Patients with underlying hypertension, diabetes, and cancer are at higher risk for developing thrombotic events. Coagulopathy in coronavirus infection is now associated with high mortality and manifests with high d-dimer elevations [102]. Lung inflammation and impaired pulmonary gas exchange contributes to cytokine storm, which leads to spike in d-dimer and pro-inflammatory response, with impaired endothelial function. Tissue factor (TF), expressed by tumor cells, contributes to thrombosis, metastasis, tumor growth, and tumor angiogenesis, leading to release of pro-coagulant microparticles into the circulation and triggering thromboembolism in patients with cancer [103]. TF on circulating tumor cells leads to coating of cells with fibrin that traps them within microvasculature, thereby contributing to worsening endothelial dysfunction [104]. In patients with pre-existing cancer diagnoses, shared COVID infection as well as hypoxia places them at even greater risk of developing and incurring thrombotic events [105]. Early heparin initiation is posited to delay the spike in inflammatory biomarkers and may reduce contributions to pro-coagulopathic state [106]. A retrospective study from China examined 449 patients classified as having severe COVID-19 infection, of which 272 had one or more chronic underlying diseases, such as hypertension and heart disease. Patients were assigned to receive various forms of heparin, with those treated with heparin having a lower mortality rate (40% vs. 64.2%, p = 0.029) [107]. Data regarding initiation and choice of anticoagulation remains limited, and further randomized clinical trials are necessary to determine prophylactic and treatment strategies for cardio-oncology patients infected with COVID-19, as they represent a population with elevated theoretical risk for suffering from thromboembolic events.