The novel coronavirus SARS-CoV-2, responsible for the 2019–2020 global (COVID-19) pandemic, is a respiratory virus associated with the development of thromboembolic complications and respiratory failure in severe cases. Increased risk of pulmonary embolism and thrombosis has been identified in COVID-19 patients, alongside accompanying elevations in potential prognostic biomarkers, including D-dimer, IL-6 and cardiac specific troponins. Our aim was to provide a scoping review of the available literature regarding thrombosis risk, other cardiovascular implications, and their biomarkers in COVID-19 to highlight potential disease mechanisms. Authors conducted a literature search in PubMed using MeSH headings “disseminated intravascular coagulation”, “pulmonary embolism”, “thromb*”, “stroke”, “myocardial infarction” and “acute lung injury”, as well as terms “COVID-19”, “SARS-CoV-2”, “2019 novel coronavirus” and “2019-nCoV”. COVID-19 disease is characterised by the interactions between hyperactive coagulation and complement systems – induced by hyper-inflammatory conditions, resulting in a pro-thrombotic state and diffuse tissue injury. There are several promising prognostic markers of disease severity, with D-dimer the most significant. The presence of thrombocytopenia appears to be a key indicator of patient deterioration. Further research is required to understand the underlying pathophysiology in COVID-19 and its implications in disease progression and patient management. Randomised trials are urgently needed to determine the safety of proposed therapeutic anticoagulation with heparin and the role for anti-platelet agents, such as Ticagrelor, in patient management. Display omitted •COVID-19 is associated with an increased risk of thrombotic complications.•COVID-19 phenotype results from inflammation, complement and coagulation interplay.•D-dimer, thrombocytopenia and IL-6 are promising markers of COVID-19 severity.•Anticoagulative therapy in COVID-19 needs further study.