Abstract
BackgroundInflammation 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.ResultsThirty-seven dogs with cardiovascular diseases (dilated cardiomyopathy, DCM (16 dogs), myxomatous mitral valve disease, MMVD (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). No significant difference was found in most of the measured parameters between MMVD and DCM patients, except for glutathione peroxidase (GPX) and NT-proBNP. In patients with CHF, TNF-α correlated positively with malondialdehyde (P = 0.014, r = 0.474) and negatively with 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).ConclusionInflammatory 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.
Highlights
Inflammation and oxidative stress can contribute to the development and progression of heart failure
Rubio and colleagues found no significant differences in a number of cytokines (IL-2, IL-6, IL-7, IL-8, IL-10, IL-15, IL-18, interferon gamma-induced protein, monocyte chemoattractant protein-1, granulocyte macrophage-colony stimulating factor, tumour necrosis factor-α (TNF-α) and interferon-gamma) between dogs with different stages of heart failure due to myxomatous mitral valve disease (MMVD) or dilated cardiomyopathy (DCM) [15]
The concentration of Tumor necrosis factor-alpha (TNF-α) was significantly (P = 0.030) higher in patients with congestive heart failure (CHF) compared to patients without CHF, while no significant difference was found in comparison to control dogs
Summary
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). Inflammatory markers are released from the cells of failing myocardium and endothelial cells, blood leukocytes, and platelets, as well as from the liver and lungs [1,2,3]. Markers of inflammation, such as C–reactive protein (CRP), cytokines, and their corresponding soluble receptors, white blood cell count (WBC) and markers of an activated immune system, have been reported to be elevated in human heart failure patients [4,5,6,7]. Rubio and colleagues found no significant differences in a number of cytokines (IL-2, IL-6, IL-7, IL-8, IL-10, IL-15, IL-18, interferon gamma-induced protein, monocyte chemoattractant protein-1, granulocyte macrophage-colony stimulating factor, tumour necrosis factor-α (TNF-α) and interferon-gamma) between dogs with different stages of heart failure due to MMVD or dilated cardiomyopathy (DCM) [15]
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