Since the emergence of the COVID-19 pandemic, the impact of the virus on the heart has become more pervasive prompting the Journal of the American College of Cardiology to issue a three-part focus seminar on COVID-19 in 2020 to address these complexities. Last month, we covered the Coronavirus and Cardiovascular Disease, Myocardial Injury, and Arrhythmia JACC Focus Seminar (accessible here). This month, we will review another JACC focus seminar entitled Coronavirus Historical Perspective, Disease Mechanisms, and Clinical Outcomes where researchers examine the model of COVID-19 induced injury as well as the potential long-term impact on the health and safety of global survivors.
Since our recent blog focused on peripheral blood cells, which contain cell populations important to the immune system, we thought this seminar, which addresses in part, the innate immune response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), would be an interesting companion piece.
According to the publication, most individuals infected (~80%) with SARS-CoV-2 experience mild, non-life-threatening symptoms and recover fully. But, elderly patients and people with comorbidities are more susceptible to serious infection and development of acute respiratory distress syndrome, lung injury, large-vessel thrombosis, and in situ microthrombi that may contribute to organ failure and increased mortality risk. The mortality rate is 8.0% in patients 70 to 79 years of age, 14.8% in patients ≥80 years of age, and 49.0% in critically ill patients.
Viral illnesses, including the coronaviruses (SARS-CoV-1, SARS-CoV-2, and MERS-CoV), incite a profound systemic inflammatory immune response resulting in tissue injury and organ failure. The innate immune response to SARS and other viruses involves Toll-like receptor (TLR)-3, which is expressed on the surface of human alveolar cells, bronchial epithelial cells, and a variety of hematopoietic immune cells. The recognition of viral RNA by TLR-3 triggers a cellular immune response where lymphocytes and monocytes become activated and increased levels of multiple proinflammatory cytokines is observed. This excessive release of cytokines can result in a COVID-19-induced cytokine storm syndrome (CS), which is a severe immune reaction that can cause lethal complications, such as progressive pneumonia, acute respiratory distress syndrome (ARDS), and organ failure. The release of inflammatory molecules also activates the coagulation system leading to a high incidence of venous and arterial thrombosis involving large and small vessels of various organs.
The clinical presentation of COVID-19 has informed several treatment guidelines where anti-cytokine and immunomodulatory drugs, as well as antithrombotic agents, are some of the therapies being utilized to combat the virus-induced inflammatory and coagulation responses. However, the long-term consequences for survivors of severe COVID-19 infection remain uncertain, but the researchers of the paper expressed concern over some early observations. Italian patients polled after recovery from infection reported at least 1 persistent symptom 2 months after the onset of their illness, with 44% noting a marked decline in their quality-of-life scores.
Additionally, while cardiac dysfunction and myocardial injury resulting from microvascular thrombosis were relatively mild and mostly reversible, it is plausible to assume that COVID-19 survivors will be more susceptible to long-term cardiac morbidity. Given the extent of alveolar epithelial injury, microvascular angiopathy, and duration of deep intensive care unit sedation in survivors of severe or critical COVID-19, it seems reasonable to anticipate similar or even more severe disabilities in this at-risk population persisting into the future. Patient follow-up studies and long-term testing will be important to understand the full extent of the impact of SARS-CoV2 on the health of the global population as the effects of the pandemic will be felt for many years to come.
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