OBJECTIVE:To evaluate the cost and effectiveness of Shenmai injection and Salvianolate for injection in adjuvant treatment of coronary heart disease with heart failure. METHODS:In prospective randomized controlled clinical study,103 pa-tients with coronary heart disease with heart failure were randomized into 2 groups:55 patients in group A received Shenmai injec-tion 50 ml added into 5% Glucose solution 250 ml intravenously on the basis of routine treatment,once a day;48 patients in group B received Salvianolate for injection 200 mg added into 5% Glucose solution 250 ml intravenously on the basis of routine treatment,once a day;treatment course lasted for 2 weeks. The improvement of clinical indicators and ADR were observed before and after treatment;2 drug treatment programs were evaluated and analyzed with pharmacoeconomics. RESULTS:Total effective rates of group A and B were 89.09% and 72.92%,with statistical significance(P<0.05);the incidence of ADR in group A and B were 9.09% and 12.50%,there was no statistical significance(P>0.05). The cost-effectiveness ratio of group A was significantly lower than that of group B,with statistical significance(P<0.05);the results of sensitivity analysis was consistent with it,indicat-ing the cost of Shenmai injection was in low level. CONCLUSIONS:Shenmai injection is more economic in adjuvant treatment of coronary heart disease with heart failure.

BACKGROUND AND OBJECTIVES: Appropriate inflammatory response is necessary for cardiac repairing after acute myocardial infarction (MI). Three-Bromo-4,5-dihydroxybenzaldehyde (BDB) is a potent antioxidant and natural bromophenol compound derived from red algae. Although BDB has been shown to have an anti-inflammatory effect, it remains unclear whether BDB affects cardiac remolding after MI. The aim of this study was to investigate the potential role of BDB on cardiac function recovery after MI in mice. METHODS: Mice were intraperitoneally injected with BDB (100 mg/kg) or vehicle control respectively 1 hour before MI and then treated every other day. Cardiac function was monitored by transthoracic echocardiography at day 7 after MI. The survival of mice was observed for 2 weeks and hematoxylin and eosin (H&E) staining was used to determine the infarct size. Macrophages infiltration was examined by immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was used to test the production of cytokines associated with macrophages. The phosphorylation status of nuclear factor (NF)-κB was determined by western blot. RESULTS: BDB administration dramatically improved cardiac function recovery, and decreased mortality and infarcted size after MI. Treatment with BDB reduced CD68+ macrophages, M1 and M2 macrophages infiltration post-MI, and suppressed the secretion of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1, and IL-6 in the injured hearts. Furthermore, BDB inhibited the phosphorylation of NF-κB in the infarcted hearts. CONCLUSIONS: These data demonstrate, for the first time, that BDB treatment facilitated cardiac healing by suppressing pro-inflammatory cytokine secretion, and indicate that BDB may serve as a therapeutic agent for acute MI.
Animals ; Blotting, Western ; Cytokines ; Echocardiography ; Enzyme-Linked Immunosorbent Assay ; Eosine Yellowish-(YS) ; Fluorescent Antibody Technique ; Heart ; Hematoxylin ; Interleukin-6 ; Interleukins ; Macrophages ; Mice ; Monocytes ; Mortality ; Myocardial Infarction ; Phosphorylation ; Recovery of Function ; Rhodophyta ; Tumor Necrosis Factor-alpha

BACKGROUND AND OBJECTIVES: Appropriate inflammatory response is necessary for cardiac repairing after acute myocardial infarction (MI). Three-Bromo-4,5-dihydroxybenzaldehyde (BDB) is a potent antioxidant and natural bromophenol compound derived from red algae. Although BDB has been shown to have an anti-inflammatory effect, it remains unclear whether BDB affects cardiac remolding after MI. The aim of this study was to investigate the potential role of BDB on cardiac function recovery after MI in mice. METHODS: Mice were intraperitoneally injected with BDB (100 mg/kg) or vehicle control respectively 1 hour before MI and then treated every other day. Cardiac function was monitored by transthoracic echocardiography at day 7 after MI. The survival of mice was observed for 2 weeks and hematoxylin and eosin (H&E) staining was used to determine the infarct size. Macrophages infiltration was examined by immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was used to test the production of cytokines associated with macrophages. The phosphorylation status of nuclear factor (NF)-κB was determined by western blot. RESULTS: BDB administration dramatically improved cardiac function recovery, and decreased mortality and infarcted size after MI. Treatment with BDB reduced CD68+ macrophages, M1 and M2 macrophages infiltration post-MI, and suppressed the secretion of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1, and IL-6 in the injured hearts. Furthermore, BDB inhibited the phosphorylation of NF-κB in the infarcted hearts. CONCLUSIONS These data demonstrate, for the first time, that BDB treatment facilitated cardiac healing by suppressing pro-inflammatory cytokine secretion, and indicate that BDB may serve as a therapeutic agent for acute MI.