The mechanism by which patent foramen ovale (PFOs) are associated with ischemic stroke is believed to be paradoxical embolism. It has been observed that people with migraine with aura have a larger than expected concomitant prevalence of PFO compared to people without migraine. Transient global amnesia is considered to have a similar pathophysiology to migraine, and an association with PFO has also been observed. The mechanisms by which obstructive sleep apnea (OSA) increases the risk of ischemic stroke are multiple and all contribute to the ischemic event. As the risk seems associated with the multiple physiological abnormalities that accompany OSA and facilitated by a PFO, stroke prevention could potentially be achieved by improving OSA and reducing the right-to-left shunt treatment, antithrombotic therapy, PFO closure. Antithrombotic therapy should be given as well, in light of the greater overall cardiovascular risk.

This chapter outlines the hemostatic response to vascular damage in the carotid artery and considers the endogenous hemostatic factors that may determine the likelihood of embolization in patients. It discusses the mechanisms involved in thrombus formation and stabilization. Platelets provide a reinforced loop in the generation of a thrombus, providing a source of thrombin to recruit new platelets and propagate clot formation. The mechanism of stabilization of a thrombus by P-selectin appears to be partly stabilization of platelet-platelet aggregates but mostly through recruitment of leucocytes via interaction of P-selectin with PSGL-1. Many factors are involved in forming a stable thrombus and consequently there are many candidates for regulating the risk of embolization. Antiplatelet and antithrombotic therapies are of benefit in limiting the growth of thrombus within the carotid vessel. In particular, adenosine diphosphate (ADP) seems to have a very specific role in regulating embolization.