Severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) and the resulting
coronavirus disease-19 (COVID-19) have led to a global pandemic associated with high fatality rates.
COVID-19 primarily manifests in the respiratory system as an
acute respiratory distress syndrome following viral entry through the
angiotensin-converting enzyme-2 (ACE2) that is present in pulmonary epithelial cells. Central in
COVID-19 is the burst of
cytokines, known as a "
cytokine storm", and the subsequent widespread endothelial activation, leading to cardiovascular complications such as
myocarditis, arrhythmias, and adverse vascular events, among others. Genetic alterations may play an additive, detrimental role in the
clinical course of patients with
COVID-19, since gene alterations concerning ACE2, major histocompatibility complex class I, and
toll-like receptors may predispose patients to a worse clinical outcome. Since the role of
inflammation is quintessential in
COVID-19, pharmacologic inhibition of various signaling pathways such as the
interleukin-1 and -6,
tumor necrosis factor-alpha,
interferon gamma,
Janus kinase-signal transducer and activator of transcription, and
granulocyte-macrophage colony-stimulating factor may ameliorate the prognosis following timely administration. Finally, frequently used, non-specific
anti-inflammatory agents such as
corticosteroids,
statins,
colchicine, and
macrolides represent additional therapeutic considerations.