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The present study aimed to investigate the relationship between serum levels of secretory vimentin and coronary artery disease (CAD). The biological effect of secretory vimentin was ascertained by experiments.We analysed serum levels of secretory vimentin in CAD patients (n = 288) and non-CAD controls (n = 195) by ELISA. To evaluate the pro-inflammatory effects of secreted vimentin, the human aortic endothelial cells (HAECs) and human peripheral blood mononuclear cells (PBMCs) were treated with recombinant vimentin or saline. Intraperitoneal injection of vimentin (1 μg/each) or saline was performed every other day for 12 weeks in ApoESerum levels of secretory vimentin were significantly increased in CAD patients than in health controls (p 0.05), and correlated with the number of diseased coronary arteries, Syntax and Gensini score (for all comparison, p 0.01). Logistic regression analysis showed that vimentin level is an independent determinant of CAD. In experiments, recombinant vimentin protein enhanced the expression of adhesion molecules and inflammatory cytokines in both endothelial cells and macrophages. This protein also promoted macrophage-endothelial cells adhesion in vitro and the recruitment of leukocytes to mesenteric venules in C57BL/6 mice. Compared with saline, intraperitoneal injection of recombinant vimentin (1 μg/each) every other day induced atherogenesis in ApoESerum vimentin levels are associated with the presence and the severity of CAD. Vimentin protein promotes atherogenesis in ApoE

Increased transcytosis of low-density lipoprotein (LDL) across the endothelium and oxidation of LDL deposited within the subendothelial space are crucial early events in atherogenesis. C1q/TNF-related protein (CTRP) 5 is a novel secreted glycoprotein and its biological functions are largely undefined.Expression of CTRP5 was analyzed in sera and atherosclerotic plaques of patients with coronary artery disease (CAD). The role of CTRP5 in atherogenesis was investigated in vitro and in vivo.We found CTRP5 serum levels were higher in patients with than without CAD (247.26 ± 61.71 vs. 167.81 ± 68.08 ng/mL, p 0.001), and were positively correlated with the number of diseased vessels (Spearman's r = 0.611, p 0.001). Increased expression of CTRP5 was detected in human coronary endarterectomy specimens as compared to non-atherosclerotic arteries. Immunofluorescence further showed that CTRP5 was predominantly localized in the endothelium, infiltrated macrophages and smooth muscle cells in the neointima. In vivo and in vitro experiments demonstrated that CTRP5 promoted transcytosis of LDL across endothelial monolayers, as well as the oxidative modification of LDL in endothelial cells. Mechanistically, we found that CTRP5 up-regulated 12/15-lipoxygenase (LOX), a key enzyme in mediating LDL trafficking and oxidation, through STAT6 signaling. Genetic or pharmacological inhibition of 12/15-LOX dramatically attenuated the deposition of oxidized LDL in the subendothelial space and the development of atherosclerosis.These data indicate that CTRP5 is a novel pro-atherogenic cytokine and promotes transcytosis and oxidation of LDL in endothelial cells via up-regulation of 12/15-LOX.

Background We investigated whether and to what extent stenosis of predominant collateral donor artery (PCDA) affects coronary collateral flow in relation to blood pressure (BP) in type 2 diabetic patients with chronic total occlusion (CTO). Methods Collateral flow index (CFI) as derived from intracoronary pressure distal to occluded segment and mean aortic pressure in 220 type 2 diabetic patients and 220 propensity score matched non-diabetic controls undergoing percutaneous coronary intervention for CTO. The severity of PCDA stenosis was graded according to lumen diameter narrowing. Results CFI decreased stepwise from mild to severe stenosis of the PCDA and was lower in diabetic patients with moderate or severe PCDA stenosis than in non-diabetic controls (0.36 ± 0.10 vs. 0.45 ± 0.08, P

Background There is increasing interest in percutaneous coronary intervention (PCI) for chronic total occlusions (CTO). Periprocedural myocardial injury (PMI) post CTO PCI is not uncommon, but true incidence and implications of PMI are not well understood. Objectives This study aimed to investigate risk factors for PMI post CTO PCI and its implications for the 1-year clinical outcome of a Chinese population. Methods Baseline characteristics, procedure features, and major adverse cardiac events (MACE) at 1 year were assessed in 629 consecutive patients who underwent CTO PCI. PMI was diagnosed as an elevation of creatine kinase MB ≥3 times ULN 12–24 hr post procedure. Multivariate analysis was performed to determine the correlates of PMI and MACE at 1-year follow-up. Results In total, PMI was detected in 115 patients (18.3%). Compared with patients without PMI, those with PMI had a higher percentage of previous coronary artery bypass grafting (CABG), right coronary occlusion and side branch occlusion, and technical success was lower in the PMI group (90.4% vs. 96.7%, P = 0.003). One-year MACE-free survival was reduced in the PMI group (87.8% vs. 95.9%, P = 0.001). The final TIMI flow 0–1 (OR 2.23, 95%CI 1.06–4.87, P = 0.02), side branch occlusion (OR 2.67, 95%CI 1.19–7.11, P = 0.009), retrograde PCI (OR 1.35, 95%CI 1.10–2.74, P = 0.04), and history of prior CABG (OR 2.41, 95%CI 1.38–5.91, P = 0.01) were independent risk factors for the occurrence of PMI. Conclusions In this unique Chinese cohort, PMI post CTO PCI was associated with several clinical and angiographic factors and exerts an adverse effect on 1-year clinical outcomes. © 2016 Wiley Periodicals, Inc.

Aims We investigated the association of the adipokine C1q/TNF-related protein (CTRP) 1 with coronary artery disease (CAD), and the biological vascular effects of CTRP1. Methods and results We analysed CTRP1 levels in sera of CAD patients ( n = 451) and non-CAD controls ( n = 686), and in coronary endarterectomy specimens ( n = 32), non-atherosclerotic internal mammary arteries ( n = 26), aortic atherosclerotic plaques ( n = 15), and non-atherosclerotic aortic samples ( n = 10). C1q/TNF-related protein-levels were higher in sera, endarterectomy specimens, aortic atherosclerotic plaques, and peripheral blood mononuclear cells (PBMCs) from CAD patients compared with controls, and were related to CAD severity. The production of CTRP1 was profusely induced by inflammatory cytokines and itself caused a concentration-dependent expression of adhesion molecules and inflammatory markers in human endothelial cells, human peripheral blood monocytes, and THP-1 cells. C1q/TNF-related protein-1 induced p38-dependent monocyte-endothelium adhesion in vitro and the recruitment of leucocytes to mesenteric venules in C57BL/6 mice. Immunohistochemistry of atherosclerotic femoral arteries exhibited CD68 and VE-cadherin loci-associated increased CTRP1 expression in plaques. Compared with saline, intraperitoneal injection of recombinant CTRP1 protein (200 μg/kg) every other day promoted atherogenesis in apoE−/− mice at 24 weeks. However, pro-atherogenic effects were significantly attenuated in CTRP1−/−/apoE−/− double-knockout mice compared with apoE−/− mice, with a consistent decrease in vascular adhesion molecule, phospho-p38 and TNF-α expression and macrophage infiltration in plaque in CTRP1−/− and double-knockout mice. Tumour necrosis factor-α-induced expression of adhesion molecules and cytokines were lower in primary endothelial cells and macrophages from CTRP−/− mice than in those from C57BL/6 mice. Conclusion C1q/TNF-related protein-1 is a marker of atherosclerosis in humans and promotes atherogenesis in mice.

The presence of calcium and magnesium affects the purity of the final product MnCl2 in hydrometallurgical treatment processes. The solvent extraction method can be used to separate Ca2+ and Mg2+ from Mn2+ solutions containing impurity ions such as Ca2+ and Mg2+. This article aims to investigate the single-stage extraction equilibrium of Ca2+, Mg2+, and Mn2+ in chloride medium using di(2-ethylhexyl)phosphoric acid in kerosene (O:A = 1:1). The results show that the pH0.5 values are 1.11, 1.56, and 2.18 for Ca2+, Mn2+, and Mg2+, respectively. The mechanism of extraction and stoichiometries of metal-containing extracted species were illustrated based on a slope analysis. The composition of the extracted species in the organic phase is proposed to be MnR2·R2H2, CaR2·R2H2, and MgR2·(R2H2)2, respectively.

Background and purpose:Patients are at risk of developing periprocedural myonecrosis after percutaneous coronary intervention (PCI). We investigated whether the use of the platelet glycoprotein (GP) IIb/IIIa receptor inhibitor tirofiban could reduce periprocedural myocardial infarction (PMI) in pati

Background The extent of coronary collateral formation is a primary determinant of the severity of myocardial damage and mortality after coronary artery occlusion. Type 2 diabetes mellitus (T2DM) represents an important risk factor for impaired collateral vessel growth. However, the mechanism of reduced coronary collateralization in type 2 diabetic patients remains unclear. Methods With the reference to the recent researches, this review article describes the pathogenic effects of T2DM on collateral development and outlines possible clinical and biochemical markers associated with reduced coronary collateralization in type 2 diabetic patients with chronic total occlusion (CTO). Results Diffuse coronary atherosclerosis in T2DM reduces pressure gradient between collateral donor artery and collateral recipient one, limiting collateral vessel growth and function. An interaction between advanced glycation end-products and their receptor activates several intracellular signaling pathways, enhances oxidative stress and aggravates inflammatory process. Diabetic condition decreases pro-angiogenic factors especially vascular endothelial growth factor and other collateral vessel growth related parameters. Numerous clinical and biochemical factors that could possibly attenuate the development of coronary collaterals have been reported. Increased serum levels of glycated albumin, cystatin C, and adipokine C1q tumor necrosis factor related protein 1 were associated with poor coronary collateralization in type 2 diabetic patients with stable coronary artery disease and CTO. Diastolic blood pressure and stenosis severity of the predominant collateral donor artery also play a role in coronary collateral formation. Conclusions T2DM impairs collateral vessel growth through multiple mechanisms involving arteriogenesis and angiogenesis, and coronary collateral formation in patients with T2DM and CTO is influenced by various clinical, biochemical and angiographic factors. This information provides insights into the understanding of coronary pathophysiology and searching for potential new therapeutic targets in T2DM.

The data presented in this article are related to the research article entitled "Increased serum TREM-1 level is associated with in-stent restenosis, and activation of TREM-1 promotes inflammation, proliferation and migration in vascular smooth muscle cells" (Wang et al., 2017) [1], which demonstrated that TREM-1 is expressed on vascular smooth cells (VSMCs) and promotes inflammation, proliferation and migration in cultured VSMCs. In this dataset, the expression of TREM-1 in leukocytes and endothelial cells of carotid artery after ligation was evaluated. The effect of TREM-1 on stenosis was analyzed in cultured human saphenous veins (HSVs) that spontaneously undergo remodeling which involves VSMC proliferation and migration.

Background Nonenzymatic glycation of apolipoproteins plays a role in the pathogenesis of the vascular complications of diabetes. Objectives This study investigated whether apolipoprotein (apo) A-IV was glycated in patients with type 2 diabetes mellitus (T2DM) and whether apoA-IV glycation was related to coronary artery disease (CAD). The study also determined the biological effects of glycated apoA-IV. Methods The authors consecutively enrolled 204 patients with T2DM without CAD (Group I), 515 patients with T2DM with CAD (Group II), and 176 healthy subjects (control group) in this study. ApoA-IV was precipitated from ultracentrifugally isolated high-density lipoprotein, and its glycation level was determined based on Western blotting densitometry (relative intensity of apoA-IV glycation). ApoA-IV NƐ-(carboxylmethyl) lysine (CML) modification sites were identified by mass spectrometry in 37 control subjects, 63 patients in Group I, and 138 patients in Group II. Saline or glycated apoA-IV (g-apoA-IV) generated by glyoxal culture was injected into apoE –/– mice to evaluate atherogenesis, and was also used for the cell experiments. Results The relative intensity and the abundance of apoA-IV glycation were associated with the presence and severity of CAD in patients with T2DM (all p –/– mice through the nuclear receptor NR4A3. G-apoA-IV with mutations (K-A) at high-frequency glycation sites exhibited more weakened proinflammatory and atherogenic effects than did g-apoA-IV both in vitro and in vivo. Conclusions ApoA-IV glycation is associated with CAD severity in patients with T2DM, and g-apoA-IV induces atherogenesis through NR4A3 in apoE –/– mice.

Whether target organ damage is associated with blood pressure (BP) variability independent of level remains debated. We assessed these associations from 10-minute beat-to-beat, 24-hour ambulatory, and 7-day home BP recordings in 256 untreated subjects referred to a hypertension clinic. BP variability indices were variability independent of the mean, maximum–minimum difference, and average real variability. Effect sizes (standardized β) were computed using multivariable regression models. In beat-to-beat recordings, left ventricular mass index (n=128) was not ( P ≥0.18) associated with systolic BP but increased with all 3 systolic variability indices (+2.97–3.53 g/m 2 ; P P ≤0.03) with systolic BP (+1.14–1.17 mg/mmol) and maximum–minimum difference (+1.18 mg/mmol); and pulse wave velocity increased with systolic BP (+0.69 m/s; P P P ≥0.15) except for increases in pulse wave velocity ( P P P ≥0.07). In conclusion, while accounting for BP level, associations of target organ damage with BP variability were readily detectable in beat-to-beat recordings, least noticeable in home recordings, with 24-hour ambulatory monitoring being informative only for pulse wave velocity.

Background Sirolimus-eluting stents (SES) with a biodegradable polymer coating have demonstrated promising results but have not been compared to SES with a durable polymer in high-risk patients. We compared the efficacy of these 2 stent types in patients with acute myocardial infarction (STEMI). Methods One thousand one hundred ninety-two STEMI patients were randomized to receive SES coated with biodegradable (n = 596) or durable polymer (n = 596). The study end-point was the composite of major adverse cardiac events (MACE) including all-cause death, recurrent myocardial infarction (MI), or target lesion revascularization (TLR) at 1-year follow-up. Secondary end-points included individual components of primary end-point and stent thrombosis. Results Compared with durable polymer SES, the noninferiority of SES with biodegradable polymer coating was established by an absolute risk difference of 0.9% in the primary end-point (12.4% vs. 13.3%, P = 0.67) and an upper limit of one-sided 95% confidence interval (CI) of 2.96% (P for noninferiority = 0.001). Rate of death, recurrent MI, and TLR were 7.9% and 8.6% (HR: 0.92; 95% CI: 0.61–1.38, P = 0.67), 2.9% and 3.5% (HR: 0.80; 95% CI: 0.42–1.54, P = 0.51), and 2.0% and 3.2% (HR: 0.62; 95% CI: 0.30–1.30, P = 0.20) in the biodegradable polymer SES and durable polymer SES group at 1-year clinical follow-up, respectively. Despite similar rates of 30-day ARC definite/probable stent thrombosis, late stent thrombosis (stent thrombosis occurring beyond 30 days) was lower with biodegradable polymer SES (0.7% vs. 2.2%, P = 0.028). Conclusions In patients undergoing primary PCI for STEMI, the use of biodegradable polymer SES was associated with noninferior 1-year rates of MACE compared with durable polymer SES. (J Interven Cardiol 2014;27:131–141)

According to the principles of simultaneous equilibrium and mass equilibrium, the thermodynamics model of the precipitation-coordination equilibrium of Ni2+−C2H8N2−C2O42−−H2O system was established, and calculation for the relationships between concentration of each substance in solution and parameters was carried out, including pH value, concentrations of ethylenediamine and oxalate by MATLAB program. The results show that Ni exists as Ni2+ and [Ni(C2O4)n]2-2n mainly at pH 6, the complex between Ni2+ and ethylenediamine is predominant. The precursor of Ni microfiber was prepared by an oxalate precipitation process using ethylenediamine as a coordination agent, and the role of ethylenediamine in the growth of the precursor fiber was discussed. The Ni microfiber can be obtained by a thermal decomposition-reduction process of the precursor in N2 and H2 mixed atmosphere. The diameters and aspect ratios of the obtained Ni microfibers are 0.2-1 μm and 20–30, respectively.

Background Glycated albumin (GA) has been shown to be a better indicator than glycosylated hemoglobin A1c (HbA1c) in terms of severity of renal impairment in patients with type 2 diabetes mellitus (T2DM). This study aimed to determine whether elevated serum GA levels are associated with an increased risk for contrast-induced acute kidney injury (CI-AKI) and worse clinical outcome in patients with T2DM and at least moderate renal insufficiency (RI) undergoing coronary angiography. Methods Serum levels of fasting blood glucose (FBG), HbA1c and GA were measured in 1030 patients with T2DM and moderate to severe RI (eGFR 15–59mL/min/1.73m 2 ). CI-AKI was defined as ≥25% increase in serum creatinine within 72h after the procedure. Receiver-operating characteristic curve was constructed to assess the predictive value of GA, HbA1c and FBG for CI-AKI. Multivariable logistic regression model was developed to identify risk factors for CI-AKI, and Kaplan–Meier curve analysis was used to compare the rates of dialysis and major adverse cardiac events (MACE) during one-year follow-up. Results The overall rate of CI-AKI was 11.1%. GA was significantly higher in patients with CI-AKI than in those without, and correlated positively with changes of renal function after the procedure. After adjusting for age, sex, left ventricular ejection fraction, multi-vessel disease, type and volume of contrast media, FBG, and HbA1c, GA remained an independent risk factor for CI-AKI. GA≥21% was associated with increased rates of dialysis and MACE during one-year follow-up in patients with or without CI-AKI. Conclusions Increased GA level serves as a valuable risk factor for CI-AKI and indicates poor one-year clinical outcome in patients with T2DM and moderate to severe RI.

Objective— In a previous study, we established diabetic and nondiabetic minipig models with coronary artery in-stent restenosis (ISR). Mass spectrometry showed that high-mobility group box (HMGB) 2 level was higher in ISR than in non-ISR tissue from diabetic minipigs. We here investigated whether serum HMGB2 levels were related to ISR in coronary artery disease patients. The effect of HMGB2 was evaluated in mice with femoral artery wire injury and in human aortic smooth muscle cells. Approach and Results— From 2513 patients undergoing coronary artery intervention and follow-up angiography at ≈1 year, 262 patients were diagnosed with ISR, and 298 patients with no ISR were randomly included as controls. Serum HMGB2 levels were significantly higher in patients with ISR than in those without ISR and were associated with ISR severity. Multivariable logistic regression analysis showed that HMGB2 level was independently associated with ISR. In experiments, HMGB2 expression was increased in vascular tissue after injury. Perivascular HMGB2 administration promoted injury-induced neointimal hyperplasia in C57Bl/6 mice compared with in the control, whereas such pathophysiological features were attenuated in Hmgb2 –/– mice. Mechanistically, HMGB2 enhanced neointimal hyperplasia in mice and proliferation and migration in human aortic smooth muscle cells by inducing reactive oxygen species through increased p47phox phosphorylation. Knocking down p47phox, however, inhibited HMGB2-induced effects in human aortic smooth muscle cells. Finally, HMGB2-induced effects were significantly declined in receptor of advanced glycation end products knockdown or deficient cells, but not in Toll-like receptor 4 knockdown or deficient cells. Conclusions— Serum HMGB2 levels were associated with ISR in patients. HMGB2 promoted neointimal hyperplasia in mice with arterial wire injury through reactive oxygen species activation.

We investigated whether serum vasostatin-2 level is related to chronic heart failure (CHF) in patients with previous myocardial infarction (MI) and MACE in 3-year follow-up. The biological effect of vasostatin-2 on ischemic HF was evaluated in animal experiments.After exclusion of the subjects not eligible, this study included 450 patients with CHF and previous MI, and 149 healthy controls. Serum vasostatin-2 level was analyzed. CHF patients were followed up for three years and major adverse cardiac events (MACE) were recorded, defined as reinfarction, target-vessel revascularization, cardiovascular death and refractory HF requiring hospitalizations.Notably, serum vasostatin-2 level was decreased in CHF patients than in controls, and significant difference was observed between CHF patients with MACE and those without (both P0.05). Vasostatin-2 level was correlated with HF stages (Spearman's r=-0.288, P0.05), LVEF (r=0.377, P0.05) and pro-BNP level (r=-0.294, P0.05). Multivariable logistic regression analysis suggested that vasostatin-2, conventional risk factors, severity of HF stages and LVEF were independently associated with MACE in CHF patients. Vasostatin-2 (100μg) or PBS was injected intraperitoneally every other day in MI rats, follow by echocardiography, hemodynamic analysis after 2months. Compared with PBS, vasostatin-2 treatment prevented ischemic HF in MI rats, accompanied with reduction of infarct size, remodeling, fibrosis and inflammation, mainly through inhibition of Rho, Wnt and TLR-4 pathways and modulation of renin-angiotensin system.Decreased serum vasostatin-2 level is associated with ischemic CHF and with MACE in three-year follow-up. Intraperitoneal injection of vasostatin-2 protects against ischemic HF in MI rats.

We investigated whether serum level of C1q/TNF-related protein (CTRP) 5 is associated with in-stent restenosis (ISR) after percutaneous coronary intervention (PCI) with drug-eluting stent (DES) implantation, and assessed the biological effects of CTRP5 in human aortic smooth muscle cells (hASMCs).Serum CTRP5 levels were assayed in 306 patients with and 306 patients without angiographic ISR at approximately one year after DES-based PCI. Multivariate logistic regression analysis was performed to determine risk factors for ISR. Notably, serum CTRP5 levels were higher in ISR patients than in non-ISR counterparts (197±84ng/mL vs. 150±74ng/mL, P0.001). Compared with the lowest tertile (125ng/mL) of CTRP5, patients with the mid (125-200ng/mL) and the highest tertile (200ng/mL) of CTRP5 had a more than 1.6-fold (adjusted OR=1.670-2.127, P≤0.039) and 7.4-fold (adjusted OR=7.478-11.264, all P0.001) increased risk of ISR (all P for trend0.001), respectively, after adjustment for potential clinical, biochemical and angiographic characteristics. To assess the biological effects of CTRP5, we stimulated hASMCs with this protein. CTRP5 concentration-dependently induced the expression of MMP-2, cyclin D1 and TNF-α in hASMCs, with activation of Notch1, TGF-β and hedgehog signaling pathways. Consistently, this protein promoted migration and proliferation of hASMCs in wound-healing, Boyden chamber and Brdu incorporation assay.Increased serum CTRP5 level is associated with ISR after PCI with DES implantation. CTRP5 promotes proliferation, inflammation and migration in vascular smooth muscle cells through activation of multiple pathways.

High-mobility group box (HMGB) family is related to inflammatory diseases. We investigated whether serum HMGB2 levels are related to myocardial infarction (MI) severity and major adverse cardiac events (MACE) during MI. We included 432 consecutive patients with ST-segment elevation myocardial infarction and 312 controls. Serum HMGB2 levels were significantly higher in MI patients than in controls. Increased HMGB2 levels were associated with MACE and negatively with ejection fraction in MI patients. HMGB2 was an independent determinant of MACE in logistic regression analysis. HMGB2 protein (10 μg) or saline was injected intramyocardially in MI rats, with or without coadministration of the NADPH oxidase inhibitor apocynin. After 72 h, pathological, echocardiographic, and hemodynamic examinations showed that HMGB2 increased infarct size and worsened cardiac function in MI rats. Moreover, HMGB2 administration enhanced reactive oxygen species (ROS) production, cell apoptosis, inflammation, and autophagosome clearance impairment, which were attenuated by coadministration of apocynin or knock down of receptor for advanced glycation end products (RAGE). In conclusion, increased serum HMGB2 levels are associated with MI severity and MACE at 1 mo. HMGB2 promotes myocardial ischemic injury in rats and hypoxic H9C2 cell damage via ROS provoked by RAGE.NEW & NOTEWORTHY We demonstrate that serum high-mobility group box 2 is associated with major adverse cardiac events at 1 mo in myocardial infarction patients. Mechanistically, high-mobility group box 2 promotes reactive oxygen species production via receptor for advanced glycation end products signaling in ischemic myocardium, thereby aggravating cell apoptosis, inflammation, and autophagosome clearance impairment. This study reveals that high-mobility group box 2 is a novel factor enhancing ischemic injury in myocardial infarction.

BACKGROUND In a meta-analysis, we investigated effects of β-blockers on central hemodynamic measurements and explored the impact of heart rate (HR) on central hemodynamics and the risk of stroke. METHODS We searched randomized controlled trials that compared β-blockers with other classes of antihypertensive drugs in reducing central systolic blood pressure (cSBP) and augmentation index (cAI) and in preventing stroke. A random-effects model was used to compute pooled estimates. RESULTS In 9 trials (n = 754), β-blockers were less efficacious in reducing cAI than all the other classes of drugs (8.6%, P < 0.001). β-blockers were also less efficacious in reducing cSBP than angiotensin converting enzyme inhibitors (7.7 mm Hg, P = 0.02) and angiotensin receptor blockers (3.6 mm Hg, P = 0.005) but not the other classes of drugs (P ≥ 0.50). In a meta-regression analysis of these 9 trials, the baseline-adjusted difference in HR between randomized groups was associated with cAI (7.0% increase for each 10 bpm decrease in HR, P = 0.02), which was associated with cSBP (1.2 mm Hg increase for each 1% increase in cAI, P = 0.009). In 5 outcome trials, the pooled OR of stroke was 1.23 (P < 0.001), which would be accounted for by the difference in cSBP derived from the above meta-regression analysis. CONCLUSIONS Slowing HR with β-blockers may increase cAI and in turn may decrease cSBP less than with other classes of drugs. This mechanism might account for a smaller reduction in the risk of stroke when using β-blockers to treat hypertension.

BACKGROUND To investigate the accuracy of the SphygmoCor and Omron HEM9000-AI devices in the estimation of central blood pressure (BP) in comparison with the simultaneous invasive catheter measurement. METHODS The radial arterial pulse was sequentially recorded by the use of the Omron and SphygmoCor devices in 33 patients, with the calibration of the brachial oscillometric BP, to derive central BPs, which were also measured simultaneously with a catheter-based fluid-filled manometer system. The procedure was repeated three times to obtain 99 pairs of noninvasive and invasive measurements. RESULTS The noninvasive central systolic BP estimations were significantly (P < 0.001) associated with the invasive measurement at the ascending aorta, with a correlation coefficient of 0.91 and 0.90 for the SphygmoCor and Omron devices, respectively. However, both devices underestimated central systolic BP with a difference of -15 mm Hg (95% confidence interval (CI), -17 to -13 mm Hg, P < 0.001) for SphygmoCor and -2 mm Hg (95% CI, -4 to 0 mm Hg, P < 0.05) for Omron. In comparison with the invasive catheter measurement at the brachial artery, the oscillometric Omron device underestimated brachial systolic BP by -19 mm Hg (95% CI, -23 to -15 mm Hg, P < 0.001). CONCLUSIONS Both devices underestimated central systolic BP, with a larger deviation by SphygmoCor. Nonetheless, these noninvasive estimations of central BP closely correlate with the invasive measurements, and can still be properly used, on the condition that device specific diagnostic thresholds become available.

BACKGROUND: This study sought to examine whether circulatory levels of endothelial dysfunction biomarkers [vascular cell adhesion molecule (sVCAM-1), intercellular adhesion molecule (sICAM-1), sE-selectin, von Willebrand factor (vWF), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1)] are associated with occurrence of late or very late stent thrombosis (ST) after percutaneous coronary intervention with sirolimus-eluting stent implantation, and to assess the possible influence of genetic variants of these proteins on ST. METHODS: Serum levels of sVCAM-1, sICAM-1, sE-selectin, vWF, t-PA and PAI-1 were measured, and polymorphisms of vWF (-1234C/T, -1185A/G and -1051G/A), t-PA (insertion/deletion) and PAI-1 genes (4G/5G) were determined in 41 patients who experienced at least one episode of late or very late ST. Eighty-two patients without ST randomly selected from the same study period served as controls. RESULTS: Serum levels of vWF, sVCAM-1 and sICAM-1 were significantly increased in patients with ST than in controls (all P

OBJECTIVES This study aimed to evaluate the impact of angiographic and intravascular ultrasound (IVUS) features on clinical outcome in nondiabetic and type 2 diabetic patients after percutaneous coronary intervention (PCI) with sirolimus-eluting stent (SES) implantation. METHODS Repeat coronary angiography with IVUS imaging was performed after SES-based PCI for de-novo lesions in 128 diabetic and 327 nondiabetic patients (189 lesions and 504 lesions, respectively). The rate of major adverse cardiac events including cardiac death, non fatal myocardial infarction (MI), and target lesion revascularization during clinical follow-up was recorded. RESULTS In-stent and in-segment late loss, intimal hyperplasia volume, and percentage volumetric obstruction were similar, but stented external elastic membrane cross-sectional area and reference/stented segment ratio were lower in diabetic than in nondiabetic patients. Incomplete stent apposition (ISA) was less frequent, but occurrence of new coronary lesions was higher in diabetic than in nondiabetic patients. Despite similar target lesion revascularization, cumulative survival rates freedom from composite cardiac death and nonfatal MI or major adverse cardiac events were reduced in diabetic patients. Cox proportional hazards model identified diabetes, left ventricular ejection fraction, minimal stent CSA, maximal ISA area, atherosclerotic progression and lesion length as independent predictors of non fatal MI or mortality at follow-up. CONCLUSION In diabetic patients, PCI with SES implantation neutralizes the excess risk of intimal hyperplasia and decreases occurrence of ISA, but could not modify the propensity of increased adverse clinical outcomes at follow-up.

Background We assessed the possible association of glycated albumin (GA) and circulatory adhesion molecules with diffuse coronary artery disease (CAD) in patients with type 2 diabetes mellitus (T2DM). Methods Six hundred and two consecutive patients with CAD, based upon angiographic features and presence or absence of T2DM, were categorized as Group I (296 patients with non-diffuse CAD but no T2DM), Group II (138 patients with diffuse CAD but no T2DM), Group III (78 patients with non-diffuse CAD and T2DM) and Group IV (90 patients with diffuse CAD and T2DM). Serum levels of glycated albumin, adhesion molecules, endogenous secretory receptor of advanced glycation end products (esRAGE) and inflammatory factors were determined. Results Serum levels of GA, hsCRP, sVCAM-1, sICAM-1 and sE-selectin were increased, while esRAGE levels were decreased in diabetic patients than in non-diabetic patients (all P

Background: The efficacy of partial vs full coverage for tandem lesions in the culprit vessel during primary percutaneous coronary intervention (PCI) after ST-elevation myocardial infarction (STEMI) was compared in the present study. Methods and Results: The 76 patients with STEMI and tandem lesions in the culprit vessel were randomized to receive stent implantation for an occluded/culprit lesion only (partial group) or complete coverage of lesions (full group). After PCI, patients in the partial group had more complete ST-segment resolution (STR) at 90 min (60.5% vs 28.9%, P=0.006), Thrombosis In Myocardial Infarction (TIMI) flow grade 3 (68.4% vs 28.9%, P=0.001), and myocardial blush grade 3 (42.1% vs 15.8%, P=0.04) than those in the full group. At 6 months, the major adverse cardiac events-free survival rate did not differ significantly between groups, but left ventricular (LV) ejection fraction was improved in the partial group. Multivariate analysis revealed pre-procedural TIMI flow grade >1 and door-to-balloon time

Background Glycated albumin is the predominant circulating Amadori-type glycated protein in vivo and plays a major role in the development of diabetic vascular complications. The aim of this study was to assess the relationship between increased serum glycated albumin level and the presence and severity of coronary artery disease (CAD) in patients with type 2 diabetes mellitus (T2DM). Methods and Results In a total of 320 consecutive patients with T2DM, coronary angiography revealed normal coronary arteries in 83 patients (control group) and significant coronary stenosis (≥70% luminal diameter narrowing) in 237, of whom 51 patients had 1-vessel disease (Group I), 80 had 2-vessel disease (Group II), and 106 had 3-vessel disease (Group III). Serum glycated albumin, hemoglobin A1c (HbA1c) and tumor necrosis factor (TNF)-α levels, lipid profile, and renal function were measured. Logistic regression analysis was performed to determine the relative risk of serum glycated albumin level for the presence and severity of CAD. Multivariate stepwise linear regression analysis was done to identify independent determinants of the glycated albumin level. Serum glycated albumin (21.2±5.3% vs 19.4±4.3%, p=0.005) and TNF-α levels (123 ±115 pg/ml vs 65±59 pg/ml, p

There is increasing interest in percutaneous coronary intervention (PCI) for chronic total occlusions (CTO). Periprocedural myocardial injury (PMI) post CTO PCI is not uncommon, but true incidence and implications of PMI are not well understood.This study aimed to investigate risk factors for PMI post CTO PCI and its implications for the 1-year clinical outcome of a Chinese population.Baseline characteristics, procedure features, and major adverse cardiac events (MACE) at 1 year were assessed in 629 consecutive patients who underwent CTO PCI. PMI was diagnosed as an elevation of creatine kinase MB ≥3 times ULN 12-24 hr post procedure. Multivariate analysis was performed to determine the correlates of PMI and MACE at 1-year follow-up.In total, PMI was detected in 115 patients (18.3%). Compared with patients without PMI, those with PMI had a higher percentage of previous coronary artery bypass grafting (CABG), right coronary occlusion and side branch occlusion, and technical success was lower in the PMI group (90.4% vs. 96.7%, P = 0.003). One-year MACE-free survival was reduced in the PMI group (87.8% vs. 95.9%, P = 0.001). The final TIMI flow 0-1 (OR 2.23, 95%CI 1.06-4.87, P = 0.02), side branch occlusion (OR 2.67, 95%CI 1.19-7.11, P = 0.009), retrograde PCI (OR 1.35, 95%CI 1.10-2.74, P = 0.04), and history of prior CABG (OR 2.41, 95%CI 1.38-5.91, P = 0.01) were independent risk factors for the occurrence of PMI.In this unique Chinese cohort, PMI post CTO PCI was associated with several clinical and angiographic factors and exerts an adverse effect on 1-year clinical outcomes.

Objective We investigated whether and to what extent cystatin C was associated with angiographic coronary collateralization in patients with stable coronary artery disease and chronic total occlusion. Methods Serum levels of cystatin C and high-sensitive C-reactive protein (hsCRP) and glomerular filtration rate (GFR) were determined in 866 patients with stable angina and angiographic total occlusion of at least one major coronary artery. The degree of collaterals supplying the distal aspect of a total occlusion from the contra-lateral vessel was graded as poor (Rentrop score of 0 or 1) or good coronary collateralization (Rentrop score of 2 or 3). Results In total, serum cystatin C was higher in patients with poor collateralization than in those with good collateralization (1.08 ± 0.32 mg/L vs. 0.90 ± 0.34 mg/L, P < 0.001), and correlated inversely with Rentrop score (adjusted Spearmen’s r = -0.145, P < 0.001). The prevalence of poor coronary collateralization increased stepwise with increasing cystatin C quartiles (P for trend < 0.001). After adjusting for age, gender, risk factors for coronary artery disease, GFR and hsCRP, serum cystatin C ≥ 0.97 mg/L remained independently associated with poor collateralization (OR 2.374, 95% CI 1.660 ~ 3.396, P < 0.001). The diagnostic value of cystatin C levels for detecting poor coronary collateralization persisted regardless of age, gender, presence or absence of diabetes, hypertension or renal dysfunction. Conclusions Serum cystatin C reflects angiographic coronary collateralization in patients with stable coronary artery disease, and cystatin C ≥ 0.97 mg/L indicates a great risk of poor coronary collaterals.

Objective To investigate whether apolipoprotein A (apoA)-I glycation and paraoxonase (PON) activities are associated with the severity of coronary artery disease (CAD) in patients with type 2 diabetes mellitus (T2DM). Methods Relative intensity of apoA-I glycation and activities of high-density lipoprotein (HDL)-associated PON1 and PON3 were determined in 205 consecutive T2DM patients with stable angina with (n = 144) or without (n = 61) significant CAD (luminal diameter stenosis ≥ 70 %). The severity of CAD was expressed by number of diseased coronary arteries, extent index, and cumulative coronary stenosis score (CCSS). Results The relative intensity of apoA-I glycation was higher but the activities of HDL-associated PON1 and PON3 were lower in diabetic patients with significant CAD than in those without. The relative intensity of apoA-I glycation increased but the activities of HDL-associated PON1 and PON3 decreased stepwise from 1 - to 3 - vessel disease patients (P for trend

Background and aims In-stent restenosis (ISR) remains a major limitation of percutaneous coronary intervention despite improvements in stent design and pharmacological agents, whereas the mechanism of ISR has not been fully clarified. In the present study, we sought to investigate the potential association of serum soluble TREM-1 (sTREM-1) levels with the incidence of ISR. The role of TREM-1 was evaluated in cultured vascular smooth muscle cells (VSMCs). Methods Out of 1683 patients undergoing coronary intervention and follow-up coronary angiography after approximately one year, 130 patients were diagnosed with ISR, and 150 gender- and age-matched patients with no ISR were randomly included as controls. Levels of sTREM-1 were determined by ELISA. The role of TREM-1 signaling in the activation of VSMCs was tested. Results Serum sTREM-1 concentrations were significantly elevated in patients with than without ISR. Multivariable logistic regression analysis showed that sTREM-1, besides conventional factors, was independently associated with the incidence of ISR. Evident expression of TREM-1 in VSMCs was detected in the neointimal and medial layers of stenotic lesions of mouse carotid ligation models. In cultured VSMCs, expression of TREM-1 was significantly induced upon exposure to lipopolysaccharide. Blocking of TREM-1 with a synthetic inhibitory peptide LP17 dramatically inhibited, whereas TREM-1-activating antibody promoted cellular inflammation, proliferation and migration in VSMCs. Conclusions These data suggest that TREM-1 is a predictive biomarker of ISR and an important mediator of cellular inflammation, migration, and proliferation in VSMCs. Pharmacological inhibition of TREM-1 may serve as a promising approach to attenuate the progression of ISR.

OBJECTIVE We investigated whether and to what extent blood pressure (BP) affects coronary collateralization in type 2 diabetic and nondiabetic patients with stable angina and chronic total occlusion. METHODS Brachial BP was measured using an inflatable cuff manometer in 431 diabetic and 287 nondiabetic patients with stable angina and angiographic total occlusion of at least one major coronary artery. They were classified according to the SBP (

Patients are at risk of developing periprocedural myonecrosis after percutaneous coronary intervention (PCI). We investigated whether the use of the platelet glycoprotein (GP) IIb/IIIa receptor inhibitor tirofiban could reduce periprocedural myocardial infarction (PMI) in patients with stable coronary artery disease undergoing elective PCI with overlapping stent implantation for long lesions.A total of 748 stable angina patients with long lesions (≥ 40 mm in length) treated with overlapping stent implantation were randomly assigned to receive tirofiban (tirofiban group; n = 373) or conventional therapy (control group; n = 375). Intravenous tirofiban was initiated before PCI and maintained for 12 hr after the procedure. The primary endpoint was PMI, defined as an elevation in CK-MB3 times the upper limit of normal 12 hr after the index procedure. The secondary endpoint was major adverse cardiac events (MACE), including cardiac death, target vessel revascularization, and recurrent MI (re-MI), at one-year of clinical follow-up. The safety end-points included Thrombolysis in Myocardial Infarction (TIMI) major bleeding and stent thrombosis.Despite comparable angiographic and procedural characteristics, in the intention-to-treatment analysis, the primary endpoint was significantly reduced in the tirofiban group (4.0% vs. 11.5%, P0.001). Multivariate analysis revealed that the adjunctive use of tirofiban was the only negative predictor of PMI (OR 0.41, 95% CI 0.28-0.81, P0.01). At one-year of clinical follow-up, the overall occurrence of MACE was significantly lower in the tirofiban group (13.4% vs. 22.7%, P = 0.001). The rate of TIMI major bleeding and stent thrombosis did not differ significantly between the two groups.Our results show that the adjunctive use of tirofiban reduces the occurrence of PMI and MACE at one year in stable coronary artery disease patients undergoing elective PCI for long lesions with overlapping stent implantation.

In a recent meta-analysis, we investigated effects of β-blockers versus other classes of antihypertensive drugs on central hemodynamic measurements and explored the impact of heart rate on central hemodynamics and the risk of stroke. The pooled estimates of nine randomized controlled trials (n=754) showed that β-blockers were less efficacious in reducing central augmentation index (cAI) than all the other classes of antihypertensive drugs (8.6 %, P

Objective: Renal dysfunction represents a risk factor for poor coronary collateral growth. We investigated whether Glomerular Filtration Rate (GFR) estimated with the cystatin C-based formula (GFRCYS) is superior to that with the creatinine-based abbreviated Modification of Diet in Renal Disease (GFRMDRD) and the Chronic Kidney Disease Epidemiology Collaboration (GFREPI) equations for evaluating coronary collateralization in type 2 diabetic patients with stable coronary artery disease. Methods: GFR was estimated with creatinine- and cystatin C- based equations in 302 diabetic and 127 nondiabetic patients with stable angina and angiographic total occlusion of at least one major coronary artery. The degree of collaterals supplying the distal aspect of a total occlusion from the contra-lateral vessel was graded as poor (Rentrop score of 0 or 1) or good collateralization (Rentrop score of 2 or 3). Results: In diabetic patients, GFRCYS correlated more closely with Rentrop score than GFRMDRD (Spearmen’s r=0.44 vs. Spearmen’s r=0.30, P=0.047) and GFREPI (Spearmen’s r=0.44 vs. Spearmen’s r=0.29, P=0.028), and area under the curve of GFRCYS was larger compared with that of GFRMDRD and GFREPI (0.78 vs. 0.68 and 0.66, P=0.001 and P

No randomized trial has been performed to compare the efficacy of an intracoronary bolus of tirofiban versus urokinase during primary percutaneous coronary intervention (PCI). We investigated whether the effects of adjunctive therapy with an intracoronary bolus of urokinase was noninferior to the effects of an intracoronary bolus of tirofiban in patients with ST-elevation myocardial infarction (STEMI) undergoing PCI.A total of 490 patients with acute STEMI undergoing primary PCI were randomized to an intracoronary bolus of tirofiban (10 µg/kg; n = 247) or urokinase (250 kU/20 ml; n = 243). Serum levels of P-selectin, von Willebrand factor (vWF), CD40 ligand (CD40L), and serum amyloid A (SAA) in the coronary sinus were measured before and after intracoronary drug administration. The primary endpoint was the rate of complete ( ≥ 70%) ST-segment resolution (STR) at 90 minutes after intervention, and the noninferiority margin was set to 15%.In the intention-to-treat analysis, complete STR was achieved in 54.4% of patients treated with an intracoronary bolus of urokinase and in 60.6% of those treated with an intracoronary bolus of tirofiban (adjusted difference: -7.0%; 95% confidence interval: -15.7% to 1.8%). The corrected TIMI frame count of the infarct-related artery was lower, left ventricular ejection fraction was higher, and the 6-month major adverse cardiac event-free survival tended to be better in the intracoronary tirofiban group. An intracoronary bolus of tirofiban resulted in lower levels of P-selectin, vWF, CD40L, and SAA in the coronary sinus compared with an intracoronary bolus of urokinase after primary PCI (P0.05).An intracoronary bolus of urokinase as an adjunct to primary PCI for acute STEMI is not equally effective to an intracoronary bolus of tirofiban with respect to improvement in myocardial reperfusion assessed by STR. This may be caused by less reduction in coronary circulatory platelet activation and inflammation.

Transradial access has been increasingly used during primary percutaneous coronary intervention (PCI) for patients with acute ST-segment elevation myocardial infarction (STEMI) in last decade. Clinical benefits of upstream use of tirfiban therapy in STEMI patients treated by primary PCI have been reported. We investigated the merits of transradial vs. transfemoral access in primary PCI for STEMI patients with upstream use of tirofiban.Patients with STEMI treated with tirofiban between December 2006 and October 2012 then by primary PCI were compared between transradial (n = 298) and transfemoral (n = 314) access. Baseline demographics, angiographic and PCI features and primary endpoint of major adverse cardiac events (MACE) at 30-day clinical follow-up were recorded.Baseline and procedural characteristics were comparable between the two groups, apart from more patients in transradial group had hypertension and were treated by thrombus aspiration during primary PCI. Significantly fewer MACE occurred in the transradial group (5.4%) compared with the transfemoral group (9.9%) at 30-day clinical follow-up. Major bleeding events at 30-day clinical follow-up were 0 in transradial group and in 2.9% of transfemoral group. Multivariate analysis confirmed transradial approach as an independent negative predictor of 30-day MACE (HR 0.68; 95%CI 0.35 - 0.91; P = 0.03).Using transradial approach in primary PCI for acute STEMI infarction patients treated with tirofiban was clearly beneficial in reducing bleeding complications and improving 30-day clinical outcomes.

BACKGROUND We previously tested the accuracy of the SphygmoCor and Omron HEM-9000AI devices in the estimation of central blood pressure. In the present study, we investigated these two devices in the estimation of central-to-brachial pressure amplification against the invasive catheter measurement. METHODS In 33 individuals undergoing cardiac catheterization, we measured central blood pressure simultaneously by the invasive catheter and each of the two noninvasive devices and brachial blood pressure by the invasive catheter and an automated oscillometric blood pressure monitor of the Omron device. Pressure amplification was calculated as central-to-brachial systolic pressure difference and pulse pressure difference and ratio. The agreement between each of these two noninvasive devices and the invasive catheter was evaluated using the Student's t-test, intraclass correlation analysis, and the Bland-Altman method. RESULTS The mean central-to-brachial systolic pressure difference and pulse pressure difference and ratio estimated by Omron were significantly lower than those measured by the catheter (P

AIMS To evaluate the efficacy and safety of a 5-in-6 double catheter (DC) technique during transradial complex PCI compared to a conventional buddy-wire or balloon-anchoring approach. METHODS AND RESULTS One hundred and eighty-seven patients who failed in stent or balloon delivery after successful wiring of the target vessel were prospectively randomised to further treatment with a 5-in-6 DC technique (DC group, n=94) or by a conventional buddy-wire or balloon-anchoring approach (control group, n=93). Baseline clinical and lesion features were comparable between the two groups. The primary endpoint of technical success was significantly higher in the DC than in the control group (97.9% and 39.8%, p

The clinical significance of ischemic chest pain before acute ST-elevation myocardial infarction (STEMI) remains an interesting issue of investigation particularly in the era of percutaneous coronary intervention (PCI). This study aimed to assess the impact of angina prior to STEMI on short-term clinical outcomes in patients with acute STEMI undergoing primary PCI.Among a total of 875 consecutive patients with STEMI undergoing primary PCI, 292 had episodes of angina within 24 hours of STEMI (PA group) and the remaining 583 were free of anginal symptoms (non-PA group). Clinical characteristics, angiographic and procedural features, and in-hospital and 30-day outcomes were compared between the two groups.Diabetes was less common (17.5% vs. 23.3%, P = 0.04) and symptom-to-door time was shortened ((191.6 ± 96.8) minutes vs. (357.2 ± 341.9) minutes, P0.001) in the PA group than in the non-PA group. Patients with angina prior to STEMI had fewer totally or nearly totally occluded infarct-related artery (TIMI flow grade 0 - 1) at initial angiography (75.0% vs. 90.7%, P0.001), and achieved more TIMI flow grade 3 after primary PCI (84.2% vs. 78.2%, P = 0.04). These were associated with higher rates of overall procedural success (95.9% vs. 91.8%, P = 0.02) and of complete ST-segment resolution at 90 minutes after the procedure (51.7% vs. 40.3%, P = 0.001). During a 30-day clinical follow-up, the left ventricular ejection fraction was significantly improved ((53.0 ± 8.6)% vs. (51.1 ± 9.7)%, P = 0.002) and the primary endpoint of major adverse cardiac events was reduced in the PA group (7.2% vs. 12.7%, P = 0.01).Presence of angina prior to acute STEMI is associated with better outcome at a 30-day clinical follow-up in patients undergoing primary PCI.

Sewage sludge (SS) applied to sloping fields at rates that exceed annual forest nutrient requirements can be a source of phosphorus (P) in runoff. This study investigates the effects of different slopes (18, 27, 36, and 45%) on P in runoff from plots amended with SS (120 Mg ha). Lateritic soil (pH 5.2) was exposed to five simulated rainfalls (90 mm h) on outdoor plots. When sludge was broadcast and mixed with surface soils, the concentrations and loss in runoff of total P in the mixed sample (MTP), total P in the settled sample (STP), total particulate P (TPP), total suspended P (TSP), and total dissolved P (TDP) were highest at 1 or 18 d after application. Initially, pollution risks to surface waters generally increased to different degrees with steeper slopes, and then diminished gradually with dwindling differences between the slopes. The runoff losses coefficient of MTP increased in the order 36 > 45 > 27 > 18%. The initial event (1 and 18 d) accounted for 67.0 to 83.6% of total runoff P losses. Particulate fraction were dominant carriers for P losses, while with the lower slopes there was higher content of P per unit particulate fraction in runoff. Phosphorus losses were greatly affected by the interaction of sludge-soil-runoff and the modification of soil properties induced by sludge amendment. It is recommended to choose lower slopes (

This study aimed to evaluate the impact of vascular response assessed by intravascular ultrasound (IVUS) imaging on clinical outcomes in elderly patients (≥ 75 years) undergoing percutaneous coronary intervention (PCI) for de novo lesions with sirolimus-eluting stent (SES) implantation. Repeat coronary angiography with IVUS was performed 1 year after SES-based PCI for de novo lesions in 136 elderly patients (≥ 75 years) and 427 younger counterparts (75 years) (219 lesions and 635 lesions, respectively). Major adverse cardiac events (MACE) including cardiac death, non-fatal myocardial infarction, and target lesion revascularization (TLR) during 2-year follow-up were recorded. Despite similar angiographic in-stent restenosis and TLR and IVUS-detected incomplete stent apposition (ISA), absolute intimal hyperplasia and percentage of volumetric obstruction were lower in elderly than in younger patients. At 2-year follow-up, cumulative survival freedom from composite death and myocardial infarction or MACE was significantly reduced in elderly patients, but very late stent thrombosis was similar in the two groups. Cox proportional hazards model identified age, diabetes, left ventricular ejection fraction, lesion length,minimal stent cross-sectional area and plaque progression as independent predictors of non-fatal myocardial infarction or mortality. In elderly patients undergoing SES-based PCI, despite similar TLR, neointimal hyperplasia was significantly lower than in younger patients. IVUS measurements except for minimal stent cross-sectional area did not correlate with stent thrombosis and clinical outcomes at 2 years.

Background Recently, a chronic total occlusion (CTO) in the non-infarct-related artery (non-IRA) was reported as an independent predictor of clinical outcome in patients with acute ST-segment elevation myocardial infarction (STEMI). The aim of this study was to investigate the clinical significance of staged revascularization for a CTO in the non-IRA for patients with STEMI. Methods A total of 136 patients with acute STEMI undergoing primary percutaneous coronary intervention (PCI) received staged revascularization (ranging 7–10days) for a CTO in the non-IRA. Cardiac mortality and major adverse cardiac events (MACE) including death, recurrent myocardial infarction, repeat revascularization, and re-hospitalization because of heart failure during 2-year follow-up were recorded. Results Recanalization of totally occluded lesions in the non-IRA was successful in 87 (64%) patients for 93 lesions but failed in 49 (36%) patients. During 2-year follow-up, cardiac mortality was lower (8.0% vs. 20.4%, p=0.036) and MACE-free survival was higher (78.2% vs. 61.2%, p=0.042) in patients with successful than in those with failed revascularization of a CTO in the non-IRA. Multivariable analysis showed that after adjustment for possible confounders, successful recanalization of a CTO in the non-IRA was an independent predictor for 2-year cardiac mortality (HR=0.145, 95% CI 0.047–0.446, P=0.001) and MACE-free survival (HR=0.430, 95%CI 0.220–0.838, P=0.013). Conclusion Successful revascularization of a CTO in the non-IRA is associated with improved clinical outcomes in patients with STEMI undergoing primary PCI.

Cadmium toxicity to 23 kinds of commonly cultivated crops of 9 families was studied by solution culture with different cadmium concentrations. Most of the studied crop seedlings showed cadmium toxicity symptoms with 0.1-0.25 mg x L(-1). The toxic effects of cadmium on the crops were quite different. The effect of Cd on shoot biomass was more obvious and stable than the other parameters at low Cd concentrations (0.1-0.5 mg x L(-1)), Therefore, shoot fresh weight was selected to be the indicator of plant sensitivity to Cd. The EC20 (effective concentration causing a 20% inhibition of shoot biomass) values of Cd for the studied crops ranged from 0.03 to 24.67 mg x L(-1). The Cd sensitivity of the crops is classified according to the response endpoint of apparent symptoms and the EC20 values. Chinese cabbage, brassica napus, youmai lettuce, mustard and pakchoi are sensitive species to Cd toxicity that can be used as ecological receptors to determine the critical value of the toxicity of soil Cd to crops or as monitoring crop species of soil Cd pollution. Cucumber is most tolerant to Cd toxicity among the studies crops.

The efficacy of partial vs full coverage for tandem lesions in the culprit vessel during primary percutaneous coronary intervention (PCI) after ST-elevation myocardial infarction (STEMI) was compared in the present study.The 76 patients with STEMI and tandem lesions in the culprit vessel were randomized to receive stent implantation for an occluded/culprit lesion only (partial group) or complete coverage of lesions (full group). After PCI, patients in the partial group had more complete ST-segment resolution (STR) at 90 min (60.5% vs 28.9%, P=0.006), Thrombosis In Myocardial Infarction (TIMI) flow grade 3 (68.4% vs 28.9%, P=0.001), and myocardial blush grade 3 (42.1% vs 15.8%, P=0.04) than those in the full group. At 6 months, the major adverse cardiac events-free survival rate did not differ significantly between groups, but left ventricular (LV) ejection fraction was improved in the partial group. Multivariate analysis revealed pre-procedural TIMI flow grade1 and door-to-balloon time90 min were positively associated with complete STR at 90 min, whereas full coverage for tandem lesions was an independent factor for poor STR (odds ratio 2.58, 95% confidence interval 1.08-5.42, P=0.03).For acute STEMI patients with tandem lesions in the culprit vessel, primary stenting for the occluded lesion only is beneficial in improving myocardial perfusion and LV function.

The impact of late incomplete stent apposition (ISA) post sirolimus eluting stent (SES) implantation in patients with acute coronary syndrome (ACS) on long-term clinical outcomes remains controversial. The aim of the present study was to evaluate the association between late ISA and clinical outcomes in patients with ACS compared with that with stable angina (SA).From February 2005 to March 2007, 54 ACS patients and 83 SA patients were enrolled in this study, late ISA was determined by means of three-dimensional volumetric intravascular ultrasound (IVUS) analyses one year after SES implantation and clinical outcomes one year post IVUS were obtained in these patients.In 219 treated lesions of the 137 patients, late ISA was documented in 25 lesions in 16 patients (20 ISA in 12 ACS patients vs. 5 ISA in 4 SA patients, P0.001). Though lumen area in reference and stented segment, neointimal hyperplasia (NIH) area and percentage of NIH in stented segment, and external elastic membrane (EEM) area in reference segment were similar between two groups, EEM area in stented segment [(15.34+/-5.44) mm2 vs. (13.83+/-4.51) mm2, P=0.026], stented/reference segment EEM area ratio (1.13+/-0.22 vs. 1.02+/-0.18, P0.001), plaque and media area [(8.43+/-3.93) mm2 vs. (7.01+/-2.93) mm2, P=0.002] was significantly lager in ACS group than that in SA group. Multivariable logistic analysis showed that ACS (OR 6.477 with 95% CI from 2.297 to 18.263, P0.001) and stent lengthor=23 mm (OR 3.680 with 95% CI from 1.181 to 11.469, P=0.025) were main independent factors of occurrence of late ISA. Incidence of main adverse cardiac events (MACE) one year post IVUS was similar between the two groups.Compared with patients with SA, ACS patients had larger stented segment EEM area, plaque and media area as well as increased incidence of ISA. However, the incidence of MACE was similar in ACS and SA patients one year after IVUS.

Current guidelines support primary percutaneous coronary intervention (primary PCI) as the first treatment of choice (as opposed to thrombolytic therapy) for patients with acute ST-segment elevation myocardial infarction (STEMI) especially when delivered within 12 hours of symptom onset. We aimed to evaluate the impact of different clinical pathways on reduction of reperfusion delay and subsequent improvement in outcomes in patients with STEMI.From November 2005 to November 2007, 546 consecutive patients with definite STEMI, who upon arrival at the emergency room were triaged to undergo primary PCI, were included. Of them, 271 patients were brought directly to catheterization laboratory (rapid group), and 275 patients were admitted to the coronary care unit (CCU) or cardiac ward first, and then transferred to the catheterization laboratory (non-rapid group). Primary endpoint was door-to-balloon (D2B) time, and secondary endpoints included infarct size assessed by peak CK-MB level and rates of major cardiac adverse events (MACE) including death, reinfarction, or target-vessel revascularization during hospitalization and at 30-day clinical follow-up.Baseline clinical characteristics, angiographic features and procedural success rates were comparable between the two groups, except that more patients received glycoprotein IIb/IIIa receptor inhibitors before angiography (84.0% and 77.1, P = 0.042) and had TIMI 3 flow in the culprit vessel at initial angiogram (17.1% and 9.2%, P = 0.007) in the non-rapid group. The D2B time was shortened ((108 +/- 44) minutes and (138 +/- 31) minutes, P0.0001), and number of patients with D2B time90 minutes was greater (22.6% and 10.9%, P0.0001) in the rapid group. The advantages associated with rapid intra-hospital transfer were enhanced if the patients presented to the hospital at regular hours. Peak CK-MB level was significantly reduced in the rapid group. In-hospital mortality (4.1% and 5.8%) and cumulative MACE rate (7.0% and 9.8%) did not significantly differ between rapid and non-rapid groups. At 30 days, cumulative death- and MACE-free survival rates were improved in the rapid group (94.5% and 89.5%, P = 0.035; 90.1% and 84.0%, P = 0.034, respectively).Clinical pathway with bypass of CCU/cardiac ward admission was associated with rapid reperfusion, smaller infarct size, and improved short-term survival for patients with STEMI undergoing primary PCI. In the future, it is essential to reduce the time delay for patients presenting at off-hours.