Objective: To determine the status of tumor necrosis factor (TNF) and other measures of immunity and inflammation in chronic heart failure (CHF) in the elderly. Design: Comparative survey study of subjects with heart failure and age-matched controls. Settings: University affiliated tertiary care VA Medical Center, Heart Failure Clinic. Patients: Twenty men with New York Class II and III heart failure and 17 age-matched controls. Interventions: None. Main outcome measure: Levels of lymphocyte mitogenesis, TNF, natural killer (NK) cell activity, elastase-Α₁-antitrypsin (E/Α) and cross-linked fibrin D-dimers (XDP). Results: TNF levels (p = 0.27), NK activity (p = 0.56), and lymphocyte mitogenesis (p = 0.67) were similar in patients and controls. E/Α levels were somewhat lower in CHF patients (p = 0.05) and XDP were similar (p = 0.59). However, TNF levels were significantly related to NK activity and to E/Α activity in elderly men with heart failure but not controls. XDP were positively related to NK in heart failure patients but not controls. Conclusion: TNF and other measures of immune function and inflammation do not appear to be significantly elevated in elderly patients with heart failure of moderate severity. However, significant relationships exist between TNF, NK activity, XDP and E/Α in the heart failure patients only, suggesting that immune activation and subclinical inflammation does exist in these patients.

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Cardiac ischemia impairs angiogenesis in response to hypoxia, resulting in ventricular remodeling. Garcinoic acid (GA), the extraction from the plant garcinia kola, is validated to attenuate inflammatory response. However, the role of GA in heart failure (HF) and neovascularization after myocardial infarction (MI) is incompletely understood. The present study is striving to explore the role of GA and the potential mechanism of which in cardiac function after MI. SD rats were randomized into sham group, MI+vehicle group, and MI+GA group in vivo. Human umbilical endothelial cells (HUVECs) were cultured in vehicle or GA, and then additionally exposed to 2% hypoxia environment in vitro. MI rats displayed a dramatically reduced myocardial injury, cardiac function and vessel density in the peri-infarcted areas. GA delivery markedly improved cardiac performance and promoted angiogenesis. In addition, GA significantly enhanced tube formation in HUVECs under hypoxia condition. Furthermore, the expressions of pro-angiogenic factors HIF-1α, VEGF-A and bFGF, and pro-angiogenic proteins phospho-VEGFR2Tyr1175 and VEGFR2, as well as phosphorylation levels of Akt and eNOS were increased by GA treatment. In conclusion, GA preserved cardiac function after MI probably via promoting neovascularization. And the potential mechanism may be partially through upregulating the expressions of HIF-1α, VEGF-A, bFGF, phospho-VEGFR2Tyr1175 and VEGFR2 and activating the phosphorylations of Akt and eNOS.