ABSTRACT
INTRODUCTION Arterial occlusion resulting from thrombosis or thromboembolism, although relatively uncommon in pregnancy, may have devastating consequences. The aetiology of arterial thrombosis, like that of venous thromboembolism, is multi-factorial (Table 14.1). In the general population atherosclerotic plaque rupture and subsequent thrombus formation is the final common path that most frequently leads to coronary, cerebral or peripheral artery occlusion. However, although early atherosclerotic lesions are evident from adolescence, other mechanisms may play an important role in promoting thrombus formation and embolism in young patients. Altered blood flow or stasis in patients with cardiac arrhythmias, cardiac valve lesions or prosthetic heart valves may result in endothelial damage and platelet activation. Exposure of blood to foreign surfaces such as prostheses and grafts causes platelet activation and hypercoagulability, which, although more generally associated with enhancing the risk of venous thrombosis, may in some circumstances increase the risk of arterial occlusion.
