**1. Introduction**

Haemostasis is a protective process that regulates and maintains stable physiology in the system. The physiology of haemostasis is extremely complex and reflects a delicate balance between the constant blood flow and immediate localised response to vascular injury. The process of haemostasis is traditionally divided into a cellular phase (involving platelets), known as the primary haemostatic phase and a fluid phase (involving plasma proteins), also called the secondary haemostatic phase [1]. It associates with other body defence mechanisms, including the immune system and the inflammatory responses [2]. During vascular injury, the increased blood pressure exerted in the blood circulation requires powerful and regulated localised pro-coagulant responses to minimise blood loss without compromising blood flow. Systemic anticoagulant and fibrinolytic components in other ways are also developed

to inhibit the extension of the pro-coagulant responses to escalate beyond the vascular endothelial control, which may result in thrombotic formation. Thus, the haemostatic system is defined as a complex, highly regulated and integrated process, comprising both activators and inhibitory pathways, including blood vessels, platelets activities, coagulation and fibrinolytic system together [3]. While the coagulation cascade is aimed at fibrin formation through the production of thrombin, which is converted to fibrinogen (FN) and subsequently to fibrin, in the fibrinolytic system, plasmin is the main enzyme that plays a key role in dissolving the already formed clots by degrading fibrin. Physiological anticoagulation mechanisms function to suppress thrombin generation or inhibit its effects. Alterations to these mechanisms could lead to hypercoagulable states. This chapter will focus on the mechanisms associated with anticoagulation and defects of the anticoagulation mechanisms, leading to hypercoagulable states. The review also gave a concise description of the clinical approaches and traditional intervention to minimise the effects of hypercoagulability, which may progress to cardiovascular diseases (CVDs).
