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| ====Pathophysiology====
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| *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.
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| *Among patients with [[COVID-19]], there is a high [[prevalence]] of the [[cardiovascular]] disease, and >7% of patients experience [[myocardial]] injury from the [[infection]].
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| *[[Myocarditis]] is an [[inflammatory]] disease of the heart characterized by [[inflammatory]] infiltrates and [[myocardial]] injury without an [[Ischemia|ischemic]] cause.
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| *The major cause of [[myocarditis]] in the United States and other developed countries is viral. Number of cases of [[myocarditis]] have been reported in [[COVID19]] patients.
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| *It has also been reported as the cause of death in some [[COVID19]] patients.
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| * [[SARS-CoV-2]] [[infection]] is caused by binding of the viral surface spike [[protein]] (primed by [[TMPRSS2]], which is a trans-membrane protease, [[serine]] 2) to the human [[angiotensin-converting enzyme 2 (ACE2) receptor]].
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| * ACE2 is expressed in the [[lung]], principally type II [[alveolar]] cells which appears to be the principal portal of entry.
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| * [[ACE2]] is highly expressed in the [[heart]] as well.
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| *[[Naive T cell|Naive]] [[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]].
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| * 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 [[Coronavirus|corona viruses]] possess cardio-[[tropism]].
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| * The primed CD 8+ [[T lymphocytes]] migrate to the cardiomyocytes and through cell-mediated [[cytotoxicity]], cause [[myocardial]] [[inflammation]].
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| * In the [[cytokine storm syndrome]], pro-inflammatory cytokines such as [[Interleukin-6]] ([[IL-6]]) are released into the circulation, which further augments [[T-lymphocytes|T-lymphocyte]] activation and causes the release of more [[Cytokine|cytokines]].
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| * This results in a positive feedback loop of immune activation and [[myocardial]] damage.
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| <references />
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