Although SARS-CoV-2 infection predominantly involves the respiratory system, clinical manifestations of the disease can be often expressed by cardiovascular symptoms. The symptoms like cough, dyspnea and fatigue can mimic the new onset of heart failure (HF) or the decompensation of preexisting one and can, in addition, complicate management and prognosis of COVID-19. In order to get a better understanding of the COVID-19 impact on clinical evolution and management of HF, we made a review of the articles published on this topic from April to December 2020. The existent data show that cardiac symptoms are present in 17% to 49% of survived patients and in about 52% of the deceased ones. HF is one of the most frequent complications of COVID-19, following acute respiratory distress syndrome and sepsis, and the preexisting HF is an independent predictor of a worse outcome. One of the mechanisms through which COVID19 patients present worsening of HF symptoms is acute myocardial injury due to endothelial damage, thrombosis, ischemia, infarction or myocardial inflammation. Other mechanisms are acute respiratory failure, new or recurrent arrhythmias, as well as molecular mechanisms, represented by ACE-2 receptors. No data have shown an increased severity of COVID-19 patients who are receiving ACEi/ARB treatment, therefore, in order to prevent cardiovascular decompensation these drugs should not be discontinued. Laboratory values, such as inflammatory markers, procalcitonin and brain natriuretic peptide (BNP), may suggest a diagnosis of COVID-19 pneumonia, or preexisting HF exacerbation. Patients with heart failure represent a group of risk for COVID-19 infection and have to respect prevention measures. The preexisting heart failure complicates the disease course in infected patients. Elevation of proinflammatory and heart failure biomarkers indicates a negative outcome, being useful for a prognostic evaluation in these patients. Heart failure treatment has to be continued, even in patients with concomitant COVID-19 infection.