Inflammation and its association with oxidative stress in dogs with heart failure

Background: Inflammation and oxidative stress can contribute to the development and progression of heart failure. This study aimed to investigate the association between inflammatory and oxidative stress markers in dogs with congestive heart failure (CHF). Associations between the disease severity marker N-terminal pro-B-type natriuretic peptide (NT-proBNP) and markers of inflammation and oxidative stress were also determined. Results Thirty-seven dogs with cardiovascular diseases (dilated cardiomyopathy (16 dogs), myxomatous mitral valve disease (21 dogs)) and ten healthy dogs were included in this prospective study. The patients were further divided into groups with (26) and without CHF (11). We found a significantly higher serum concentration of C-reactive protein (P = 0.012), white blood cell ( P  = 0.001), neutrophil ( P  = 0.001) and monocyte counts ( P  = 0.001) in patients with CHF compared to control dogs. The concentration of tumor necrosis factor-alpha (TNF-α) was significantly higher in patients with CHF compared to patients without CHF (P = 0.030). In patients with CHF, TNF-α correlated positively with malondialdehyde (P = 0.014, r = 0.474) and negatively with glutathione peroxidase (GPX) (P = 0.026, r = − 0.453), and interleukin-6 correlated negatively with GPX (P = 0.046, r = − 0.412). NT -proBNP correlated positively with malondialdehyde (P = 0.011, r = 0.493). In patients without CHF none of the inflammatory and oxidative stress markers correlated significantly. Furthermore, in the group of all cardiac patients, GPX activity significantly negatively correlated with NT-proBNP ( P  = 0.050, r = − 0.339) and several markers of inflammation, including TNF–α ( P  = 0.010, r = − 0.436), interleukin-6 ( P  = 0.026, r = − 0.382), white blood cell ( P  = 0.032, r = − 0.369), neutrophil ( P  = 0.027, r = − 0.379) and monocyte counts ( P  = 0.024, r = − 0.386). Conclusion Inflammatory and oxidative stress markers are linked in canine CHF patients, but not in patients without CHF. These results suggest complex cross communication between the two biological pathways in advanced stages of CHF.