Protective effect of metformin on myocardial injury in metabolic syndrome patients following percutaneous coronary intervention.

OBJECTIVES: The present study tested the hypothesis that pretreatment with metformin decreases postprocedural myocardial injury and improves clinical outcomes in metabolic syndrome patients following percutaneous coronary intervention (PCI). METHODS: We enrolled 152 metabolic syndrome patients with no prior history of metformin treatment. Patients scheduled for elective coronary intervention were randomized to the metformin or control group 7 days before the procedure. Creatine kinase-MB (CK-MB) and troponin I levels were measured at baseline and 8 and 24 h after the procedure, and clinical outcomes were monitored for 1 year. RESULTS: Post-PCI myocardial injury as indicated by CK-MB elevation (14.5 vs. 32.9%, p = 0.008) and troponin I elevation (14.5 vs. 34.2%, p = 0.005) was significantly lower in the metformin group than in the control group. Postprocedural peak values of CK-MB (2.70 ± 4.30 vs. 6.29 ± 8.03 ng/ml, p < 0.001) and troponin I (0.02 ± 0.05 vs. 0.07 ± 0.10 ng/ml, p = 0.001) were also significantly lower in the metformin group than in the control group. At 1 year, the composite endpoint of death from any cause, post-PCI myocardial infarction (MI), MI after PCI hospitalization or ischemia-driven target lesion revascularization occurred in 7.9% of metformin-treated patients and 28.9% of controls (hazard ratio 0.25, 95% CI 0.10-0.62, log rank p = 0.001). CONCLUSIONS: A 7-day metformin pretreatment regimen (250 mg 3 times a day) significantly reduces postprocedural myocardial injury and improves 1-year clinical outcomes in metabolic syndrome patients undergoing PCI.

[Changes in plasma levels of atrial natriuretic peptide, endothelin-1 and von Willebrand factor among newborns with persistent pulmonary hypertension].

OBJECTIVE: To investigate the changes in plasma levels of atrial natriuretic peptide (ANP), endothelin-1 (ET-1) and von Willebrand factor (vWF), and their significance among newborns with persistent pulmonary hypertension (PPH). METHODS: Sixty-six newborns with PPH (case group) (mild: 26 cases; moderate: 21 cases; severe: 19 cases), as well as 40 newborns without PPH (control group) who were hospitalized in the same period, were enrolled. The control group underwent echocardiography on admission. The case group underwent echocardiography before treatment (with refractory hypoxemia) and after 7 days of treatment for measurement of pulmonary artery systolic pressure (PASP). Meanwhile, plasma levels of ANP, ET-1 and vWF were measured using ELISA. RESULTS: Before treatment, the case group had significantly higher plasma levels of ANP, ET-1 and vWF than the control group (P<0.05), and these indices increased as PASP rose. After 7 days of treatment, the children with mild or moderate PPH showed normal PASP, and their plasma levels of ANP, ET-1 and vWF were not significantly different from those of control group. The children with severe PPH had significant decreases in all indices, but they were significantly higher than those of the control group. Plasma levels of ANP, ET-1 and vWF were significantly positively correlated with PASP before and after treatment (P<0.01). CONCLUSIONS: Changes in plasma levels of ANP, ET-1 and vWF can reflect PASP in newborns with PPH during treatment. Dynamic monitoring of these indices can help to judge the severity of PPH and guide treatment.