Cardiovascular complications in the Post-Acute COVID-19 syndrome (PACS)
•The presence of stress-related (Takotsubo) cardiomyopathy has also been demonstrated in COVID-19.•The proposed mechanisms of cardiac damage during the acute phase of COVID-19 include both direct -viral penetration- and indirect routes -hypoxic injury and systemic inflammation.•SARS-CoV-2 infection,...
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Published in: | International journal of cardiology. Heart & vasculature Vol. 40; p. 101012 |
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01-06-2022
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Abstract | •The presence of stress-related (Takotsubo) cardiomyopathy has also been demonstrated in COVID-19.•The proposed mechanisms of cardiac damage during the acute phase of COVID-19 include both direct -viral penetration- and indirect routes -hypoxic injury and systemic inflammation.•SARS-CoV-2 infection, especially in its severe form, is associated with an increased risk for venous thromboembolism (VTE).•Unfractionated heparin (UFH) is the first-line treatment for hemodynamic instability and emergency reperfusion for PASC.•Further studies are needed to offer current screening for the occurrence of cardiovascular problems especially myocardial infarction and heart failure in COVID-19 patients.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) or coronavirus disease 2019 (COVID-19) initially surfaced in December 2019 from Wuhan, China, sweeping the world with various strains, forcing the WHO to declare a pandemic epidemic in March 2020. Furthermore, COVID-19 manifests with a wide array of presentations from fever and fatigue to severe respiratory and cardiovascular complications. Post-COVID-19 syndrome is poorly understood affecting COVID-19 survivors at all levels of disease severity. The disease is most associated with post-discharge dyspnea and fatigue. However, other persistent symptoms as chest pains, palpitations, smell, and taste dysfunctions. Patients with high concentrations of CRP and creatinine in the acute phase of Covid-19 are more prone to cardiac sequelae. Therefore, high levels of cardiac-sensitive troponin and hypokalaemia can also be used for risk stratification. Furthermore, Cardiac damage can manifest as myocarditis, pericarditis, rhythm abnormalities. The use of different diagnostic modalities like electrocardiogram (ECG), echocardiogram, and cardiac magnetic resonance imaging (MRI)(CMR) to evaluate the myocardial damage were studied. However, Cardiovascular complications are a common manifestation of PASC, classification of severity of cardiac symptoms and the emergence of CMR as a diagnostic tool needs more evidence. |
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AbstractList | The severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) or coronavirus disease 2019 (COVID-19) initially surfaced in December 2019 from Wuhan, China, sweeping the world with various strains, forcing the WHO to declare a pandemic epidemic in March 2020. Furthermore, COVID-19 manifests with a wide array of presentations from fever and fatigue to severe respiratory and cardiovascular complications. Post-COVID-19 syndrome is poorly understood affecting COVID-19 survivors at all levels of disease severity. The disease is most associated with post-discharge dyspnea and fatigue. However, other persistent symptoms as chest pains, palpitations, smell, and taste dysfunctions. Patients with high concentrations of CRP and creatinine in the acute phase of Covid-19 are more prone to cardiac sequelae. Therefore, high levels of cardiac-sensitive troponin and hypokalaemia can also be used for risk stratification. Furthermore, Cardiac damage can manifest as myocarditis, pericarditis, rhythm abnormalities. The use of different diagnostic modalities like electrocardiogram (ECG), echocardiogram, and cardiac magnetic resonance imaging (MRI)(CMR) to evaluate the myocardial damage were studied. However, Cardiovascular complications are a common manifestation of PASC, classification of severity of cardiac symptoms and the emergence of CMR as a diagnostic tool needs more evidence. •The presence of stress-related (Takotsubo) cardiomyopathy has also been demonstrated in COVID-19.•The proposed mechanisms of cardiac damage during the acute phase of COVID-19 include both direct -viral penetration- and indirect routes -hypoxic injury and systemic inflammation.•SARS-CoV-2 infection, especially in its severe form, is associated with an increased risk for venous thromboembolism (VTE).•Unfractionated heparin (UFH) is the first-line treatment for hemodynamic instability and emergency reperfusion for PASC.•Further studies are needed to offer current screening for the occurrence of cardiovascular problems especially myocardial infarction and heart failure in COVID-19 patients. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) or coronavirus disease 2019 (COVID-19) initially surfaced in December 2019 from Wuhan, China, sweeping the world with various strains, forcing the WHO to declare a pandemic epidemic in March 2020. Furthermore, COVID-19 manifests with a wide array of presentations from fever and fatigue to severe respiratory and cardiovascular complications. Post-COVID-19 syndrome is poorly understood affecting COVID-19 survivors at all levels of disease severity. The disease is most associated with post-discharge dyspnea and fatigue. However, other persistent symptoms as chest pains, palpitations, smell, and taste dysfunctions. Patients with high concentrations of CRP and creatinine in the acute phase of Covid-19 are more prone to cardiac sequelae. Therefore, high levels of cardiac-sensitive troponin and hypokalaemia can also be used for risk stratification. Furthermore, Cardiac damage can manifest as myocarditis, pericarditis, rhythm abnormalities. The use of different diagnostic modalities like electrocardiogram (ECG), echocardiogram, and cardiac magnetic resonance imaging (MRI)(CMR) to evaluate the myocardial damage were studied. However, Cardiovascular complications are a common manifestation of PASC, classification of severity of cardiac symptoms and the emergence of CMR as a diagnostic tool needs more evidence. • The presence of stress-related (Takotsubo) cardiomyopathy has also been demonstrated in COVID-19. • The proposed mechanisms of cardiac damage during the acute phase of COVID-19 include both direct -viral penetration- and indirect routes -hypoxic injury and systemic inflammation. • SARS-CoV-2 infection, especially in its severe form, is associated with an increased risk for venous thromboembolism (VTE). • Unfractionated heparin (UFH) is the first-line treatment for hemodynamic instability and emergency reperfusion for PASC. • Further studies are needed to offer current screening for the occurrence of cardiovascular problems especially myocardial infarction and heart failure in COVID-19 patients . The severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) or coronavirus disease 2019 (COVID-19) initially surfaced in December 2019 from Wuhan, China, sweeping the world with various strains, forcing the WHO to declare a pandemic epidemic in March 2020. Furthermore, COVID-19 manifests with a wide array of presentations from fever and fatigue to severe respiratory and cardiovascular complications. Post-COVID-19 syndrome is poorly understood affecting COVID-19 survivors at all levels of disease severity. The disease is most associated with post-discharge dyspnea and fatigue. However, other persistent symptoms as chest pains, palpitations, smell, and taste dysfunctions. Patients with high concentrations of CRP and creatinine in the acute phase of Covid-19 are more prone to cardiac sequelae. Therefore, high levels of cardiac-sensitive troponin and hypokalaemia can also be used for risk stratification. Furthermore, Cardiac damage can manifest as myocarditis, pericarditis, rhythm abnormalities. The use of different diagnostic modalities like electrocardiogram (ECG), echocardiogram, and cardiac magnetic resonance imaging (MRI)(CMR) to evaluate the myocardial damage were studied. However, Cardiovascular complications are a common manifestation of PASC, classification of severity of cardiac symptoms and the emergence of CMR as a diagnostic tool needs more evidence. |
ArticleNumber | 101012 |
Author | Vorla, Monica Elseidy, Sheref A. Fatima, Amina Elbadawy, Merihan A. Awad, Ahmed K. Mandal, Debvarsha Mohamad, Tamam |
Author_xml | – sequence: 1 givenname: Sheref A. surname: Elseidy fullname: Elseidy, Sheref A. organization: Internal medicine department, University of Texas health sciences, Houston, TX – sequence: 2 givenname: Ahmed K. surname: Awad fullname: Awad, Ahmed K. email: ahmedkawad@gmail.com organization: Faculty of Medicine, Ain Shams University, Cairo, Egypt – sequence: 3 givenname: Monica surname: Vorla fullname: Vorla, Monica organization: Department of internal medicine, University of Louisville School of Medicine, Louisville, Ky – sequence: 4 givenname: Amina surname: Fatima fullname: Fatima, Amina organization: University of Louisville School of Medicine, Louisville, Ky – sequence: 5 givenname: Merihan A. surname: Elbadawy fullname: Elbadawy, Merihan A. organization: Faculty of Medicine, Ain Shams University, Cairo, Egypt – sequence: 6 givenname: Debvarsha surname: Mandal fullname: Mandal, Debvarsha organization: University of Louisville School of Medicine, Louisville, Ky – sequence: 7 givenname: Tamam surname: Mohamad fullname: Mohamad, Tamam organization: Cardiovascular Disease Department, Wayne State University, Detroit, MI |
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Keywords | Myocardial infarction TMPRS2 IL PACS TTE VTE RAAS NOAC TNF-Alpha CMR DAMPs COVID-19 CVD CAMKII ACE2 UFH Post covid sequelae Cardiovascular diseases SARS-CoV 2 WHO DAMPs, damage-associated molecular patterns VTE, venous thromboembolism RAAS, Renin-Angiotensin Aldosterone System dysregulation TTE, transthoracic echocardiogram CMR, Cardiac magnetic resonance imaging UFH, Unfractionated heparin CAMKII, calmodulin-dependent protein kinase II COVID-19, Coronavirus disease 2019 PACS, Post-Acute COVID-19 syndrome SARS-CoV 2, severe acute respiratory syndrome coronavirus 2 TMPRS2, transmembrane protease serine 2 IL, interleukin NOAC, novel oral anticoagulation CVD, Cardiovascular disease ACE2, Angiotensin-converting enzyme 2 WHO, World health organization TNF-Alpha, Tumor necrosis factor-alpha |
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