Changes of plasma activated Factor XII type A (XIIaA) concentrations following percutaneous coronary intervention (PCI)

Abstract

A significant short-lasting increase in specific types of XIIa (namely XIIaA) was observed following PCI. These increases are most likely induced by the concomitant treatment with heparin.

Specific types of activated Factor XII increase following thrombolytic therapy with tenecteplase

“…Heparin-induced changes in XIIa concentration could not be demonstrated in STEMI patients treated with heparin alone [3], however, the documentation of a heparin effect on different types of XIIa remains sparse. Obviously, this lack of knowledge necessitates further research, and recently we were able to demonstrate an increase in the specific types of XIIa secondary to the use of unfractionated heparin [22]. To date, whether a A clinical benefit of fibrin-specific thrombolytics as compared to non-selective thrombolytics has been postulated, and might theoretically result in a lower complication rate due to less activation of the contact system.…”

Activated factor XII type A predicts long‐term mortality in patients admitted with chest pain

“…The alkaline phosphatase conjugated secondary antibody was a monoclonal antibody against XIIa. Further details of the assay have been recently reported [26,27].…”

“…However, recent research indicates that in vivo XIIa exists in multiple forms, and that the predominant species is a 53 kD molecule consisting of the catalytic chain linked via a disulfide bridge to a truncated heavy chain that has lost one fibronectin finger domain and one EGF domain. It has also been shown that in vivo XIIa can exist in the circulation complexed to various other proteins, and is also associated with lipoproteins and cellular material in addition to being present in the aqueous phase of plasma [26,27]. One of these recently discovered forms of XIIa, termed XIIaA, is comprised of a circulating form of the 53 kD species that can be readily measured in plasma, without the requirement of adding agents to dissociate it from binding partners, whereas a form termed XIIaR requires addition of an agent (such as a detergent) to disrupt the association with its binding partners before it can be measured.…”

Factor XII: a novel target for safe prevention of thrombosis and inflammation

“…The Risk in Acute Coronary Syndrome (RACS) study group in Stavanger, Norway, found that increased plasma levels of FXIIa on admission to hospital were associated with higher mortality in 870 patients with chest pain . FXIIa levels were also increased following percutaneous coronary intervention and associated with risk factors for coronary heart disease such as smoking, blood pressure, serum cholesterol level and alcohol intake in the Northwick Park Heart Study . Individuals with severe FXI deficiency were found to have a lower risk for ischaemic stroke and deep vein thrombosis .…”