Using circulating O-sulfotyrosine in the differential diagnosis of acute kidney injury and chronic kidney disease.

BACKGROUND: Sulfation of tyrosine, yielding O-sulfotyrosine, is a common but fixed post-translational modification in eukaryotes. Patients with increased circulating O-sulfotyrosine levels experience a faster decline in renal function with progression to end-stage renal disease (ESRD). In the present study, we measured serum O-sulfotyrosine levels in individuals with chronic kidney disease (CKD) and acute kidney injury (AKI) to explore its ability to differentiate AKI from CKD. METHODS: A total of 135 patients (20 with AKI and 115 with CKD) were recruited prospectively for liquid chromatography-mass spectrometry assessment of circulating O-sulfotyrosine. We also studied C57BL/6 mice with CKD after 5/6 nephrectomy (Nx). Blood samples were drawn from the tail vein on Day 1, 3, 5, 7, 14, 30, 60, and 90 after CKD. Serum separation and characterization of creatinine, blood urea nitrogen (BUN), and O-sulfotyrosine was performed. Thus, the time-concentration curves of the O-sulfotyrosine level demonstrate the variation of kidney dysfunction. RESULTS: The serum levels of O-sulfotyrosine were markedly increased in patients with CKD compared with AKI. Median O-sulfotyrosine levels in CKD patients versus AKI, respectively, were as follows:243.61 ng/mL(interquartile range [IQR] = 171.90-553.86) versus 126.55 ng/mL (IQR = 48.19-185.03, P = 0.004). In patients with CKD, O-sulfotyrosine levels were positively correlated with creatinine, BUN, and Cystatin C (r = 0.63, P < 0.001; r = 0.49, P < 0.001; r = 0.61, P < 0.001, respectively) by the multivariate linear regression analysis (ß = 0.71, P < 0.001; ß = 0.40, P = 0.002; ß = 0.73, P < 0.001, respectively). However, this association was not statistically significant in patients with AKI (r = - 0.17, P = 0.472; r = 0.11, P = 0.655; r = 0.09, P = 0.716, respectively). The receiver operating characteristic (ROC) analysis illustrated that the area under the curve was 0.80 (95% confidence interval [CI] 0.71-0.89; P < 0.001) and the optimal cut-off value of serum O-sulfotyrosine suggesting AKI was < 147.40 ng/mL with a sensitivity and specificity of 80.90 and 70.00% respectively. In animal experiments, serum levels of O-sulfotyrosine in mice were elevated on Day 7 after 5/6 nephrectomy (14.89 ± 1.05 vs. 8.88 ± 2.62 ng/mL, P < 0.001) until Day 90 (32.65 ± 5.59 vs. 8.88 ± 2.62 ng/mL, P < 0.001). CONCLUSION: Serum O-sulfotyrosine levels were observed correlated with degrading renal function and in CKD patients substantially higher than those in AKI patients. Thus serum O-sulfotyrosine facilitated the differential diagnosis of AKI from CKD.

Increased glycated albumin and decreased esRAGE levels in serum are related to negative coronary artery remodeling in patients with type 2 diabetes: an Intravascular ultrasound study.

BACKGROUND: Negative coronary artery remodeling is frequent in patients with diabetes, but its mechanism remains unclear. We here evaluated the association of serum levels of glycated albumin (GA) and endogenous secretory receptor for advanced glycation end products (esRAGE) with coronary artery remodeling in type 2 diabetic patients. METHODS: Serum levels of GA and esRAGE were measured and intravascular ultrasound was performed in 136 consecutive diabetic patients with 143 coronary intermediate lesions. The remodeling index (RI) was calculated as the ratio between external elastic membrane (EEM) area at the lesion site and EEM area at the reference segment. Negative remodeling (NR) was defined as an RI < 0.95 and intermediate or positive remodeling as an RI ≥ 0.95. RESULTS: Mean plaque burden at the lesion site was 70.96 ± 9.98%, and RI was 0.96 ± 0.18. Negative coronary arterial remodeling existed in 81 (56.6%) lesions. RI correlated closely with serum esRAGE level (r = 0.236, P = 0.005) and was inversely related to serum GA level (r = - 0.240, P = 0.004) and plasma low-density lipoprotein cholesterol (LDL-C) (r = - 0.206, P = 0.014) and total cholesterol levels (r = - 0.183, P = 0.028). Generalized estimating equations logistic regression analysis identified esRAGE (OR 0.037; 95% CI 0.012-0.564, P = 0.021), GA (OR 1.093; 95% CI 1.013-1.179, P = 0.018) and LDL-C (OR 1.479; 95% CI 1.072-2.835, P = 0.023) as independent predictors for negative remodeling. CONCLUSIONS: In diabetic patients, negative coronary artery remodeling is associated with increased GA and decreased esRAGE levels in serum.

Association of Serum HMGB2 Levels With In-Stent Restenosis: HMGB2 Promotes Neointimal Hyperplasia in Mice With Femoral Artery Injury and Proliferation and Migration of VSMCs.

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.

Increased carbamylation level of HDL in end-stage renal disease: carbamylated-HDL attenuated endothelial cell function.

It is thought that carbamylated modification plays a crucial role in the development and progression of cardiovascular disease (CVD) in patients with end-stage renal disease (ESRD). However, information on the biological effects of carbamylated high-density lipoprotein (C-HDL) in ESRD is poor. The present study investigated the carbamylation level of HDL in ESRD and the effects of C-HDL on endothelial repair properties. HDL was isolated from healthy control subjects (n = 22) and patients with ESRD (n = 30). The carbamylation level of HDL was detected using ELISA. Isolated C-HDL for use in tissue culture experiments was carbamylated in vitro to a similar extent to that observed in ESRD. Human arterial endothelial cells were treated with C-HDL or native HDL to assess their migration, proliferation, and angiogenesis properties. HDL-associated paraoxonase 1 activity was also determined by spectrophotometry assay. Compared with healthy control subjects, the carbamylation level of HDL in ESRD patients was increased and positively correlated with blood urea concentration. In vitro, C-HDL significantly inhibited migration, angiogenesis, and proliferation in endothelial cells. Mechanistic studies revealed that HDL-associated paraoxonase 1 activity was decreased and negatively correlated with the carbamylation level of HDL in ESRD patients. In addition, C-HDL suppressed the expression of VEGF receptor 2 and scavenger receptor class B type I signaling pathways in endothelial cells. In conclusion, the present study identified a significantly increased carbamylation level of HDL in ESRD. Furthermore, C-HDL inhibited endothelial cell repair functions.

Impact of angina prior to acute ST-elevation myocardial infarction on short-term outcomes after primary percutaneous coronary intervention: results from the Shanghai Registry of Acute Coronary Syndrome (SRACE).

BACKGROUND: 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. METHODS: 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. RESULTS: 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, P < 0.001) 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%, P < 0.001), 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). CONCLUSION: Presence of angina prior to acute STEMI is associated with better outcome at a 30-day clinical follow-up in patients undergoing primary PCI.

Increased serum vWF and sVCAM-1 levels are associated with late or very late angiographic stent thrombosis after sirolimus-eluting stent implantation.

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<0.01). No significant difference was observed in the genotype and allele distribution of the vWF, t-PA and PAI-1 gene polymorphisms. Multivariable logistic regression analysis showed that vWF, sVCAM-1, discontinuation of clopidogrel therapy and left ventricular ejection fraction of less than 50% were independent determinants of late ST. CONCLUSION: Increased serum vWF and sVCAM-1 levels are associated with late ST, suggesting that endothelial dysfunction contributes to the development of late or very late ST.

[Intravascular ultrasound evaluation on the efficacy of national made Firebird stents comparing with Cypher stents].

OBJECTIVE: Intravascular ultrasound (IVUS) was used to compare the effects on neointimal hyperplasia inhibition between national made Firebird stents and Cypher stents in patients with coronary artery disease. METHODS: From May 2003 to March 2007, 215 patients with 317 native lesions received either Firebird stent (147 lesions of 108 patients, Firebird group) or Cypher stent implantation (138 lesions of 107 patients, Cypher group). Quantitative coronary angiography (QCA) and IVUS were performed at one-year follow-up. RESULTS: The baseline clinical and angiographic characteristics between the two groups were similar, but post procedural minimal lumen diameter was significantly larger in Firebird group than that in Cypher group [(2.88 +/- 0.43) mm vs. (2.78 +/- 0.33) mm, P < 0.05]. follow-up QCA results showed that in-stent late loss [(0.17 +/- 0.29) mm vs. (0.16 +/- 0.27) mm, P > 0.05] and in-segment late loss [(0.18 +/- 0.36) mm vs. (0.20 +/- 0.32) mm, P > 0.05] was similar between Firebird group and Cypher group, while stent cross sectional area (CSA) [(6.99 +/- 2.25) mm(2) vs. (6.46 +/- 1.71) mm(2), P < 0.05], lumen CSA [(6.89 +/- 2.30) mm(2) vs. (6.36 +/- 1.73) mm(2), P < 0.05], stent volume [(162.5 +/- 68.9) m(3) vs. (140.8 +/- 57.9) mm(3), P < 0.01], lumen volume [(160.4 +/- 69.5) mm(3) vs. (138.6 +/- 57.6) mm(3), P < 0.01] and minimal stent CSA [(5.40 +/- 1.85) mm(2) vs. (4.92 +/- 1.43) mm(2), P < 0.05] were larger in Firebird group than those in Cypher group. IVUS analysis showed that there was no significant difference in neointimal hyperplasia volume [(2.09 +/- 5.46) mm(3) vs. (2.23 +/- 6.50) mm(3), P > 0.05] and percentage of volume obstruction [(1.68 +/- 5.84)% vs. (1.59 +/- 4.10)%, P > 0.05] between the two groups. CONCLUSION: Implantation of Firebird stent was associated with low restenosis rate and both Firebird and Cypher stents equally and effectively inhibited neointimal hyperplasia.

Intra-coronary administration of soluble receptor for advanced glycation end-products attenuates cardiac remodeling with decreased myocardial transforming growth factor-beta1 expression and fibrosis in minipigs with ischemia-reperfusion injury.

BACKGROUND: The cardioprotective effects of soluble receptor for advanced glycation end-products (sRAGE) have not been evaluated in large animals and the underlying mechanisms are not fully understood. This study aimed to evaluate the effects of intra-coronary administration of sRAGE on left ventricular function and myocardial remodeling in a porcine model of ischemia-reperfusion (I/R) injury. METHODS: Ten male minipigs with I/R injury were randomly allocated to receive intra-coronary administration of sRAGE (sRAGE group, n = 5) or saline (control group, n = 5). Echocardiography was performed before and 2 months after infarction. Myocardial expression of transforming growth factor (TGF)-beta1 was determined by immunohistochemistry and fibrosis was evaluated by Sirius red staining. RESULTS: As compared with the baseline values in the control animals, left ventricular end-diastolic volume (from (19.5 +/- 5.1) to (32.3 +/- 5.6) ml, P < 0.05) and end-systolic volume (from (8.3 +/- 3.2) to (15.2 +/- 4.1) ml, P< 0.05) were significantly increased, whereas ejection fraction was decreased (from (61.6 +/- 13.3)% to (50.2 +/- 11.9)%, P < 0.05). No obvious change in these parameters was observed in the sRAGE group. Myocardial expression of TGF-beta1 was significantly elevated in the infarct and non-infarct regions in the control group, as compared with sRAGE group (both P< 0.01). Fibrotic lesions were consistently more prominent in the infarct region of the myocardium in the control animals (P < 0.05). CONCLUSION: Intra-coronary sRAGE administration attenuates RAGE-mediated myocardial fibrosis and I/R injury through a TGF-beta1-dependent mechanism, suggesting a clinical potential in treating RAGE/ligand-associated cardiovascular diseases.

Impact of angiographic and intravascular ultrasound features on clinical outcome after sirolimus-eluting stent implantation for de-novo lesions in nondiabetic and type 2 diabetic patients.

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.

Partial vs full coverage for tandem lesions in culprit vessel during primary coronary intervention in patients with acute ST-elevation myocardial infarction--the PERFECT-AMI study.

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 <90 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). CONCLUSIONS: 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.

[Association between late incomplete stent apposition after sirolimus eluting stent implantation and clinical outcomes in patients with acute coronary syndrome].

OBJECTIVE: 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). METHODS: 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. RESULTS: 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, P<0.001). 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, P<0.001), 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, P<0.001) and stent length>or=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. CONCLUSION: 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.

Serial assessment of left ventricular remodeling and function by echo-tissue Doppler imaging after myocardial infarction in streptozotocin-induced diabetic swine.

BACKGROUND: The aim of this study was to determine the value of Doppler tissue imaging (DTI) in detecting serial changes in left ventricular (LV) geometry and function after myocardial infarction (MI) in diabetic swine. METHODS: Thirteen minipigs with streptozotocin-induced diabetes for 1 month and 13 controls were subjected to occlusion of the left anterior descending coronary artery. Echocardiography and DTI were performed before, 30 minutes, 90 minutes, and 4 weeks after left anterior descending coronary artery occlusion. RESULTS: At baseline, LV end-diastolic volume and mass were greater in pigs with diabetes. After MI, LV ejection fractions and systolic mitral annular velocities were decreased and LV chambers dilated in both groups, which were exacerbated in animals with diabetes. At 30 minutes, 90 minutes, and 4 weeks after MI, strain rates were significantly lower in both infarct and noninfarct areas in the diabetic group than in controls. CONCLUSIONS: DTI proved to be a useful tool in the serial assessment of subclinical LV dysfunction after MI in pigs with diabetes.

Impact of moderate or severe renal insufficiency on long-term outcomes in patients undergoing drug-eluting stent based coronary intervention.

AIMS: 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. METHODS: 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 CrCl<60 ml/min (RI group; n=460) and those with CrCl> or =60 ml/min (control group; n=714). Hazard ratio for mortality and myocardial infarction was further evaluated for patients with severe (CrCl<30 ml/min), moderate (CrCl 30-59 ml/min), mild RI (CrCl 60-89 ml/min) and normal renal function (CrCl> or =90 ml/min). RESULTS: 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%, P<0.001), cardiac death (5.7% vs. 1.1%, P<0.001) 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 CrCl<60 ml/min, diabetes, left ventricular ejection fraction <0.50 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. CONCLUSIONS: Irrespective of whether drug-eluting stent implantation reduces TVR, the presence of moderate or severe RI is still associated with unfavorable long-term outcomes.

Moderate-severe renal insufficiency is a risk factor for sirolimus-eluting stent thrombosis. The RIFT study.

OBJECTIVE: The RIFT study aimed to observe the impact of renal insufficiency (RI) on the incidence of stent thrombosis (ST) after percutaneous coronary intervention. METHODS: The RIFT study enrolled 1,174 patients undergoing revascularization exclusively with sirolimus-eluting stents. The occurrence of ST and major adverse cardiac events were compared between patients with (n = 309) and without (n = 865) RI, and independent predictors of ST were also identified. RESULTS: During follow-up (mean 18.9 +/- 9.2 months), the rate of ST was significantly higher in patients with than without RI [5.5% (n = 17) vs. 1.7% (n = 15), p < 0.001], and the presence of severe RI (estimated glomerular filtration rate <30 ml/min.1.73 m(2)) was an independent predictor of ST (odds ratio = 4.5, 95% confidence interval 1.4-15, p = 0.011). In patients with RI and diabetes or left ventricular ejection fraction (LVEF) <50%, the incidence of ST was significantly increased [13.0% (n = 10) vs. 3.6% (n = 7), p = 0.010; 11.6% (n = 8) vs. 1.9% (n = 3), p = 0.004, respectively] compared to those with diabetes or LVEF <50% alone. The influence of RI on ST was not significant in patients with multivessel disease, calcified or bifurcation lesions, and target lesion revascularization. CONCLUSIONS: These findings substantiate the importance of long-term antiplatelet therapy for patients with RI after drug-eluting stent implantation.

Acute coronary syndrome is an independent risk factor for late incomplete stent apposition after sirolimus-eluting stent implantation.

BACKGROUND: Late incomplete stent apposition (ISA) may occur after drug-eluting stent implantation, affecting long-term clinical outcomes. This study aimed to evaluate the impact of clinical presentations of coronary artery disease on late ISA after percutaneous coronary intervention (PCI) with sirolimus-eluting stents (SES) by means of three-dimensional volumetric intravascular ultrasound (IVUS) analyses. METHODS: One hundred and thirty-seven patients with coronary artery disease received SES implantation during PCI and had repeat angiography with IVUS examination. All patients were followed up one year after the procedure. RESULTS: In overall 219 treated lesions (137 patients), late ISA was identified in 25 lesions (16 patients). Clinical diagnosis of acute coronary syndrome (ACS) and use of long stents were more common in patients with than in those without late ISA. Patients with late ISA had greater external elastic membrane (EEM) area in stented segment ((15.34 +/- 5.44) vs (13.83 +/- 4.51) mm(2), P = 0.026), stented-to-reference segment EEM area ratio (1.13 +/- 0.22 vs 1.02 +/- 0.18, P < 0.001), and plaque and media area ((8.43 +/- 3.93) vs (7.01 +/- 2.93) mm(2), P = 0.002) than in those without late ISA. Multivariate Logistic regression analysis showed that clinical diagnosis of ACS and use of long stents were independent risk factors for late ISA (OR 6.477, 95% CI 2.297 - 18.263, P < 0.001; OR 3.680, 95% CI 1.181 - 11.469, P = 0.025; respectively). During one-year follow-up after IVUS examination, the rate of very late stent thrombosis tended to be higher in patients with than in those without late ISA (18.7% vs 3.3%, P = 0.051). CONCLUSIONS: The occurrence of late ISA after SES implantation may be related to clinical status, use of long stents, and marked positive vessel remodeling. Late ISA tended to increase the rate of very late stent thrombosis during follow-up, highlighting the importance of long-term dual antiplatelet therapy for these patients.