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The present coronavirus disease (COVID-19) has emerged as a global pandemic, infecting millions and killing thousands of patients. Even though many questions remain unanswered, knowledge on the pathophysiology of COVID-19 has improved substantially around many aspects, including the development of the virus, the role of ACE2 receptors, the type and severity of organ involvement, the importance of coagulopathy and endotheliopathy, and the role of disproportionate cytokine response [1]. There is growing evidence that patients with COVID-19 are in fact having a heterogeneous disease, going well beyond the differences in lung compliance and ventilation-to-perfusion mismatch [2]. Elucidating the variable phenotypes and the underlying pathophysiology can be a key step to individualize therapy.
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Shrestha et al. (2020) studied this question.
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