Abstract
Hemostatic processes contribute to gradual fibrin deposition within atherosclerotic plaques and overt thrombus formation subsequent to plaque disruption. Activation of sympathetic nervous system (SNS) affects blood coagulation, fibrinolysis and platelet activation by several mechanisms. Given the significance of increased hemostatic activity in atherosclerosis and thrombosis and the important role of the SNS in cardiovascular disease, sympathetic activation and catecholamine effects might contribute to arterial thrombus formation. In particular, chronic stimulation of the SNS and concomitant hypercoagulable changes could contribute to gradual fibrin deposition at sites of atherosclerotic lesions and, in patients with endothelial dysfunction, acute stress response could trigger rupture of an atherosclerotic plaque. Further studies are needed to better understanding the regulation of the SNS-hemostasis axis.
Highlights
Given the significance of increased hemostatic activity in atherosclerosis and thrombosis and the important role of the sympathetic nervous system (SNS) in cardiovascular disease, sympathetic activation and catecholamine effects might contribute to arterial thrombus formation
Chronic stimulation of the SNS and concomitant hypercoagulable changes could contribute to gradual fibrin deposition at sites of atherosclerotic lesions and, in patients with endothelial dysfunction, acute stress response could trigger rupture of an atherosclerotic plaque
Hemostatic processes contribute to gradual fibrin deposition within atherosclerotic plaques and overt thrombus formation subsequent to plaque disruption [1]
Summary
Hemostatic processes contribute to gradual fibrin deposition within atherosclerotic plaques and overt thrombus formation subsequent to plaque disruption [1]. Given the significance of increased hemostatic activity in atherosclerosis and thrombosis and the important role of the SNS in cardiovascular disease, sympathetic activation and catecholamine effects might contribute to arterial thrombus formation. Chronic stimulation of the SNS and concomitant hypercoagulable changes could contribute to gradual fibrin deposition at sites of atherosclerotic lesions and, in patients with endothelial dysfunction, acute stress response could trigger rupture of an atherosclerotic plaque.
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