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Due to advances in medical treatments, a substantial proportion of heart failure (HF) patients with reduced left ventricular ejection fraction (EF, HFrEF) have experienced partial or complete recovery of EF, termed HFrecEF, and markedly improved clinical outcomes. In the present study, we sought to investigate the relationship between glycemic control and the incidence of HFrecEF in hospitalized HFrEF patients with type 2 diabetes mellitus (T2DM).A total of 463 hospitalized T2DM patients with HFrEF were consecutively enrolled. Follow-up echocardiogram was performed after around 12 months. Patients who had an absolute EF improvement ≥10% and a second EF 40% were classified into HFrecEF, and those who did not meet these criteria were defined as persistent HFrEF.During the 12-month follow-up, 44.5% of T2DM patients developed HFrecEF. Patients with HFrecEF had significantly lower HbA1c level than those with persistent HFrEF (6.5% [IQR 5.8% ∼ 7.2%] vs. 6.7% [IQR 6.1% ∼ 7.8%], P = 0.003), especially in HF of an ischemic etiology. HbA1c levels were inversely correlated with changes in EF during follow-up. After multivariate adjustment, every 1% increase in HbA1c conferred a 17.4% (OR: 0.826 [95% CI 0.701-0.968]) lower likelihood of HFrecEF. Compared to patients with good glycemic control (HbA1c ≤ 6.2%), those with poor glycemic control (HbA1c 7.1%) had a 52.0% (OR: 0.480 [95% CI 0.281-0.811] decreased likelihood of HFrecEF.This study demonstrates that uncontrolled HbA1c level is associated with compromised development of HFrecEF in T2DM patients with HF, especially in those with an ischemic etiology.

Objective This study aimed to evaluate the relationship between coronary collateralization and in-stent restenosis (ISR) in stable coronary artery disease patients with chronic total occlusion (CTO) after percutaneous coronary intervention (PCI) with drug-eluting stent (DES) implantation. Methods The degree of coronary collaterals supplying the distal aspect of a total occlusion from the contra-lateral vessel was graded according to Rentrop classification in 216 patients with stable angina undergoing successful DES based PCI for CTO. Univariable and multivariable logistic regression analyses were performed to assess the potential factors related to angiographic ISR during follow-up. Results Despite similar number of diseased coronary arteries, good collateralization (Rentrop score 2 or 3) was more frequently associated with right coronary artery occlusion (60%), whereas poor collaterals (Rentrop score 0 or 1) occurred more often in left anterior descending artery occlusion (40%). Despite similar number of CTO intervened, stent length was longer in patients with good collateralization (59±27mm vs 47±23mm, p =0.001). At mean 18months, the rate of ISR did not significantly differ between patients with good collateralization and those with poor collateralization (12.7% vs 20.2%, p =0.148). At multivariable analysis, age (OR 1.058, 95%CI 1.015–1.104, p =0.008), history of diabetes mellitus (OR 2.382, 95%CI 1.109–5.116, p =0.026) and reference CTO vessel diameter (OR 0.219, 95% CI 0.051–0.951, p =0.043) were independent risk factors for ISR while Rentrop collateral grade (OR 0.795, 95% CI 0.365–1.732, p =0.414) was not associated with ISR. Conclusions The occurrence of ISR after successful DES based PCI for CTO may be not influenced by coronary collateralization.

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

Glycated albumin (GA) and the endogenous secretory receptor for advanced glycation endproducts (esRAGE) may modulate risk related to atherosclerosis. We tested the hypothesis that elevated GA and reduced esRAGE in serum are associated with adverse clinical outcomes in patients with type 2 diabetes and stable coronary artery disease (CAD).We determined GA and esRAGE serum levels in 576 consecutive patients with type 2 diabetes and stable CAD undergoing sirolimus-eluting stent (SES)-PCI. The primary endpoint was the incidence of major adverse cardio-cerebral events (MACCE) including cardiac death, non-fatal myocardial infarction, and non-fatal stroke during a 2-year follow-up. The secondary endpoint was the occurrence of clinically driven repeat revascularization during a 2-year follow-up. The prognostic value of GA and esRAGE was determined with the Cox-proportional hazard model after adjustment for covariates.A total 40 patients (6.9%) experienced MACCE, and 108 (18.8%) patients underwent repeat coronary revascularization during the follow-up. Serum GA (HR=1.22, 95% CI 1.16-1.28; HR=1.15, 95% CI 1.11-1.19, respectively; for both p0.001) and esRAGE (HR=0.60, 95% CI 0.40-0.87; HR=0.75, 95% CI 0.61-0.92, respectively; for both p0.01) levels remained independent predictors of the primary and secondary endpoints after adjustment for possible confounders.Serum GA and esRAGE are novel predictors of long-term clinical outcomes in patients with type 2 diabetes and stable CAD. Increased serum GA and decreased esRAGE are associated with a poor prognosis in such patients.

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.

Background We investigated whether an additional intracoronary tirofiban bolus administration following upstream intravenous treatment could further improve myocardial reperfusion and clinical outcome in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Methods A total of 453 eligible STEMI patients were randomly allocated to intracoronary bolus administration of tirofiban (10μg/kg; n=229) or saline (10mL; n=224) during primary PCI, followed by intravenous tirofiban infusion (0.15μg/kg/min) for 24–36h. Serum levels of P-selectin, vWF, CD40L and serum amyloid A (SAA) in the coronary sinus were measured before and after intracoronary bolus administration. The primary endpoint was ST-segment resolution (STR) at 90min after the procedure. Second endpoints included corrected TIMI frame count (cTFC), left ventricular volumes and ejection fraction (EF), and major adverse cardiac events (MACE) at 30-day and 6-month follow-up. Results Intracoronary tirofiban administration resulted in a higher rate of completed STR (59.0% vs. 44.6%, P=0.002), lower cTFC (21.6±5.4 vs. 23.7±7.8, P=0.048), and significantly reduced coronary sinus levels of P-selectin, vWF, CD40L and SAA. Patients treated with intracoronary tirofiban had a trend toward less MACE at 30days (3.1% vs. 6.7%, P=0.072). At 6months, left ventricular end-systolic volume was smaller, EF was higher and MACE-free survival was improved (96.1% vs. 90.6%, P=0.020) in the intracoronary tirofiban group. Conclusions An additional intracoronary tirofiban bolus administration following upstream intravenous treatment reduces coronary circulatory platelet activation and inflammatory process, and significantly improves myocardial reperfusion and left ventricular function as well as 6-month MACE-free survival for STEMI patients undergoing primary PCI.

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.

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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.

We sought to examine the impact of moderate or severe renal insufficiency (RI) on long-term clinical outcomes after successful percutaneous coronary intervention (PCI) with drug-eluting stent implantation.All-cause mortality and major adverse cardiac events were prospectively determined for 1174 patients after successful PCI with drug-eluting stent implantation. Based on estimated creatinine clearance (CrCl) levels, long-term outcomes were compared between patients with CrCl60 ml/min (RI group; n=460) and those with CrClor =60 ml/min (control group; n=714). Hazard ratio for mortality and myocardial infarction was further evaluated for patients with severe (CrCl30 ml/min), moderate (CrCl 30-59 ml/min), mild RI (CrCl 60-89 ml/min) and normal renal function (CrClor =90 ml/min).Patients in RI group were older, lower body weight and hemoglobin, more female gender, and less cigarette smokers than those in control group. During follow-up (averaged 19.2 months) after successful PCI, all-cause death (8.3% vs. 1.5%, P0.001), cardiac death (5.7% vs. 1.1%, P0.001) and occurrence of non-fatal myocardial infarction (2.2% vs. 0.4%, P=0.005) were significantly higher, but rate of target vessel revascularization (TVR) was lower (5.7% vs. 9.6%, P=0.017) in RI group than in control group. Multivariate analysis revealed that CrCl60 ml/min, diabetes, left ventricular ejection fraction0.50 and anemia were independent risk factors for mortality and non-fatal myocardial infarction. Compared with patients with normal renal function, hazard ratio for a composite of mortality and myocardial infarction was 1.079 (P=0.907), 5.067 (P=0.007) and 8.828 (P=0.002) in patents with mild, moderate and severe RI, respectively.Irrespective of whether drug-eluting stent implantation reduces TVR, the presence of moderate or severe RI is still associated with unfavorable long-term outcomes.

The potential role of hydration in prevention of contrast-induced nephropathy (CIN) still remains to be unclear.Nine-hundred and thirty-six patients scheduled for percutaneous coronary intervention (PCI) were enrolled into the present study, and divided into normal (serum creatinine1.5 mg/dl) and abnormal (serum creatineor =1.5 mg/dl) groups according to their baseline serum concentration of creatinine. Each group was further randomly divided into two subgroups: hydration and nonhydration. All patients in abnormal group took twice orally loading dose of 1200 mg acetylcysteine (ATLS) at 12 h before scheduled time for coronary angiogram and immediately after procedure. Creatinine concentration was remeasured at the time of admission (just before catheterization), every day for the following three days. The primary end point during 6-month follow-up included clinical driven revascularization (either PCI or CABG), death from all causes, and requiring emergency renal-replacement therapy.The incidence of CIN was more commonly in abnormal group that in normal group (6.52% vs. 37.68%, p0.001). Hydration had potentials in prevention of CIN only in patients with elevated baseline concentration of creatinine. Multivariate analysis demonstrated that the following variables remained to be significant factors correlating with CIN: ageor =70 years (odds ration [OR] 5.27, 95% confidence interval [CI] 1.94 to 13.07, p=0.0007), contrast volumeor =320 ml (OR 3.26, 95% CL 2.14 to 7.58, p=0.01), diabetes mellitus (OR 9.86, 95% CL 5.38 to 31.67, p0.0001), and peripheral arterial disease (OR 11.25, 95% CL 5.12 to 43.19, p0.0001). Patients with CIN in abnormal group had worse clinical outcomes, compared to patients with CIN in normal group.Patients with CIN and preexisting renal insufficiency had worse clinical outcomes. Hydration with 0.45% sodium chloride alone had no potential effect on the occurrence of CIN in patients with normal renal function. Combination of hydration with ATLS could reduce the incidence of CIN in patients at high risk.