The cellular and clinical manifestations of COVID-19 from a cardiological perspective

What is it about?

After acquiring a sufficiently high viral load in the upper cavity, SARS-CoV-2 infects the goblet and ciliated cells in charge of sputum expectoration. The diffusion through the mucous layer allows the ease of infection of alveolar epithelial type II cells and systemic organs that express ACE2. The resulting illness, named coronavirus disease 2019 (COVID-19), is multifaceted and unpredictable and can manifest with early smell disorders in over 80% of cases or result in the most severe conditions like sepsis-like shock or respiratory failure in 14% of cases. Globally, it has been observed that 1 in 16 patients has encountered fatal consequences (WHO situation report 132, May–June 2020), and several infected patients were old and malnourished. Importantly, epidemiological data have been shown that preexisting cardiovascular conditions could be another central virulence factor for disease progression. In addition, clinical findings showed that not a few numbers of COVID-19 patients encounter several implications of cardiological nature, including hypoxemia, sustained activation of the endothelium, nonischemic injuries, leukocyte polarization, thrombi-derived ischemic damages, dysrhythmias, and autonomic dysfunctions.

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Photo by jesse orrico on Unsplash

Photo by jesse orrico on Unsplash

Why is it important?

Since each structure and function of the cardiovascular system shows severe implications, it is crucial to discuss from a cardiological perspective the relationship between SARS-CoV-2 infection and the cardiovascular system in order to shed some light on the mechanisms that can lead to cardiac symptoms or fatal consequences in COVID-19 patients.

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