**8. Summary**

In summary, there is evidence that OSA results in elevated levels of fibrinogen and increased platelet activity, promotes platelet adhesion and aggregation, and results in an impaired fibrinolytic capacity. A hypercoagulable state and impaired fibrinolysis promote thrombotic events, and this might be one of the several underlying mechanisms linking OSA with an adverse cardio- and cerebrovascular outcome. Several other pathophysiological consequences of OSA that differ between phenotypes of OSA, clustering of cardiovascular risk factors, and comorbidities might define the vascular risk that OSA induces in an individual. However, hypercoagulability, fibrinolysis, and haemostasis are potential therapy targets that can be influenced either via the coagulation system or the endothelium.

**Supplementary Materials:** The following are available online at https://www.mdpi.com/article/10 .3390/ijms22062834/s1.

**Author Contributions:** The manuscript was drafted and was critically reviewed and approved by all authors. The figures and tables were created by M.M. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research received no external funding.

**Institutional Review Board Statement:** Not applicable.

**Informed Consent Statement:** Not applicable.

**Data Availability Statement:** Not applicable.

**Acknowledgments:** Andras Bikov is supported by the NIHR Manchester BRC.

**Conflicts of Interest:** The authors declare no conflict of interest.
