Plasminogen activator inhibitor-1 (PAI-1) activity post myocardial infarction: the role of acute phase reactants, insulin-like molecules and promoter (4G/5G) polymorphism in the PAI-1 gene

High PAI-1 levels post acute myocardial infarction (AMI) are associated with a poor outcome. Concentrations of insulin-like molecules, proinflammatory cytokines and an insertion (5G)/deletion (4G) polymorphism in the promoter of the PAI-1 gene, all influence circulating PAI-1 levels. We studied the determinants of PAI-1 in 123 patients immediately following and at 6 months after AMI. Within 24 h of AMI, PAI-1 levels were related to those of proinsulin-like molecules but not to levels of cytokines (interleukin-1β, interleukin-6 or tumour necrosis factor-α), to genotype, or to interactions between genotype and cytokine concentration. PAI-1 levels 6 months after AMI were related to concentrations of interleukin-1β but not to genotype. We have found no evidence that subjects with the 4G/4G polymorphism have higher PAI-1 levels on admission or 6 months after AMI. In these patients, levels of PAI-1 are related to concentrations of proinsulin-like molecules and of proinflammatory cytokines.