In the one year since SARS-CoV-2 (COVID-19) arrived on the scene, the virus has precipitated nothing short of a serious global health crisis. One of the virus’s less-obvious dimensions has been its impact on the human cardiovascular system.
Over the past year, COVID-19 has been associated with several critical cardiovascular complications. So much so that even patients with no history of cardiovascular disease seem to be at risk of developing cardiovascular complications as a result of COVID-19. Indeed, patients with severe COVID-19 infection commonly experience thrombotic disorders with elevated D-dimer, sepsis, disseminated intravascular coagulation (DIC) with high mortality rates.
Several large-scale studies have shown that 18.8%-36.2% of COVID-19 patients show thrombocytopenia at the time of admission into hospital and in cumulative, 31% of ICU patients experience thrombotic complications. Even though there is overwhelming evidence of a hypercoagulable state in COVID-19 patients, the molecular events and underlying mechanisms still remain largely a mystery.
The role of platelets
It is well known that platelets play an important role in thrombosis and hemostasis. During infection, activated platelets adhere to the sub-endothelium and their hyperactivity can result in thrombus formation, leading to arterial ischemia and pulmonary embolisms. Many viral infections, such as hepatitis C (HCV), Ebola, human immunodeficiency virus (HIV), dengue virus (DV) and influenza, directly lead to the activation of platelets triggering uncontrolled coagulation cascades, resulting in lung injury. We know that SARS-CoV-2 uses a spike protein to bind to ACE2 receptors on the host cell for entry and multiplication, but we have little insight into how this influences platelets.
This story is from the January 2021 edition of Future Medicine India.
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This story is from the January 2021 edition of Future Medicine India.
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