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Abstract Background Second-generation drug-eluting stents (DES) have raised the bar of clinical performance. These stents are mostly made from cobalt chromium alloy. A newer generation DES has been developed from platinum chromium alloy, but clinical data regarding the efficacy and safety of the platinum chromium-based everolimus-eluting stent (PtCr-EES) is limited, with no comparison data against the cobalt chromium-based zotarolimus-eluting stent (CoCr-ZES). In addition, an antiplatelet regimen is an integral component of medical therapy after percutaneous coronary intervention (PCI). A 1-week duration of doubling the dose of clopidogrel (double-dose antiplatelet therapy (DDAT)) was shown to improve outcome at 1 month compared with conventional dose in acute coronary syndrome (ACS) patients undergoing PCI. However in Asia, including Korea, the addition of cilostazol (triplet antiplatelet therapy (TAT)) is used more commonly than doubling the dose of clopidogrel in high-risk patients. Methods In the 'Harmonizing Optimal Strategy for Treatment of coronary artery stenosis - sAfety & effectiveneSS of drug-elUting stents & antiplatelet REgimen' (HOST-ASSURE) trial, approximately 3,750 patients are being prospectively and randomly assigned in a 2 × 2 factorial design according to the type of stent (PtCr-EES vs CoCr-ZES) and antiplatelet regimen (TAT vs DDAT). The first primary endpoint is target lesion failure at 1 year for the stent comparison, and the second primary endpoint is net clinical outcome at 1 month for comparison of antiplatelet therapy regimen. Discussion The HOST-ASSURE trial is the largest study yet performed to directly compare the efficacy and safety of the PtCr-EES versus CoCr-ZES in an 'all-comers' population. In addition, this study will also compare the clinical outcome of TAT versus DDAT for 1-month post PCI. Trial registration ClincalTrials.gov number NCT01267734.

Abstract: Silver nanoparticles were synthesized from the reaction of silver nitrate (AgNO3) with a 1wt% aqueous solution of polysorbate 20, polysorbate 40, polysorbate 60, polysorbate 80, and Brij 97, respectively, under microwave irradiation. The resulting nanoparticles were effectively dispersed throughout water and characterized by UV–vis spectra and transmission electron microscopy (TEM). The reaction time of 45s was investigated by monitoring the color change of the nanoparticle solution. The peaks in the UV–vis spectra showed surface plasmon resonance characteristics inherent in silver nanoparticles. The nanoparticles were reacted with 4-aminothiophenol in water, followed by addition of diethyl ether and fullerene[C60] in toluene and stirring for 24h. The resulting fullerene[C60]-silver nanoparticles were characterized by UV–vis and MALDI–TOF–MS spectra. [Copyright &y& Elsevier]

Background: There are limited data on the long-term outcome of platinum chromium-based everolimus-eluting stents (PtCr-EES) vs. cobalt chromium-based zotarolimus-eluting stents (CoCr-ZES).Methods and Results:A total of 3,755 patients undergoing percutaneous coronary intervention (PCI) were randomized 2:1 to PtCr-EES or CoCr-ZES, and 96.0% of patients completed the 3-year clinical follow-up. The primary outcome was target lesion failure (TLF), defined as a composite of cardiac death, target vessel-related myocardial infarction (MI), and clinically-driven target lesion revascularization (TLR). At 3 years, TLF occurred in 5.3% and in 5.4% of the PtCr-EES and CoCr-ZES groups, respectively (hazard ratio 0.978; 95% confidence interval 0.730-1.310, P=0.919). There were no significant differences in the individual components of TLF. Routine angiographic follow-up was performed in 38.9% of the total patients. In a landmark analysis of the subgroup that had follow-up angiography, the clinically-driven TLR rate of CoCr-ZES was significantly higher than PtCr-EES group during the angiography follow-up period (P=0.009). Overall definite and probable stent thrombosis rates were very low in both groups (0.5% vs. 0.6%, P=0.677)., Conclusions: PtCr-EES and CoCr-ZES had similar and excellent long-term outcomes in both efficacy and safety after PCI in an all-comer population.

Previously, we reported that dibenzylbutyrolactone lignans (DBLLs) from the fruit of Forsythia koreana NAKAI (Oleaceae) has anti-inflammatory, antioxidant, and anti-asthmatic effects. In this study, to clarify the anti-inflammatory mechanisms of DBLL, we evaluated the effects of DBLLs on lipopolysaccharide-stimulated inducible nitric oxide synthetase (iNOS) and cyclooxygenase-2 (COX-2) expressions, nitric oxide (NO) and prostaglandin E(2) (PGE(2)) productions, nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) activations, inhibitor of κB (IκB) and inhibitor of κB kinase (IKK) phosphorylations in cytosolic proteins, and cytotoxicity in Raw264.7 cells. DBLLs potently suppressed both the enzyme expression and DNA-binding activity of NF-κB. Arctiin, arctigenin (1.0 µM) and matairesinol (10 µM) inhibited the expression of iNOS by 37.71±2.86%, 32.51±4.28%, and 27.44±2.65%, respectively, and arctiin, arctigenin (0.1 µM) and matairesinol (1.0 µM) inhibited COX-2 expression by 37.93±7.81%, 26.70±4.61% and 29.37±5.21%, respectively. The inhibitory effects of DBLLs on NO and PGE(2) productions were the same patterns as those seen for the reductions in iNOS and COX-2 expression, respectively. Arctiin, arctigenin (1.0 µM) and matairesinol (10 µM) significantly (p<0.05) inhibited NF-κB DNA binding by 44.85±6.67%, 44.16±6.61%, and 44.79±5.62%, respectively, and arctiin (0.1 µM) and arctigenin (1.0 µM) significantly (p<0.05) inhibited the phosphorylation of IκB by 20.58±3.86% and 25.99±6.18%, respectively. Furthermore, arctiin, matairesinol (1.0 µM) and arctigenin (10 µM) inhibited the phosphorylation of IKK by 38.80±6.64%, 38.33±6.65%, and 38.57±8.14%, respectively. In addition, DBLLs potently inhibited the lipopolysaccharide (LPS)-induced activation of MAPKs (SAPK/c-Jun NH(2)-terminal kinase (JNK), p38, and extracellular signal receptor-activated kinase (ERK)1/2). Overall, arctiin was the most effective; its effect was nearly the same as that of 10 µM helenalin. These findings suggest that treatment with non-toxic DBLLs inhibits not only NF-κB and NF-κB-regulated protein activation, but also potently inhibits the activations of specific MAPKs.

Lp(a) and coronary artery calcification (CAC) have recently been reported as predictors of plaque instability, but this is surrounded by much controversy. We investigated the influence of Lp(a) and CAC compared other acute coronary syndrome (ACS) risk factors. 698 patients diagnosed with at least minimal coronary artery obstructive disease from a coronary angiography were randomly selected using SPSS. Lp(a), other lipid profiles and past histories were checked, and CAC semi quantitatively graded on stored fluoroscopic images. The prevalence of CAC was significantly higher in the ACS than the non-ACS group (38.0% vs. 29.9%, p=0.026). The serum level of Lp(a) (26.89 +/- 30.64 vs. 20.85 +/- 21.63, p < 0.01) and prevalence of positive Lp(a) (> 35 mg/dl) was higher in the ACS group (24% vs. 15.7%, p < 0.01). The risk of ACS was higher in the patients with both CAC and elevated an Lp(a) than in those with only one (OR: 2.16, p=0.009, 95% CI; 1.213 - 3.843 vs. OR: 1.79, p < 0.001, 95% CI; 1.300 - 2.456). The risk of ACS was increased 1.451 times (p=0.040, 95% CI; 1.071- 2.071) in patients with CAC and 1.648 times (p=0.014, 95% CI; 1.107- 2.455) in patients with a Lp(a) > 35 mg/dl. In the younger patients (< 60 years), the Lp(a), but not the CAC, was an independent risk factor for ACS (OR=2.248, p=0.005, 95% CI; 1.281-3.943). In the older patients (> 60 years), CAC, but not the Lp(a), was an independent risk factor (OR=1.775, p=0.021, 95% CI; 1.090 - 2.890). Both the Lp(a) and CAC were risk factors for ACS, and they had a synergistic effect on its development. In the younger Lp(a), and the older CAC, was the more potent risk factor for ACS, respectively.