Complement activation in acute myocardial infarction: An early marker of inflammation and tissue injury?

•C3d levels were significantly higher in AMI patients since the admission to discharge from hospital in a longitudinal study.•Increase of C3d, sC5b9 and AGP levels in AMI patients occurred previously to classical markers of myocardial damage.•C3d and sC5b9 are potential candidates as early biomarkers for myocardial inflammation and damage in AMI. Acute myocardial infarction (AMI) is a potentially fatal condition, being a major cause of death worldwide. Ischemia suffered during AMI causes tissue damage, leading to an inflammatory process. Moreover, myocardial injury can generate damage-associated molecular patterns that activate pattern recognition molecules including some complement proteins. Here we investigated products of complement activation, C3d and soluble C5b9 (sC5b9), as potential biomarkers for myocardial injury and inflammation, as well as serum cytokines (IL-6 and TNF-alpha), alpha-1-acid glycoprotein (AGP), and classical markers of myocardial necrosis (creatine kinase, creatine kinase-MB isoform, myoglobin and troponin-I) in a longitudinal study of patients with AMI (from admission, 6 h and 12 h post admission, and at discharge from hospital). Individuals undergoing cardiac catheterization (CC) with normal coronary arteries and asymptomatics with no history of cardiovascular disease or invasive procedures were included as controls. Plasma C3d was higher in AMI at admission, 6 h, 12 h, and discharge vs CC (p