Abstract 3741: Stress Promotes Arterial Thrombosis through Activation of the Sympathetic Nervous System
Background: Several lines of evidence demonstrate a correlation between stress and cardiovascular mortality and morbidity. Myocardial infarction can be triggered by life threatening events such as earthquakes or missile attacks, and even every day stressful situations such as anger were shown to correlate with adverse cardiovascular events, primarily caused by arterial thrombus formation. The sympathetic nervous system is known to mediate various stress-related effects; however, a mechanism linking stress and thrombosis has not been described.
Methods: To investigate the influence of acute stress on arterial thrombosis, mice were subjected to a restraint stress protocol for 20 hours. Subsequently, arterial thrombosis was induced by photochemical injury in vivo. Furthermore, coagulation times (PT, aPTT) and tissue factor activity were assayed in plasma and carotid artery, respectively. In addition, tail bleeding time was assessed. To investigate the role of the sympathetic nervous system, chemical sympathectomy was performed by treating mice with 6-Hydroxydopamine (OHDA) or control vehicle, respectively.
Results: Time to thrombotic occlusion was significantly decreased in stressed mice as compared to controls (−26.7 ± 4.0 minutes, p<0.001, n=5). In sympathectomized mice stress failed to decrease time to occlusion (−8.1 ± 5.6 minutes, n.s., n=5); Sympathectomy alone had no effect on time to occlusion as compared to vehicle treatment. Tissue factor activity, tail bleeding time, and coagulation times remained unchanged under all conditions, indicating an unaltered state of vessel wall tissue factor, systemic coagulation and platelet function, respectively.
Conclusions: Stress enhances arterial thrombosis via the sympathetic nervous system. The link between increased sympathetic activity and thrombus formation is still under investigation. These findings may open novel perspectives for the understanding of stress-induced cardiovascular events.