Myocardial infarction after meningococcal infection: a potential inflammatory link or a challenging puzzle?

There is evidence that systemic inflammatory response and infectious diseases are associated with an increased risk of vascular events such as stroke and myocardial infarction in humans. However, the potential triggering effect of infectious diseases in carciovascular phenomena is typically underreported, overlooked and unexplored. The remarkable discovery of the link between cytokine networks and the pathophysiology of infectious diseases, together with studies of the CD14+ Toll-like receptor 4 (TLR4), has increased our knowledge of the inflammatory cascade within the vascular compartment as well as of coronary artery disease. In addition, meningococcal sepsis can trigger an important host inflammatory response characterized by systemic production of cytokines and chemokines, as well as activation of complement and nitric oxide pathways. However, the exact mechanism involved and the multiple pathogenic links by which infection influences acute cardiovascular events have not been explored, presenting a challenging puzzle for researchers. Determining cytokine concentrations could prove to be a valuable tool in evaluating the pathophysiology of myocardial infarction during infectious processes. The knowledge gained could guide the development of new strategies for reducing the occurrence of adverse cardiovascular events.