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Pathophysiology

Studies have demonstrated that COVID-19 interacts with the cardiovascular system, thereby causing myocardial injury and dysfunction as well as increasing morbidity among patients with underlying cardiovascular conditions. Among patients with COVID-19, there is a high prevalence of the cardiovascular disease, and >7% of patients experience myocardial injury from the infection.[1] Myocarditis is an inflammatory disease of the heart characterized by inflammatory infiltrates and myocardial injury without an ischemic cause.[2] The major cause of myocarditis in the United States and other developed countries is viral.[3] [4] Number of cases of myocarditis have been reported in COVID19 patients.[5][6][7][8] It has also been reported as the cause of death in some COVID19 patients.[9]

SARS-CoV-2 infection is caused by binding of the viral surface spike protein (primed by TMPRSS2, which is a transmembrane protease, serine 2) to the human angiotensin-converting enzyme 2 (ACE2) receptor.[10] ACE2 is expressed in the lung, principally type II alveolar cells which appears to be the principal portal of entry.[11] ACE2 is highly expressed in the heart as well.[12] Naïve T lymphocytes can be primed for viral antigens via antigen-presenting cells and cardio-tropism by the heart-produced hepatocyte growth factor (HGF) which binds c-Met, an HGF receptor on T lymphocytes.[13] The viral RNAs of Middle East Respiratory Syndrome coronavirus (MERS-CoV) and SARS-CoV were found in the heart tissues of infected animals, suggesting that these coronaviruses possess cardiotropism.[14][15] The primed CD8+ T lymphocytes migrate to the cardiomyocytes and through cell-mediated cytotoxicity, cause myocardial inflammation. In the cytokine storm syndrome, proinflammatory cytokines such as Interleukin-6 (IL-6) are released into the circulation, which further augments T-lymphocyte activation and causes the release of more cytokines.[16] This results in a positive feedback loop of immune activation and myocardial damage.[17][2]

  1. ↑ Clerkin, Kevin J.; Fried, Justin A.; Raikhelkar, Jayant; Sayer, Gabriel; Griffin, Jan M.; Masoumi, Amirali; Jain, Sneha S.; Burkhoff, Daniel; Kumaraiah, Deepa; Rabbani, LeRoy; Schwartz, Allan; Uriel, Nir (2020). "COVID-19 and Cardiovascular Disease". Circulation. 141 (20): 1648–1655. doi:10.1161/CIRCULATIONAHA.120.046941. ISSN 0009-7322.
  2. ↑ 2.0 2.1 Esfandiarei, Mitra; McManus, Bruce M. (2008). "Molecular Biology and Pathogenesis of Viral Myocarditis". Annual Review of Pathology: Mechanisms of Disease. 3 (1): 127–155. doi:10.1146/annurev.pathmechdis.3.121806.151534. ISSN 1553-4006.
  3. ↑ Caforio, A. L. P.; Pankuweit, S.; Arbustini, E.; Basso, C.; Gimeno-Blanes, J.; Felix, S. B.; Fu, M.; Helio, T.; Heymans, S.; Jahns, R.; Klingel, K.; Linhart, A.; Maisch, B.; McKenna, W.; Mogensen, J.; Pinto, Y. M.; Ristic, A.; Schultheiss, H.-P.; Seggewiss, H.; Tavazzi, L.; Thiene, G.; Yilmaz, A.; Charron, P.; Elliott, P. M. (2013). "Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases". European Heart Journal. 34 (33): 2636–2648. doi:10.1093/eurheartj/eht210. ISSN 0195-668X.
  4. ↑ Kociol, Robb D.; Cooper, Leslie T.; Fang, James C.; Moslehi, Javid J.; Pang, Peter S.; Sabe, Marwa A.; Shah, Ravi V.; Sims, Daniel B.; Thiene, Gaetano; Vardeny, Orly (2020). "Recognition and Initial Management of Fulminant Myocarditis". Circulation. 141 (6). doi:10.1161/CIR.0000000000000745. ISSN 0009-7322.
  5. ↑ Zeng, Jia-Hui; Liu, Ying-Xia; Yuan, Jing; Wang, Fu-Xiang; Wu, Wei-Bo; Li, Jin-Xiu; Wang, Li-Fei; Gao, Hong; Wang, Yao; Dong, Chang-Feng; Li, Yi-Jun; Xie, Xiao-Juan; Feng, Cheng; Liu, Lei (2020). "First case of COVID-19 complicated with fulminant myocarditis: a case report and insights". Infection. doi:10.1007/s15010-020-01424-5. ISSN 0300-8126.
  6. ↑ Inciardi, Riccardo M.; Lupi, Laura; Zaccone, Gregorio; Italia, Leonardo; Raffo, Michela; Tomasoni, Daniela; Cani, Dario S.; Cerini, Manuel; Farina, Davide; Gavazzi, Emanuele; Maroldi, Roberto; Adamo, Marianna; Ammirati, Enrico; Sinagra, Gianfranco; Lombardi, Carlo M.; Metra, Marco (2020). "Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiology. doi:10.1001/jamacardio.2020.1096. ISSN 2380-6583.
  7. ↑ Han, Seongwook; Kim, Hyun Ah; Kim, Jin Young; Kim, In-Cheol (2020). "COVID-19-related myocarditis in a 21-year-old female patient". European Heart Journal. 41 (19): 1859–1859. doi:10.1093/eurheartj/ehaa288. ISSN 0195-668X.
  8. ↑ Esposito, Antonio; Godino, Cosmo; Basso, Cristina; Cappelletti, Alberto Maria; Tresoldi, Moreno; De Cobelli, Francesco; Vignale, Davide; Villatore, Andrea; Palmisano, Anna; Gramegna, Mario; Peretto, Giovanni; Sala, Simone (2020). "Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection". European Heart Journal. 41 (19): 1861–1862. doi:10.1093/eurheartj/ehaa286. ISSN 0195-668X.
  9. ↑ 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.
  10. ↑ Hoffmann, Markus; Kleine-Weber, Hannah; Schroeder, Simon; Krüger, Nadine; Herrler, Tanja; Erichsen, Sandra; Schiergens, Tobias S.; Herrler, Georg; Wu, Nai-Huei; Nitsche, Andreas; Müller, Marcel A.; Drosten, Christian; Pöhlmann, Stefan (2020). "SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor". Cell. 181 (2): 271–280.e8. doi:10.1016/j.cell.2020.02.052. ISSN 0092-8674.
  11. ↑ Zhao, Yu; Zhao, Zixian; Wang, Yujia; Zhou, Yueqing; Ma, Yu; Zuo, Wei (2020). doi:10.1101/2020.01.26.919985. Missing or empty |title= (help)
  12. ↑ Tikellis, Chris; Thomas, M. C. (2012). "Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease". International Journal of Peptides. 2012: 1–8. doi:10.1155/2012/256294. ISSN 1687-9767.
  13. ↑ Komarowska, Izabela; Coe, David; Wang, Guosu; Haas, Robert; Mauro, Claudio; Kishore, Madhav; Cooper, Dianne; Nadkarni, Suchita; Fu, Hongmei; Steinbruchel, Daniel A.; Pitzalis, Costantino; Anderson, Graham; Bucy, Pat; Lombardi, Giovanna; Breckenridge, Ross; Marelli-Berg, Federica M. (2015). "Hepatocyte Growth Factor Receptor c-Met Instructs T Cell Cardiotropism and Promotes T Cell Migration to the Heart via Autocrine Chemokine Release". Immunity. 42 (6): 1087–1099. doi:10.1016/j.immuni.2015.05.014. ISSN 1074-7613.
  14. ↑ Agrawal, Anurodh Shankar; Garron, Tania; Tao, Xinrong; Peng, Bi-Hung; Wakamiya, Maki; Chan, Teh-Sheng; Couch, Robert B.; Tseng, Chien-Te K.; García-Sastre, A. (2015). "Generation of a Transgenic Mouse Model of Middle East Respiratory Syndrome Coronavirus Infection and Disease". Journal of Virology. 89 (7): 3659–3670. doi:10.1128/JVI.03427-14. ISSN 0022-538X.
  15. ↑ Schaecher, Scott R.; Stabenow, Jennifer; Oberle, Christina; Schriewer, Jill; Buller, R. Mark; Sagartz, John E.; Pekosz, Andrew (2008). "An immunosuppressed Syrian golden hamster model for SARS-CoV infection". Virology. 380 (2): 312–321. doi:10.1016/j.virol.2008.07.026. ISSN 0042-6822.
  16. ↑ 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.
  17. ↑ Iakimov VP (1977). "[F. Engels' theory of the origin of man and modern anthropologic findings]". Arkh Anat Gistol Embriol. 72 (6): 5–11. PMID 409380.
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