Ricerc@Sapienza

Background: Offspring of patients with early myocardial infarction have a higher risk to develop cardiovascular events; the underlying physiopathology is still unclear.
Several lines of evidence support a role for oxidative stress in atherogenesis and NADPH oxidase-2 (NOX-2) is considered a major source of O2- in human. Thus, oxidative stress regulates arachidonic acid metabolism via activation of platelet phospholipase-A2.
Furthermore, recent studies suggested that changes of gut microbiota is associated to cardiovascular disease. In particular, lipopolysaccharide (LPS) derived from Gram-negative bacteria, is believed to play a role in causing atherosclerosis by increase of oxidative stress and inflammation.
The aim of this study is to address NOX-2 activity as well as serum thromboxane B2 (TXB2), 8-isoPGF2-alpha and LPS in offspring of patients with premature myocardial infarction.
Methods: Ninety-two consecutive subjects, including 46 offspring of patients with premature myocardial infarction and 46 healthy subjects (HS) matched for age and gender, will be recruited.
A cross sectional study will be performed to compare serum activity of soluble NOX-2-dp (sNOX-2-dp), blood levels of isoprostanes and serum TXB2 in these two groups; LPS and zonuline levels will be analyzed. Serum zonulin, will be assessed as measure of gut permeability.
Univariate and multivariate analysis will be performed to to define the independent predictors of sNOX-2-dp and serum isoprostanes.

This study want to evaluate if Nox-2 activation is a key determinant of oxidative stress and platelet activation in offspring of patients with premature myocardial infarction and if gut mycrobiota could play a role in this pathogenic process.