Background: Heart-type fatty acid-binding protein (H-FABP) is proposed as an early biomarker for acute myocardial infarction (AMI), but its prognostic value is unclear in acute coronary syndrome (ACS). We evaluated the prognostic value of the H-FABP concentration relative to cardiac troponin T (cTnT) in the early hours of ACS. Methods: Serum concentrations of H-FABP and cTnT were measured on admission in 328 consecutive patients hospitalized for ACS within 6 h after the onset of chest pain [AMI, 241 (73.5%) patients; ST-segment elevation myocardial infarction, 154 (47.0%) patients; and emergent coronary angiography within 24 h after admission, 287 (87.5%) patients]. Cardiac events, which were defined as cardiac death or subsequent nonfatal AMI, were monitored for 6 months after admission. Results: During the 6-month follow-up period, there were 25 cardiac events, including 15 cardiac deaths and 10 subsequent nonfatal AMIs. Stepwise multivariate analyses including clinical, electrocardiographic, and biochemical variables revealed that increased H-FABP (above the median of 9.8 g/L), but not increased cTnT (above the median of 0.02 g/L), was independently associated with

Objective:Nicorandil, an opener of ATP-sensitive K+ channels, was used to treat angina in patients with coronary artery disease. In this study, we aim to investigate the cardioprotective effects of single oral dose of nicorandil in patients undergoing selective percutaneous coronary intervention (PCI).Methods:One hundred and thirty-eight patients with acute coronary syndrome undergoing PCI from July 2011 to October 2012 were randomly divided into control group (group 1, n=47), 10 mg oral nicorandil group (group 2, n=45), and 20 mg oral nicorandil group (group 3, n=46) about 2 hours before procedure, respectively. Cardiac troponin I (cTnI) levels were determined at 20 ~ 24 hours after PCI.Results:There was a significant difference in the rate of any cTnI elevation among the three groups (group 1: 36.17%, group 2: 20.00%, group 3: 15.22%, p=0.0176). With respect to the frequency of cTnI elevation ≥3 and 5×the upper limit of normal (ULN), there also had statistical difference among the three groups (17.02% in group 1, 8.89% in group 2, and 4.35% in group 3, respectively for cTnI elevation ≥3× ULN, p=0.0428; 12.77% in group 1, 6.67% in group 2, and 2.17% in group 3, respectively, for cTnI elevation ≥5× ULN, p=0.0487). Logistic regression analysis showed that LVEF (OR=0.915, 95% CI=0.853-0.981) and the use of nicorandil (OR=0.516, 95% CI=0.267-0.996) before PCI were independent protective factors of myocardial injury.Conclusion:Single oral dose of nicorandil (10 mg, 20 mg) 2 hours before the PCI procedure could decrease the incidence of peri-procedure myocardial injury and PCI-related myocardial infarction.

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How to provide effective prevention and treatment of myocardial ischemia/reperfusion (I/R) injury and study of the mechanism underlying I/R injury are hotspots of current research. This study aimed to elucidate the effect and cardioprotective mechanism of vitamin C (VC) on myocardial I/R injury. Our study introduced two different I/R models: I/R in vitro and oxygen-glucose deprivation/recovery (OGD/R) in primary neonatal rat cardiac myocytes. We used the mitochondrial permeability transition pore (mPTP) opener lonidamine (LND) and the mitochondrial K ATP (mitoK ATP ) channel inhibitor 5-hydroxydecanoate (5-HD) to analyze the underlying mechanisms. We found that post-treatment with VC decreased I/R injury in our models. Post-treatment with VC significantly decreased I/R-induced injury, attenuated apoptosis, and maintained the functional integrity of mitochondria via alleviation of Ca 2 overload, reactive oxygen species burst, inhibition of the opening of mPTP, and prevention of mitochondrial membrane potential (ΔΨm) depolarization. VC post-treatment increased the phosphorylation of Akt and glycogen synthase kinase (GSK)-3β. The present results demonstrate that VC might protect the myocardium from I/R-induced injury by inhibiting the mPTP opening via activation of mitoK ATP channels. VC mediates cardioprotection via activation of the phosphatidyl inositol 3-kinase (PI3K)-Akt signaling pathway. These findings may contribute toward the development of novel strategies for clinical cardioprotection against I/R injury. Key words vitamin C (VC); ischemia/reperfusion (I/R) injury; ischemic post-treatment; mitochondrial K ATP (mitoK ATP ) channelIn recent years, cardiovascular disease has become a great threat to human life and health. Prolonged myocardial ischemia can cause tissue damage and even cell death. A key treatment of coronary heart disease is blood reperfusion of the myocardium. However, restoration of blood supply followed by myocardial cell function and structural damage results in a pathophysiological state known as ischemia/reperfusion (I/R) injury.1) The reduction occurrence of I/R injury has become a focus of current research.In 1986, Murry first put forward a self-defensive protective mechanism of the myocardial cell known as myocardial ischemia preadaptation (ischemic preconditioning; IPC), and transient ischemic preconditioning can improve myocardial ischemia and reperfusion of longer than damage tolerance ability.2) However, ischemic preconditioning poses challenges including safety and operability, and individual differences of clinical application of IPC is restricted. Thus, several studies have proposed drug post-treatment (pharmacological preconditioning; PPC), namely the simulation of IPC via a variety of drugs result in less I/R injury. 3)In myocardial I/R injury, the integrity of the mitochondrial membrane and its functions have undergone major changes, such as depolarization of the mitochondrial membrane potential (ΔΨm), interruption of mitochondrial respiratory chain electron transfer, inhibi...

1. Additive beneficial effects on cardiovascular disease have been reported for amlodipine and atorvastatin. However, it is still unclear whether the combination of amlodipine and atorvastatin has additive beneficial effects on the regression of advanced cardiac hypertrophy in hypertension. In the present study, the effects of the drug combination on advanced cardiac hypertrophy were investigated in elderly spontaneously hypertensive rats (SHR). 2. Elderly SHR (36 weeks old) were randomly allocated into four groups of 12: (i) a vehicle-treated control group; (ii) an amlodipine (10 mg/kg per day)-treated group; (iii) an atorvastatin (10 mg/kg per day)-treated group; and (iv) a group treated with a combination of amlodipine and atorvastatin (both at 10 mg/kg per day). Drugs were administered by oral gavage every morning for a period of 12 weeks before hearts were harvested for analysis. 3. Combined administration of amlodipine and atorvastatin significantly suppressed cardiomyocyte hypertrophy, interstitial fibrosis and upregulation of hypertrophic and profibrotic genes, and also improved left ventricular diastolic dysfunction to a greater extent than did amlodipine monotherapy. Further beneficial effects of combination therapy on advanced cardiac hypertrophy were associated with a greater reduction of NADPH oxidase-mediated increases in cardiac reactive oxygen species (ROS), rather than decreased blood pressure and serum cholesterol levels. 4. To elucidate the underlying molecular mechanisms, we examined cardiovascular NADPH oxidase subunits and found that amlodipine clearly attenuated the expression of p47(phox) and p40(phox) and slightly but significantly reduced p22(phox) and Rac-1 levels in heart tissue. Combination treatment with amlodipine plus atorvastatin led to a further reduction in p22(phox), p47(phox) and Rac-1 protein levels compared with amlodipine alone. 5. In conclusion, combined amlodipine and atorvastatin treatment has a greater beneficial effect on advanced cardiac hypertrophy compared with amlodipine monotherapy. The benefits are likely to be related to the additive effects of the drugs on the suppression of NADPH oxidase-mediated ROS generation.