Myocardial damage with a consequent rise in cardio-specific troponin level is a frequent phenomenon in severe cases of coronavirus disease 2019 (COVID-19). Its causes are capillary endothelial cell dysfunction, associated carditis, low oxygenization, and increased sympathetic tone, which all worsen myocardial stiffness and microvascular dysfunction (MD). They lead to severe myocardial dysfunction, arrhythmia, acute congestive heart failure, and a significant rise in death cases. During COVID-19, no specific cardiological treatment is started. As adjuvant therapy, anxiolytics in COVID-19 are widely used, but not in all anxious patients who had been infected with coronavirus. Anxiolytics can be useful to moderate MD and immunosuppressive effect of anxiety. The favorable effects of trimetazidine (TMZ) and Coenzyme Q10 (CoQ10) in the treatment of myocardial ischemia and heart failure had previously been proven, and also their anti-inflammatory effects had been suspected; however, they have not yet been used in COVID-19 cases. TMZ promotes glucose-mediated ATP production, which requires less oxygen, which explains its advantageous cardiac effects. Since it lowers serum and myocardial tissue proinflammatory cytokine levels and inhibits myocardial macrophage infiltration, it was suspected that TMZ might represent a novel therapeutic agent to prevent and treat sepsis-induced myocardial dysfunction. CoQ10 plays an important role in cellular ATP production; however, its concentration is decreased in cardiovascular diseases and in influenza patients. Due to its anti-inflammatory effect, CoQ10 has been suspected to have a key therapeutic target in influenza infection. We suggest considering these medicines to alleviate myocardial damage and inflammation in COVID-19.