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====Pathophysiology==== | ====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. | *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. | *Among patients with [[COVID-19]], there is a high [[prevalence]] of the [[cardiovascular]] disease, and >7% of patients experience [[myocardial]] injury from the [[infection]]. | ||
*[[Myocarditis]] is an inflammatory disease of the heart characterized by inflammatory infiltrates and myocardial injury without an ischemic cause. | *[[Myocarditis]] is an [[inflammatory]] disease of the heart characterized by [[inflammatory]] infiltrates and [[myocardial]] injury without an [[Ischemia|ischemic]] cause. | ||
*The major cause of myocarditis in the United States and other developed countries is viral. | *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. | ||
*It has also been reported as the cause of death in some COVID19 patients. | *It has also been reported as the cause of death in some [[COVID19]] patients. | ||
* [[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]]. | * [[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]]. | ||
* ACE2 is expressed in the lung, principally type II alveolar cells which appears to be the principal portal of entry. | * ACE2 is expressed in the [[lung]], principally type II [[alveolar]] cells which appears to be the principal portal of entry. | ||
* [[ACE2]] is highly expressed in the heart as well. | * [[ACE2]] is highly expressed in the [[heart]] as well. | ||
* 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. | *[[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]]. | ||
* 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 corona viruses possess cardio-tropism. | * 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]]. | ||
* The primed CD 8+ T lymphocytes migrate to the cardiomyocytes and through cell-mediated cytotoxicity, cause myocardial inflammation. | * The primed CD 8+ [[T lymphocytes]] migrate to the cardiomyocytes and through cell-mediated [[cytotoxicity]], cause [[myocardial]] [[inflammation]]. | ||
* In the [[cytokine storm syndrome]], pro-inflammatory 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. | * 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]]. | ||
* This results in a positive feedback loop of immune activation and myocardial damage. | * This results in a positive feedback loop of immune activation and [[myocardial]] damage. | ||
<references /> | <references /> | ||
Revision as of 17:10, 20 June 2020
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.
- Myocarditis is an inflammatory disease of the heart characterized by inflammatory infiltrates and myocardial injury without an ischemic cause.
- 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.
- It has also been reported as the cause of death in some COVID19 patients.
- 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.
- ACE2 is expressed in the lung, principally type II alveolar cells which appears to be the principal portal of entry.
- ACE2 is highly expressed in the heart as well.
- 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.
- 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 corona viruses possess cardio-tropism.
- The primed CD 8+ T lymphocytes migrate to the cardiomyocytes and through cell-mediated cytotoxicity, cause myocardial inflammation.
- In the cytokine storm syndrome, pro-inflammatory 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.
- This results in a positive feedback loop of immune activation and myocardial damage.