Genetic basis of procoagulant and fibrinolytic perioperative adverse events

Abstract Thrombotic adverse outcomes contribute to significant morbidity and mortality after major invasive surgery. Surgery creates an acute phase or ‘stress’ response, that causes the release of prothrombotic proteins and thrombocytosis. Some patients exhibit an exaggerated response. In cardiothoracic surgery the same acute phase response contributes to a variety of adverse outcomes from abnormal bleeding to coronary artery thrombosis and stroke. A number of genetic variants or polymorphisms have been elucidated that have bearing on peri-operative risk and adverse outcomes. These polymorphisms have been correlated with venous thrombosis, accelerated atherosclerosis, unstable angina and acute myocardial infarction (MI) in the non-surgical setting. The contribution of these polymorphisms to adverse outcomes after surgery is being investigated. By understanding some key polymorphisms and potentially testing for them in the future, we may be better able to target expensive pharmacological therapies as well as predicting or preventing certain adverse prothrombotic outcomes.