Myocardial dysfunction during sepsis and pneumonia has been variously associated with increased circulating cytokines and prostanoids, endothelin upregulation, impaired oxygen utilization, and increased levels of C-reactive protein (Kumar et al., 1996; Merx and Weber, 2007; Musher et al., 2007; Hunter and Doddi, 2010; Singanayagam et al., 2012). This evidence concerns the gene CRP and pneumonia.