Hypertensive emergencies are associated with elevated markers of inflammation, coagulation, platelet activation and fibrinolysis.

Data from in vitro and animal experiments suggest that progressive endothelial damage with subsequent activation of coagulation and inflammation have a key role in hypertensive crisis. However, clinical investigations are scarce. We hypothesized that hypertensive emergencies are associated with enhanced inflammation, endothelial- and coagulation activation. Thus, we enrolled 60 patients admitted to an emergency department in a prospective, cross-sectional study. We compared markers of coagulation, fibrinolysis (prothrombin fragment F(1+2), plasmin-antiplasmin complexes, plasmin-activator inhibitor, tissue plasminogen activator), platelet- and endothelial activation and inflammation (P-selectin, C-reactive protein, leukocyte counts, fibrinogen, soluble vascular adhesion molecule-1, intercellular adhesion molecule-1, myeloperoxidase and asymmetric dimethylarginine) between hypertensive emergencies, urgencies and normotensive patients. In hypertensive emergencies, markers of inflammation and endothelial activation were significantly higher as compared with urgencies and controls (P<0.05). Likewise, plasmin-antiplasmin complexes were 75% higher in emergencies as compared with urgencies (P<0.001), as were tissue plasminogen-activator levels (∼30%; P<0.05) and sP-selectin (∼40%; P<0.05). In contrast, similar levels of all parameters were found between urgencies and controls. We consistently observed elevated markers of thrombogenesis, fibrinolysis and inflammation in hypertensive emergencies as compared with urgencies. Further studies will be needed to clarify if these alterations are cause or consequence of target organ damage.