Sattar, N.; Pell, J.P.; Ho, F.K.; Niedzwiedz, C.L.; Hastie, C.E.; Anderson, J.; et al. Multimorbidity, polypharmacy, and COVID-19 infection within the UK Biobank cohort. PLoS ONE 2020, 15, e0238091.
  13. Sánchez-Sánchez, E.; Ramírez-Vargas, G.; Avellaneda-López, Y.; Orellana-Pecino, J.I.; García-Marín, E.; Díaz-Jimenez, J. Eating habits and physical activity of the Spanish population during the COVID-19 pandemic period. Nutrients 2020, 12, 2826.
  14. Gao, Y.D.; Ding, M.; Dong, X.; Zhang, J.J.; Azkur, A.K.; Azkur, D.; Gan, H.; Sun, Y.L.; Fu, W.; Li, W.; et al. Risk factors for severe and critically ill COVID-19 patients: A review. Allergy 2021, 76, 428–455.
  15. Nolen, S.C.; Evans, M.A.; Fischer, A.; Corrada, M.M.; Kawas, C.H.; Bota, D.A. Cancer-Incidence, prevalence and mortality in the oldest-old. A comprehensive review. Mech. Ageing Dev. 2017, 164, 113–126.
  16. Quagliariello, V.; Bonelli, A.; Caronna, A.; Conforti, G.; Iovine, M.; Carbone, A.; Berretta, M.; Botti, G.; Maurea, N. SARS-CoV-2 Infection and Cardioncology: From Cardiometabolic Risk Factors to Outcomes in Cancer Patients. Cancers 2020, 12, 3316.
  17. Huang, Y.; Hu, Z.; Hu, D.; Quan, Z.; Zhou, X.; Fan, G.; Chen, X.; Liu, X.; Zhang, Z.; Chen, G.; et al. Clinical characteristics, risk factors and cardiac manifestations of cancer patients with COVID-19. J. Appl. Physiol. 2021.
  18. Gonçalves, T.; Gonçalves, S.; Guarnieri, A.; Risegato, R.C.; Guimarães, M.P.; de Freitas, D.C.; Razuk-Filho, A.; Benedito Junior, P.B.; Parrillo, E.F. Prevalence of obesity and hypovitaminosis D in elderly with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Clin. Nutr. ESPEN 2020, 40, 110–114.
  19. Vanderbeke, L.; Van Mol, P.; Van Herck, Y.; De Smet, F.; Humblet-Baron, S.; Martinod, K.; Antoranz, A.; Arijs, I.; Boeckx, B.; Bosisio, F.M.; et al. Monocyte-driven atypical cytokine storm and aberrant neutrophil activation as key mediators of COVID-19 disease severity. Nat. Commun. 2021, 12, 4117.
  20. Basso, C.; Leone, O.; Rizzo, S.; De Gaspari, M.; van der Wal, A.C.; Aubry, M.C.; Bois, M.C.; Lin, P.T.; Maleszewski, J.J.; Stone, J.R. Pathological features of COVID-19-associated myocardial injury: A multicentre cardiovascular pathology study. Eur. Heart J. 2020, 41, 3827–3835.
  21. Tai, S.; Tang, J.; Yu, B.; Tang, L.; Wang, Y.; Zhang, H.; Zhu, W.; Xiao, K.; Wen, C.; Tan, C.; et al. Association between cardiovascular burden and requirement of intensive care among patients with mild COVID-19. Cardiovasc. Ther. 2020, 2020, 9059562.
  22. Terpos, E.; Ntanasis-Stathopoulos, I.; Elalamy, I.; Kastritis, E.; Sergentanis, T.N.; Politou, M.; Psaltopoulou, T.; Gerotziafas, G.T.; Dimopoulos, M. A Hematological findings and complications of COVID-19. Am. J. Hematol. 2020, 95, 834–847.
  23. Klok, F.A.; Kruip, M.J.H.A.; van der Meer, N.J.M.; Arbous, M.S.; Gommers, D.A.M.P.J.; Kant, K.M.; Kaptein, F.H.J.; van Paassen, J.; Stals, M.A.M.; Huisman, M.V.; et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb. Res. 2020, 191, 145–147.
  24. Dobesh, P.P.; Trujillo., T.C. Coagulopathy, venous thromboembolism, and anticoagulation in patients with COVID-19. Pharmacotherapy 2020, 40, 1130–1151.
  25. Kermani-Alghoraishi, M.; Ghahramani, R. A review of venous thromboembolism phenomena in COVID-19 patients. Curr. Probl. Cardiol. 2020, 46, 100692.
  26. Benito, N.; Filella, D.; Mateo, J.; Fortuna, A.M.; Gutierrez-Alliende, J.E.; Hernandez, N.; Gimenez, A.M.; Pomar, V.; Castellvi, I.; Corominas, H.; et al. Pulmonary thrombosis or embolism in a large cohort of hospitalized patients with COVID-19. Front. Med. 2020, 7, 557.
  27. Voicu, S.; Delrue, M.; Chousterman, B.G.; Stépanian, A.; Bonnin, P.; Malissin, I.; Deye, N.; Neuwirth, M.; Ketfi, C.; Mebazaa, A.; et al. Imbalance between procoagulant factors and natural coagulation inhibitors contributes to hypercoagulability in the critically ill COVID-19 patient: Clinical implications. Eur. Rev. Med. Pharmacol. Sci. 2020, 24, 9161–9168.
  28. Chen, J.; Wang, X.; Zhang, S.; Lin, B.; Wu, X.; Wang, Y.; Wang, X.; Yang, M.; Sun, J.; Xie, Y. Characteristics of acute pulmonary embolism in patients with COVID-19 associated pneumonia from the city of Wuhan. Clin. Appl. Thromb. Hemost. 2020, 26.
  29. Bouchard, B.A.; Tracy, P.B. The participation of leukocytes in coagulant reactions. J. Thromb. Haemost. 2003, 1, 464–469.
  30. Bautista-Vargas, M.; Bonilla-Abadía, F.; Cañas, C.A. Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID-19. J. Thromb. Thrombolysis 2020, 50, 479–483.
  31. Levi, M.; van der Poll, T. Inflammation and coagulation. Crit. Care Med. 2010, 38, S26–S34.
  32. Bester, J.; Matshailwe, C.; Pretorius, E. Simultaneous presence of hypercoagulation and increased clot lysis time due to IL-1beta, IL-6 and IL-8. Cytokine 2018, 110, 237–242.
  33. Roncati, L.; Ligabue, G.; Nasillo, V.; Lusenti, B.; Gennari, W.; Fabbiani, L.; Malagoli, C.; Gallo, G.; Giovanella, S.; Lupi, M.; et al. A proof of evidence supporting abnormal immunothrombosis in severe COVID-19: Naked megakaryocyte nuclei increase in the bone marrow and lungs of critically ill patients. Platelets 2020, 31, 1085–1089.
  34. Tang, N.; Li, D.; Wang, X.; Sun, Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J. Thromb. Haemost. 2020, 18, 844–847.
  35. Zhang, L.; Yan, X.; Fan, Q.; Liu, H.; Liu, X.; Liu, Z.; Zhang, Z. D-dimer levels on admission to predict in-hospital mortality in patients with COVID-19. J. Thromb. Haemost. 2020, 18, 1324–1329.
  36. Bray, M.A.; Sartain, S.E.; Gollamudi, J.; Rumbaut, R.E. Microvascular thrombosis: Experimental and clinical implications. Transl. Res. 2020, 225, 105–130.
  37. Del Turco, S.; Vianello, A.; Ragusa, R.; Caselli, C.; Basta, G. COVID-19 and cardiovascular consequences: Is the endothelial dysfunction the hardest challenge? Thromb. Res. 2020, 196, 143–151.
  38. Montone, R.A.; Iannaccone, G.; Meucci, M.C.; Gurgoglione, F.; Niccoli, G. Myocardial and microvascular injury due to coronavirus disease 2019. Eur. Cardiol. 2020, 15, e52.
  39. Zuo, Y.; Warnock, M.; Harbaugh, A.; Yalavarthi, S.; Gockman, K.; Zuo, M.; Madison, J.A.; Knight, J.S.; Kanthi, Y.; Lawrence, D.A. Plasma tissue plasminogen activator and plasminogen activator inhibitor-1 in hospitalized COVID-19 patients. Sci. Rep. 2021, 11, 580.
  40. Whyte, C.S.; Morrow, G.B.; Mitchell, J.L.; Chowdary, P.; Mutch, N.J. Fibrinolytic abnormalities in acute respiratory distress syndrome (ARDS) and versatility of thrombolytic drugs to treat COVID-19. J. Thromb. Haemost. 2020, 18, 1548–1555.
  41. Connors, J.M.; Levy, J.H. Thromboinflammation and the hypercoagulability of COVID-19. J. Thromb. Haemost. 2020, 18, 1559–1561.
  42. Iba, T.; Levy, J.H.; Levi, M.; Thachil, J. Coagulopathy in COVID-19. J. Thromb. Haemost. 2020, 18, 2103–2109.
  43. Zhou, F.; Yu, T.; Du, R.; Fan, G.; Liu, Y.; Liu, Z.; Xiang, J.; Wang, Y.; Song, B.; Gu, X.; et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet 2020, 395, 1054–1062.
  44. Simadibrata, D.M.; Lubis, A.M. D-dimer levels on admission and all-cause mortality risk in COVID-19 patients: A meta-analysis. Epidemiol. Infect. 2020, 148, e202.
  45. Roncon, L.; Zuin, M.; Zonzin, P. Age-adjusted D-dimer cut-off levels to rule out venous thromboembolism in COVID-19 patients. Thromb. Res. 2020, 190, 102.
  46. Li, X.; Xu, S.; Yu, M.; Wang, K.; Tau, Y.; Zhou, Y.; Shi, J.; Zhou, M.; Wu, B.; Yang, Z.; et al. Risk factors for severity and mortality in adult COVID-19 inpatients in Wuhan. J. Allergy Clin. Immunol. 2020, 146, 110–118.
  47. Oxley, T.J.; Mocco, J.; Majidi, S.; Kellner, C.P.; Shoirah, H.; Singh, I.P.; De Lacey, R.A.; Shigematsu, T.; Ladner, T.R.; Yaeger, K.A.; et al. Large-vessel stroke as a presenting feature of COVID-19 in the young. N. Engl. J. Med. 2020, 382, 360.
  48. Cantador, E.; Núñez, A.; Sobrino, P.; Espejo, V.; Fabia, L.; Vela, L. Incidence and consequences of systemic arterial thrombotic events in COVID-19 patients. J. Thromb. Thrombolysis 2020, 50, 543–547.
  49. Rey, J.R.; Caro-Codón, J.; Pineda, D.P.; Merino, J.L.; Iniesta, A.M.; López-Sendón, J.L. Arterial thrombotic complications in hospitalized patients with COVID-19. Rev. Esp. Cardiol. (Engl. Ed.) 2020, 73, 769–771.
  50. Hess, D.C.; Eldahshan, W.; Rutkowski, E. COVID-19-related stroke. Transl. Stroke Res. 2020, 11, 322–325.
  51. Kumar, D.R.; Hanlin, E.; Glurich, I.; Mazza, J.J.; Yale, S.H. Virchow’s contribution to the understanding of thrombosis and cellular biology. Clin. Med. Res. 2010, 8, 168–172.
  52. Sharma, A.; Sharma, C.; Raina, S.; Singh, B.; Dadhwal, D.S.; Dogra, V.; Gupta, S.; Bhandari, S.; Sood, V. A randomized open-label trial to evaluate the efficacy and safety of triple therapy with aspirin, atorvastatin, and nicorandil in hospitalised patients with SARS Cov-2 infection: A structured summary of a study protocol for a randomized controlled trial. Trials 2021, 22, 451.
  53. Khateri, S.; Mohammadi, H.; Khateri, R.; Moradi, Y. The prevalence of underlying diseases and comorbidities in COVID-19 patients; an updated systematic review and meta-analysis. Arch. Acad. Emerg. Med. 2020, 8, e72.
  54. Long, B.; Brady, W.J.; Koyfman, A.; Gottlieb, M. Cardiovascular complication in COVID-19. Am. J. Emerg. Med. 2020, 38, 1504–1507.
  55. Sriram, K.; Insel, P.A. Inflammation and thrombosis in COVID-19 pathophysiology: Proteinase-activated and purinergic receptors as drivers and candidate therapeutic targets. Physiol. Rev. 2021, 101, 545–567.
  56. Musher, D.M.; Abers, M.; Corrales-Medina, V.F. Acute infection and myocardial infarction. N. Engl. J. Med. 2019, 380, 171–176.
  57. Kim, I.C.; Kim, H.A.; Park, J.S.; Nam, C.W. Updates of cardiovascular manifestations in COVID-19: Korean experience to broaden worldwide perspectives. Korean Circ. J. 2020, 50, 543–554.
  58. Walker, C.; Deb, S.; Ling, H.; Wang, Z. Assessing the elevation of cardiac biomarkers and the severity of COVID-19 infection: A meta-analysis. J. Pharm. Pharm. Sci. 2020, 23, 396–405.
  59. Kim, I.C.; Song, J.E.; Lee, H.J.; Park, J.H.; Hyun, M.; Lee, J.Y.; Kim, H.A.; Kwon, Y.S.; Park, J.S.; Youn, J.C.; et al. The implication of cardiac injury score on in-hospital mortality of coronavirus disease 2019. J. Korean Med. Sci. 2020, 35, e349.
  60. Fan, Z.X.; Yang, J.; Zhang, J.; He, C.; Wu, H.; Yang, C.J.; Zheng, T.; Ma, C.; Xiang, Z.J.; Zhai, Y.H.; et al. Analysis of influencing factors related to elevated serum troponin I level for COVID-19 patients in Yichang, China. Cardiovasc. Diagn. Ther. 2020, 10, 678–686.
  61. Danwang, C.; Endomba, F.T.; Nkeck, J.R.; Wouna, D.L.A.; Robert, A.; Noubiap, J.J. A meta-analysis of potential biomarkers associated with severity of coronavirus disease 2019 (COVID-19). Biomark. Res. 2020, 8, 37.
  62. Li, X.; Pan, X.; Li, Y.; An, N.; Xing, Y.; Yang, F.; Tian, L.; Sun, J.; Gao, Y.; Shang, H.; et al. Cardiac injury associated with severe disease or ICU admission and death in hospitalized patients with COVID-19: A meta-analysis and systematic review. Crit. Care 2020, 24, 468.
  63. Henry, B.M.; Aggarwal, G.; Wong, J.; Benoit, S.; Vikse, J.; Plebani, M.; Lippi, G. Lactate dehydrogenase levels predict coronavirus disease 2019 (COVID-19) severity and mortality: A pooled analysis. Am. J. Emerg. Med. 2020, 38, 1722–1726.
  64. Setiati, S.; Harimurti, K.; Safitri, E.D.; Ranakusuma, R.W.; Saldi, S.R.F.; Azwar, M.K.; Marsigit, J.; Pitoyo, Y.; Widyaningsih, W. Risk factors and laboratory test results associated with severe illness and mortality in COVID-19 patients: A systematic review. Acta. Med. Indones. 2020, 52, 227–245.
  65. Zhu, Y.; Du, Z.; Zhu, Y.; Li, W.; Miao, H.; Li, Z. Evaluation of organ function in patients with severe COVID-19 infections. Med. Clin. (Engl. Ed.) 2020, 155, 191–196.
  66. Wang, K.; Qiu, Z.; Liu, J.; Fan, T.; Liu, C.; Yian, P.; Wang, Y.; Ni, Z.; Zhang, S.; Luo, J.; et al. Analysis of the clinical characteristics of 77 COVID-19 deaths. Sci. Rep. 2020, 10, 16384.
  67. Fan, Q.; Zhu, H.; Zhao, J.; Zhuang, L.; Zhang, H.; Xie, H.; Zhang, R.; Granada, J.F.; Xiang, X.; Hu, W.; et al. Risk factors for myocardial injury in patients with coronavirus disease 2019 in China. ESC Heart Fail. 2020, 7, 4108–4117.
  68. Bangalore, S.; Sharma, A.; Slotwiner, A.; Yatskar, L.; Harari, R.; Shah, B.; Ibrahim, H.; Friedman, G.H.; Thompson, C.; Alviar, C.L.; et al. ST-Segment elevation in patients with COVID-19—A case series. N. Engl. J. Med. 2020, 382, 2478–2480.
  69. Bavishi, C.; Bonow, R.O.; Trivedi, V.; Abbott, J.D.; Messerli, F.H.; Bhatt, D.L. Special article—Acute myocardial injury in patients hospitalized with COVID-19 infection: A review. Prog. Cardiovasc. Dis. 2020, 63, 682–689.
  70. Hendren, N.S.; Drazner, M.H.; Bozkurt, B.; Cooper, L.T., Jr. Description and proposed management of the acute COVID-19 cardiovascular syndrome. Circulation 2020, 9, 1903–1914.
  71. Guo, H.; Shen, Y.; Wu, N.; Sun, X. Myocardial injury in severe and critical coronavirus disease 2019 patients. J. Card. Surg. 2020, 36, 82–88.
  72. Shi, S.; Qin, M.; Shen, B.; Cai, Y.; Liu, T.; Yang, F.; Gong, W.; Liu, X.; Liang, J.; Zhao, Q.; et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol. 2020, 5, 802–810.
  73. Gu, Z.C.; Zhang, C.; Kong, L.C.; Shen, L.; Li, Z.; Ge, H.; Lin, H.W.; Pu, J. Incidence of myocardial injury in coronavirus disease 2019 (COVID-19): A pooled analysis of 7,679 patients from 53 studies. Cardiovasc. Diagn. Ther. 2020, 10, 667–677.
  74. Solano-López, J.; Zamorano, J.L.; Pardo Sanz, A.; Amat-Santos, I.; Sarnago, F.; Gutiérrez Ibañes, E.; Sanchis, J.; Rey Blas, J.R.; Gómez-Hospital, J.A.; Santos Martínez, S.; et al. Risk factors for in-hospital mortality in patients with acute myocardial infarction during the COVID-19 outbreak. Rev. Esp. Cardiol. (Engl. Ed.) 2020, 73, 985–993.
  75. Budoff, M.J.; Mayrhofer, T.; Ferencik, M. Prognostic value of coronary artery calcium in the PROMISE study (prospective multicenter imaging study for evaluation of chest pain). Circulation 2017, 136, 1993–2005.
  76. Dillinger, J.G.; Benmessaoud, F.A.; Pezel, T.; Voicu, S.; Sideris, G.; Chergui, N.; Hamzi, L.; Chauvin, A.; Leroy, P.; Gautier, J.F.; et al. COVID Research Group of Lariboisiere Hospital. Coronary artery calcification and complications in patients with COVID-19. JACC Cardiovasc. Imaging 2020, 13, 2468–2470.
  77. Fovino, L.N.; Cademartiri, F.; Tarantini, G. Subclinical coronary artery disease in COVID-19 patients. Eur. Heart J. Cardiovasc. Imaging 2020, 21, 1055–1056.
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to : , ,
View Times: 266
Revisions: 2 times (View History)
Update Date: 23 Sep 2021