COVID-19 patients are susceptible to hypoxemia due to reduced lung performance, impaired gas exchange across the inflamed alveoli and abnormal ventilation/perfusion. This will lead to decreased myocardial oxygen supply, myocardial ischemia and impaired calcium homeostasis. The disturbance in calcium balance will trigger the activation of the NLRP3 inflammasome and different inflammatory components which consequently lead to the death of cardiomyocytes (Moccia et al., 2020; Zheng et al., 2020). Additionally, the systemic response to pneumonia includes an increase in sympathetic activity causing severe tachycardia and increased peripheral resistance. Subsequently, a rapid heart rate together with vasoconstriction may result in elevated myocardial oxygen requirements and a shortened diastolic interval, the period during which coronary perfusion occurs. The mismatch between myocardial oxygen demand and supply can lead to cardiac ischemia and infarction, especially in the presence of pre-existing coronary artery disease (Corrales-Medina, Musher, Shachkina, & Chirinos, 2013). Volume overload due to impaired sodium and water metabolism (Dreyfuss, Leviel, Paillard, Rahmani, & Coste, 1988), transient disturbance of endothelial function and vascular tone (Benson, Akbarian, Adler, & Abelmann, 1970; Kumar, Wallace, Ramirez, Benson, & Abelmann, 1970) and cardiac arrhythmias (Cilli et al., 2018) may also contribute to decreased left ventricular function or worsening of HF in patients with COVID-19.