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• Beside these, our study has some limitations. The number of patients evaluated in the study is insufficient. Furthermore, levels of TNF-alpha and other cytokines that are asserted to be influenced by pentoxifylline could be investigated. In this study, we hypothesized that inhibition of TNF-alpha may provide improvement in heart failure because TNF-alpha levels are elevated in these patients. Because TNF-alpha contributes to progression of heart failure by accelerating apoptosis. Significance of TNF-alpha in pathophysiology of heart failure is not well defined. Moreover, in the recent studies, although pentoxifylline treatment improved symptoms and ejection fraction, a notable reduction was not seen in the serum levels of TNF-alpha. Therefore it can be speculated that potential effects reported in the previous studies can act via different mechanisms. Consequently, no additional benefit was observed in clinical and echocardiographic parameters with addition of pentoxifylline to standart treatment protocol in patients with heart failure. Despite existence of studies resulted positively, the potantial role of pentoxifylline in heart failure therapy is still controversial. As a result, more extensive clinical researches with larger study populations are needed.