INTRODUCTION

The diagnostic and therapeutic approach to thrombosis is dependent upon not only the vascular territory at risk but also the mechanism of thrombosis (Table 15.1). The composition of thrombus is dynamically dependent upon the local environment in which clot formation occurs. Arterial thrombi are more likely to be “white” clots, rich in platelets. By principles of physics, shear stress is highest at the fluid–endothelium interface in settings of typical arterial laminar flow. Erythrocytes and leukocytes predominate in the center of the flow and platelets are concentrated closer to the arterial wall as the larger blood cells are propelled with blood flow. The platelets' proximity to the endothelium allows for rapid platelet plug formation in case of arterial injury, which is a key adaptation for survival from trauma. Prothrombotic shear-dependent factors released by the endothelium – including von Willebrand factor, tissue factor, and adhesion molecules–allow for rapid activation of platelets in this setting. Hence, thrombus formation under high-shear conditions (i.e., within arteries) is more platelet-dependent with initial thrombus more platelet-rich until local rheology changes with the occlusiveness of the thrombus and low-shear dynamics predominate resulting in greater fibrin deposition.

The principles of Virchow's triad still hold true – stasis, endothelial injury, and hypercoagulability – for venous thrombosis. These same factors also increase fibrin deposition after initial platelet adhesion in arterial thrombosis resulting in occlusive arterial thrombi and also within the chambers of the heart resulting in thromboemboli.