Hypertension is associated with the flow of blood under high pressures, yet the complications of hypertension, such as myocardial infarction or stroke are paradoxically thrombotic rather than haemorrhagic. This could be explained by increasing evidence which suggests that hypertension fulfils the pre-requisites of the Virchows triad for thrombogenesis, leading to a prothrombotic or hypercoagulable state. Hypertension leads to changes in the platelets, endothelium and the coagulation and fibrinolytic pathways which help to promote the induction and the maintenance of this prothrombotic state. These changes can to a certain extent be reversed by the treatment of hypertension, although different antihypertensive agents may have variable effects in reversing these changes. Some of the effects may be simply related to normalisation of blood pressure, but certain groups of drugs such as those acting on the renin-angiotensin-aldosterone system appear to have an effect over and above this. Anti-platelet agents have also been shown to confer a degree of benefit to ‘high risk’ hypertensive patients. The study of the prothrombotic state in hypertension is therefore of paramount importance, as understanding the pathogenic processes underlying it can help prevent many of the complications associated with this condition.
Keywords: hypertension, thrombosis, antihypertensive agents, antiplatelet agents, platelet activation, endothelial dysfunction
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