The Contact Activation System: Problems and Paradoxes for Cardiac Anesthesiologists
Coagulation and inflammation are intertwined, an important concept that makes sense from a teleological perspective. Any loss of surface integrity or vascular injury requires hemostasis and also prevention of infection. This “cross-talk” between the 2 systems has been the subject of both fascination and exasperation for clinicians.1 What remains underappreciated, however, is the role of the contact activation system in regulating these responses.
In this issue of the Journal, Tanaka et al provide a detailed review of hereditary angioedema (HAE), a disorder typically due to reduced quantity and/or activity of complement component-1 esterase inhibitor (C1-INH).2 Like most regulatory proteins involved in hemostasis and inflammation, C1-INH has many targets for its inhibitory functions. These include inhibition of not only serine proteases of the complement system but the contact activation system as well. HAE represents a particularly challenging condition for cardiac anesthesiologists to manage because of contact activation that occurs during extracorporeal circulation.
In searching for what might be a revolutionary way to manage CPB, understanding pathology of the contact activation system, such as HAE, represents a critically important point for cardiac anesthesiologists to consider.
