Abstract
Congenital heart disease (CHD) often requires surgical intervention, and is sometimes associated with life-threatening post-operative complications. We have investigated some factors of the innate immune system involved in the initiation or regulation of complement lectin pathway activation (MASP-1, MASP-2 MASP-3, MAp19, MAp44, ficolin-3) and related them to complications and prognosis in 190 pediatric patients undergoing CHD repair with the use of cardiopulmonary bypass (CPB). Patients with MAp44 levels ≤1.81 µg/ml more frequently experienced low cardiac output syndrome (LCOS), renal insufficiency, systemic inflammatory response syndrome (SIRS) and multiorgan dysfunction (MODS). Low MASP-3 (≤5.18 µg/ml) and high MASP-1 (≥11.7 µg/ml) levels were often associated with fatal outcome. Low ficolin-3 concentrations (≤10.1 µg/ml) were more common among patients experiencing SIRS and MODS than in those without complications. However, patients suffering from SIRS and MODS with low ficolin-3 had a much better prognosis (91% survival vs. 37% among other patients; p = 0.007). A discriminating value of 12.7 µg/ml ficolin-3 yielded 8% vs. 60% mortality (p = 0.001). Our data extend the knowledge concerning involvement of proteins of the lectin pathway in development of post-CPB complications. The potential prognostic value of low preoperative MAp44 and high preoperative ficolin-3 seems promising and warrants independent confirmation.
Highlights
MASP-2 MASP-3, MAp19, MAp44, ficolin-3) and related them to complications and prognosis in 190 pediatric patients undergoing Congenital heart disease (CHD) repair with the use of cardiopulmonary bypass (CPB)
Patients may be affected by hospital-acquired infections, low cardiac output syndrome (LCOS) and systemic inflammatory response syndrome (SIRS) which may further lead to multiple organ dysfunction syndrome (MODS)
The last is activated by specific pattern-recognition molecules (PRMs), i.e., ficolins and some collectins, complexed with enzymes belonging to the MASP family
Summary
MASP-2 MASP-3, MAp19, MAp44, ficolin-3) and related them to complications and prognosis in 190 pediatric patients undergoing CHD repair with the use of cardiopulmonary bypass (CPB). Patients with MAp44 levels ≤1.81 μg/ml more frequently experienced low cardiac output syndrome (LCOS), renal insufficiency, systemic inflammatory response syndrome (SIRS) and multiorgan dysfunction (MODS). Patients may be affected by hospital-acquired infections, low cardiac output syndrome (LCOS) and systemic inflammatory response syndrome (SIRS) which may further lead to multiple organ dysfunction syndrome (MODS). The last is activated by specific pattern-recognition molecules (PRMs), i.e., ficolins and some collectins, complexed with enzymes belonging to the MASP (mannose-binding lectin serine protease) family. PRM-MASP complexes are considered important players of the first-line antimicrobial innate immune defense Beside microbial structures, their activation can be triggered by apoptotic cells, necrotic debris or other aberrant self-structures[9]. A substrate for the MASP-3 protease is profactor D, which leads to generation of factor D, an enzyme involved in the initiation of the alternative pathway of complement[12,13]. MASP-1 and MASP-2 may contribute to thrombogenesis from their ability to cleave fibrinogen, factor XIII, prothrombin and thrombin activatable fibrinolysis inhibitor (TAFI)[17,18,19]
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