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Background: The deterioration of renal function is a strong prognostic predictor in patients with coronary artery disease. Although percutaneous coronary intervention (PCI) has sometimes resulted in improved renal function (IRF) in acute coronary syndrome (ACS) patients, its clinical implications have not been fully elucidated. This study aimed to investigate the prevalence and predictors of IRF after PCI and its relationship with long-term renal outcomes., Methods: In this retrospective observational cohort study, we examined data from 177 ACS patients with non-dialysis advanced renal dysfunction (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m 2 ) who underwent PCI. Patients with and without IRF were compared in terms of baseline demographic, clinical, and procedural characteristics and renal outcomes. IRF was defined as a 20% increase in eGFR from baseline at 7 or 30 days after the index PCI., Results: IRF was observed in 66 (37.3%) patients. ST-elevation myocardial infarction and shock during PCI were independent predictors of IRF. Patients were followed up for a median of 695 days. Kaplan-Meier analyses demonstrated that patients with IRF had the lower incidence of initiation of permanent dialysis than those without IRF (Log-rank P = 0.015)., Conclusions: IRF was relatively common in non-dialysis patients with ACS and advanced renal dysfunction who underwent PCI. ST-elevation myocardial infarction and shock, which may be indicative of hemodynamic instability during PCI, were independent predictors of IRF. Further, IRF was associated with favorable renal outcomes. Hemodynamic stabilization may be important for improving the short-term and long-term renal outcomes of high-risk patients., Competing Interests: Declaration of competing interest H.I. received lecture fees from Astellas Pharma Inc., Astrazeneca Inc., Daiichi-Sankyo Pharma Inc., and MSD K. K. T.M. received lecture fees from Bayel Pharmaceutical Co., Ltd., Daiichi-Sankyo Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD K. K., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., Novartis Pharma K. K., Pfizer Japan Inc., Sanofi-Aventis K. K., and Takeda Pharmaceutical Co., Ltd. T.M. received an unrestricted research grant for the Department of Cardiology, Nagoya University Graduate School of Medicine from Astellas Pharma Inc., Daiichi-Sankyo Co., Ltd., Dainippon Sumitomo Pharma Co., Ltd., Kowa Co., Ltd., MSD K. K., Mitsubishi Tanabe Pharma Co., Nippon Boehringer Ingelheim Co., Ltd., Novartis Pharma K. K., Otsuka Pharma Ltd., Pfizer Japan Inc., Sanofi-Aventis K. K., Takeda Pharmaceutical Co., Ltd., and Teijin Pharma Ltd., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Background: Cilostazol has been reported to prevent atherosclerotic events in the general population. However, data have been limited whether there are beneficial effects of cilostazol use on long-term clinical outcomes after endovascular therapy in hemodialysis (HD) patients with peripheral artery disease (PAD)., Methods and Results: This study consisted of 595 HD patients undergoing endovascular therapy for a clinical diagnosis of PAD. They were divided into two groups: patients receiving 100mg cilostazol twice daily in conjunction with standard therapy (n=249 patients, cilostazol group) and those not administered cilostazol (n=346 patients, control group). A propensity score analysis was performed to adjust for baseline differences between the two groups. The propensity score-adjusted 10-year event-free survival rate from major adverse cardiovascular events (MACE) was significantly higher in the cilostazol group than in the control group [58.6% vs. 43.7%, hazard ratio (HR) 0.57; 95% confidence interval (CI) 0.41-0.79; p=0.0010]. Notably, the adjusted stroke-free rate was significantly higher in the cilostazol group than in the control group (81.6% vs. 74.7%; HR=0.48; 95% CI, 0.25-0.92, p=0.028). Even after adjusting for other confounders, treatment with cilostazol was an independent predictor for prevention of MACE and stroke (p=0.0028 and p=0.039, respectively)., Conclusions: Cilostazol administration improves long-term clinical outcomes including prevention of MACE and stroke after endovascular therapy in HD patients with PAD., (Copyright © 2015. Published by Elsevier Ltd.)

Objective: Lower extremity bypass surgery has been widely performed to treat critical limb ischemia (CLI) in patients on hemodialysis (HD). However, the clinical outcome still remains unclear. We investigated the limb salvage rate after infrapopliteal bypass surgery in HD patients with CLI., Methods: From April 2006 to January 2013, 226 patients with 236 limbs who electively underwent bypass surgery for treatment of CLI due to infrapopliteal disease were enrolled. Patients were grouped by those who were on HD (n = 177) and those who were not (n = 49). They were monitored for 5 years or until December 2013 if the follow-up period was <5 years. Amputation-free survival, defined as freedom from major amputation or all-cause death, was primarily evaluated. Incidence of reintervention was also analyzed., Results: Ulcer/gangrene was present in 206 patients (91.2%), and 233 limbs (98.7%) were treated using autogenous vein. Age was younger (67 ± 9 vs 72 ± 9 years; P = .0011) and ulcer/gangrene was more prevalent (93.8% vs 81.6%, P = .0080) in HD patients than in non-HD patients. During the follow-up period (median, 28 months), 33 (14.6%) major amputations and 28 reinterventions (12.4%) occurred, and 65 patients (28.8%) died. The 5-year amputation-free survival rate was significantly lower in HD patients than in non-HD patients (43.6% vs 78.8%, P = .0033), and the adjusted hazard ratio (HR) for amputation or death for HD patients was 2.36 (95% confidence interval [CI], 1.13-4.92; P = .022). Compared with non-HD patients, the status of HD was similarly an independent risk of major amputation (72.4% vs 92.5%; adjusted HR, 4.36; 95% CI, 1.04-18.3; P = .045) and mortality (56.9% vs 83.2%; adjusted HR, 2.81; 95% CI, 1.30-6.09; P = .0085). However, freedom from reintervention was comparable between the two groups (84.3% vs 86.8%; P = .89). In HD patients, body mass index (HR, 0.86; 95% CI, 0.76-0.96; per 1 kg/m(2) increase; P = .014) and C-reactive protein (HR, 1.06; 95% CI, 1.01-1.11; P = .014) independently predicted major amputation. Elevated C-reactive protein levels were also associated with death (HR, 1.04; 95% CI, 1.01-1.09; P = .047)., Conclusions: The clinical outcome after infrapopliteal bypass surgery was poorer in HD patients with CLI compared with non-HD patients. Malnutrition or chronic inflammation was associated with poor outcome in HD patients with CLI due to infrapopliteal occlusive disease., (Copyright © 2015 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.)

High low-density lipoprotein-cholesterol to high-density lipoprotein-cholesterol (L/H) ratio is associated with progressions of coronary arteriosclerosis and chronic kidney disease. On the other hand, renal function markedly declined after acute myocardial infarction (AMI). The aims of the present study were (1) to identify what type of patients with AMI would have high L/H ratio at follow-up and (2) to evaluate whether decline in renal function after AMI had accelerated or not in patients with high L/H ratio. The 190 eligible AMI patients who underwent primary percutaneous coronary intervention (PCI) and received atorvastatin (10 mg) were divided into one of two groups according to the L/H ratio at 6-month follow-up: L/H >2 group (n = 81) or L/H ≤2 group (n = 109). The characteristics on admission in the two groups were examined. Furthermore, changes in serum creatinine (sCr) and estimated glomerular filtration rate (eGFR) during 1- and 6-month follow-up were compared between the two groups. L/H >2 group were significantly younger and had greater body mass index (BMI) and worse lipid profile on admission compared with L/H ≤2 group. Percentage increase in sCr and percentage decrease in eGFR during 1-month follow-up in L/H >2 group tended to be greater than in L/H ≤2 group, and those during 6-month follow-up were significantly greater (16.5 ± 2.77 vs. 9.79 ± 2.23 %, p = 0.03 and 11.8 ± 1.93 vs. 2.75 ± 3.85 %, p = 0.04, respectively). In AMI patients undergoing primary PCI, those who were young and had large BMI and poor lipid profile on admission were likely to have a high L/H ratio at follow-up despite statin therapy. In addition, the decline in renal function after AMI had significantly accelerated in patients with high L/H ratio.

Objectives: Diabetes mellitus (DM) and high fasting glucose levels are reportedly risk factors for contrast-induced nephropathy after invasive coronary angiography in patients with renal dysfunction. Cystatin C (CyC) is a sensitive marker for detecting early impairment of renal function. Using CyC, we investigated whether DM would be a risk for worsening renal function after coronary computed tomography angiography (CCTA) in patients with preserved renal function., Methods: Two hundred twenty-eight patients scheduled for CCTA were enrolled. The serum CyC at preprocedure and 1 day after procedure, urinary microalbumin at preprocedure, and oral fluid volume for 24 hours after procedure were measured. The percentage changes in CyC from preprocedure to 1 day after procedure (%CyC) were also calculated., Results: Ninety-eight patients had DM. The %CyC and urinary microalbumin were significantly greater in DM patients than in non-DM patients. The percentage of patients showing a %CyC of 10% or greater was significantly greater in DM patients than in non-DM patients (27% vs 8%, P < 0.01). Using multivariate regression analysis, oral fluid volume and urinary microalbumin were independent predictors for a %CyC of 10% or greater in DM patients (β = - 0.428 [P < 0.0001] and β = 0.464 [P < 0.0001], respectively)., Conclusions: Diabetes mellitus is a risk factor for worsening changes in renal function after CCTA, even in patients with preserved renal function. In particular, elevated microalbuminuria and low oral fluid intake are high-risk factors for renal functional deterioration.

Background: Percutaneous coronary intervention (PCI) with drug-eluting stent (DES) is widely performed in patients with coronary artery disease, but the high restenosis rate remains a major clinical problem after implantation of DES in patients on hemodialysis (HD). Until now, there are limited reports regarding the long-term clinical outcome after implantation of DES in this patient population., Methods and Results: We compared bare metal stent (BMS) and DES for long-term clinical outcomes, such as target lesion revascularization (TLR), in HD patients undergoing PCI. BMS and DES were implanted in 204 and 301 patients, respectively. Baseline and lesion characteristics were comparable between the 2 groups. By Kaplan-Meier analysis, event rates of major adverse cardiac events for 6 years were significantly lower in the DES group than in the BMS group (42.5% vs. 58.0%, P=0.036). Although there were no significant differences in TLR rates between patients treated with DES and those with BMS at 1 year after PCI (17.8% vs. 21.3%, P=0.32), patients treated with DES had significantly lower rates of TLR compared with those treated with BMS beyond the 1-year follow-up after PCI (16.4% vs. 30.9%, P=0.019)., Conclusions: In patients on HD, implantation of DES might be more effective for preventing TLR in the medium to long follow-up period than BMS, although restenosis after PCI with DES is common in the short term.

Chronic kidney disease (CKD) is an independent risk factor for cardiac mortality. Accelerated atherosclerosis is frequently seen in patients with CKD. However, even in drug eluting stent era, higher restenosis rate after percutaneous coronary intervention (PCI) for coronary artery disease remains a clinical limitation in patients with CKD. Similar tendency is also seen when treated with endovascular therapy (EVT) for peripheral artery disease. Thus, management for atherosclerotic disease is very difficult in patients with CKD. Recent reports have shown that improvement of devices and/or intensive medical treatment may contribute better clinical outcomes after PCI or EVT in patients with CKD. In addition, inflammatory markers such as C-reactive protein may predict worse clinical outcomes including restenosis in such population.

Background/aims: Adiponectin is an adipocyte-derived protein with antiatherogenic properties. Chronic kidney disease (CKD) is one of the risk factors for cardiovascular disease. We investigated the potential association between adiponectin and carotid arteriosclerosis in patients with predialysis CKD., Methods: We enrolled 95 CKD patients without dialysis and 81 non-CKD patients. Intima-media thickness (IMT) and plaque score (PS) in the common carotid artery were measured using an ultrasound system. Carotid arteriosclerosis was defined as IMT >1.2 mm and/or PS >5.0 mm., Results: The prevalence of CKD was independently associated with carotid arteriosclerosis after adjustment for other risk factors. Higher adiponectin levels were observed in CKD patients compared with non-CKD patients. Adiponectin levels were not independently correlated with the presence of carotid arteriosclerosis in all subjects. To evaluate the association between adiponectin and carotid arteriosclerosis among a CKD population, we divided the CKD patients into 2 groups according to a cutoff level of adiponectin determined by ROC analysis. The prevalence of carotid arteriosclerosis was significantly higher in the low-adiponectin group than in the high-adiponectin group among CKD patients. After adjusting for other risk factors, low levels of adiponectin were independently correlated with carotid arteriosclerosis in CKD patients., Conclusion: Our data document that adiponectin is associated with increased risk of carotid atherosclerosis in a predialysis CKD population., (Copyright © 2011 S. Karger AG, Basel.)

Background: Percutaneous coronary intervention (PCI) using drug-eluting stents significantly reduces the risk of restenosis in the general population. However, in patients on hemodialysis, adverse cardiac events are frequently seen even if treated with drug-eluting stents. Recent studies suggest that C-reactive protein (CRP) reflects vascular wall inflammation and can predict adverse cardiac events. We evaluated possible prognostic values of CRP on outcomes in patients on hemodialysis undergoing PCI with drug-eluting stents., Methods and Results: A total of 167 patients undergoing PCI with sirolimus-eluting stents for stable angina (322 lesions) were enrolled. They were divided into tertiles according to serum CRP levels. We analyzed the incidence of major adverse cardiovascular events including cardiovascular death, nonfatal myocardial infarction, and target lesion revascularization after PCI as well as quantitative coronary angiographic data. The mean follow-up was 31 months (SD, 14). Major adverse cardiac events occurred in 11 patients (19.6%) of the lowest tertile, in 22 patients (39.3%) of the middle tertile, and in 28 patients (50.9%) of the highest tertile during follow-up period (P=0.0009). There was a progressive increase in neointimal growth after sirolimus-eluting stent implantation during follow-up because preprocedural CRP levels were higher, despite similar angiographic data just after PCI. Angiographic restenosis at 6 to 8 months after PCI was seen in 10.6% in the lowest tertile, 17.9% in the middle tertile, and 32.0% in the highest tertile (P=0.0007)., Conclusions: Increased preprocedural serum CRP levels would predict higher major adverse cardiac events and restenosis rates after sirolimus-eluting stents implantation in patients on hemodialysis.

Circulating CD34-positive (CD34(+)) cells, a population that includes endothelial progenitor cells, are believed to contribute to vascular homeostasis. Here we determine the prognostic value of CD34(+) cell measurements in 216 chronic hemodialysis patients. A total of 43 cardiovascular events and 13 deaths occurred over an average 23 months follow-up in this cohort. A cutoff number for circulating CD34(+) cells was determined by receiver operating characteristic curve analysis to maximize the power of the CD34(+) cell count in predicting future cardiovascular events. Based on this, 93 patients were categorized as having low and 123 patients as having high numbers of CD34(+) cells, determined by flow cytometry at the time of enrollment. Both cumulative cardiovascular event-free survival and all-cause survival were significantly less in the group of patients with low numbers of CD34(+) cells. By multivariate analyses, a low level of circulating CD34(+) cells was an independent and significant predictor for both cardiovascular events and all-cause mortality. Our study shows that a reduced number of circulating CD34(+) cells is significantly associated with vascular risks and all-cause mortality in patients on chronic hemodialysis. These cells may be a useful biomarker.

Background: The proportion of young females among the patients who undergo percutaneous coronary intervention (PCI) is relatively small, and information on their clinical characteristics is limited. This study investigated the clinical characteristics and prognostic factors for future cardiac events in young females who underwent PCI. Methods: This multicenter observational study included 187 consecutive female patients aged < 60 years who underwent PCI in seven hospitals. The primary composite endpoint was the incidence of cardiac death, nonfatal myocardial infarction, and target vessel revascularization. Results: The mean patient age was 52.1 ± 6.1 years and 89 (47.6%) had diabetes, and renal dysfunction (an estimated glomerular filtration rate < 60 mL/min/1.73 m2) was observed in 38 (20.3%). During a median follow-up of 3.3 years, the primary endpoint occurred in 28 patients. The Cox proportional hazards models showed that renal dysfunction was an independent predictor for the primary endpoint (hazard ratio 3.04, 95% confidence interval 1.25–7.40, p = 0.01), as well as multivessel disease (hazard ratio 2.79, 95% confidence interval 1.12–6.93, p = 0.03). Patients with renal dysfunction had a significantly higher risk for the primary endpoint than those without renal dysfunction. Conclusions: Renal dysfunction was strongly associated with future cardiac events in young females who underwent PCI. [ABSTRACT FROM AUTHOR]

Contrast-associated acute kidney injury (CA-AKI) is a complication of percutaneous coronary intervention (PCI). Because proteinuria is a sentinel marker of renal dysfunction, we assessed its role in predicting CA-AKI in patients undergoing PCI. A total of 1,254 patients undergoing PCI were randomly assigned to a derivation (n = 840) and validation (n = 414) dataset. We identified the independent predictors of CA-AKI where CA-AKI was defined by the new criteria issued in 2020, by a multivariate logistic regression in the derivation dataset. We created a risk score from the remaining predictors. The discrimination and calibration of the risk score in the validation dataset were assessed by the area under the receiver-operating characteristic curves (AUC) and Hosmer–Lemeshow test, respectively. A total of 64 (5.1%) patients developed CA-AKI. The 3 variables of the risk score were emergency procedures, serum creatinine, and proteinuria, which were assigned 1 point each based on the correlation coefficient. The risk score demonstrated a good discriminative power (AUC 0.789, 95% CI 0.766–0.912) and significant calibration. It was strongly associated with the onset of CA-AKI (Cochran-Armitage test, p < 0.0001). Our risk score that included proteinuria was simple to obtain and calculate, and may be useful in assessing the CA-AKI risk before PCI. [ABSTRACT FROM AUTHOR]

Background: The combined influence of CKD and worsening renal function (WRF) on clinical outcomes in patients undergoing primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) has not been fully understood.Methods: We analyzed 443 patients diagnosed with AMI who underwent primary PCI. Based on their estimated glomerular filtration rate (eGFR), they were classified into two groups: a high eGFR group (eGFR ≥ 45 mL/min/1.73 m2, n = 381) and a low eGFR group (eGFR < 45 mL/min/1.73 m2, n = 63). WRF was defined as an increase in serum creatinine levels ≥ 0.3 mg/dL above the admission value during the course of hospitalization. The primary end-point was set as all-cause mortality.Results: WRF was observed in 88 patients (19.8%). The median follow-up duration was 769 (interquartile range 397-1314) days. The all-cause mortality rate was significantly lower in the high eGFR than in the low eGFR group (5.5 vs. 28.6%, respectively, at 1500 days, P < 0.001). In patients with WRF, the all-cause and cardiac mortality rates were significantly higher than in patients without WRF, and these results were consistent between the high and low eGFR sub-groups. Multivariate Cox proportional hazards model analysis showed that low eGFR and WRF remained independent predictors of all-cause mortality [(hazard ratio 2.61, 95% confidence interval 1.27-5.36, P = 0.009) and (hazard ratio 2.59, 95% confidence interval 1.34-5.01, P = 0.005), respectively].Conclusions: Both eGFR at baseline and WRF were observed to be important predictors of mortality in patients with AMI undergoing primary PCI. WRF showed a significant effect on mortality even in patients with high eGFR. [ABSTRACT FROM AUTHOR]

Background: Coronary artery calcification (CAC) is an independent predictor of cardiovascular morbidity and mortality in chronic kidney disease (CKD) patients. The aim of the present study was to evaluate the predictive value of CAC scores for the incidence of contrast-induced nephropathy (CIN) after cardiac catheterization in non-dialyzed CKD patients. Methods: The present study evaluated a total of 140 CKD patients who underwent cardiac catheterization. Patients were stratified into two groups based on the optimal cut-off value of the CAC score, which was graded by a non-triggered, routine diagnostic chest computed tomography scan: CAC score ≥8 (high CAC group); and CAC score <8 (low CAC group). CIN was defined as an increase of >10 % in the baseline serum cystatin C level at 24 h after contrast administration. Results: The mean estimated glomerular filtration rate levels were 41.1 mL/min/1.73 m, and the mean contrast dose administered was 37.5 mL. Patients with high CAC scores exhibited a higher incidence of CIN than patients with low CAC scores (25.5 vs. 3.2 %, p < 0.001). After multivariate adjustment for confounders, the CAC score predicted CIN (odds ratio 1.68, 95 % confidence interval 1.28-2.21, p < 0.001). Moreover, the C-index for CIN prediction significantly increased when the CAC scores were added to the Mehran risk score (0.855 vs. 0.760, p = 0.023). Conclusion: CAC scores, as evaluated using semi-quantitative methods, are a simple and powerful predictor of CIN. Incorporating the CAC score in the Mehran risk score significantly improved the predictive ability to predict CIN incidence. [ABSTRACT FROM AUTHOR]

The purpose of this study was to investigate the relationship between abdominal aortic calcification (AAC) and coronary artery calcification (CAC) in chronic kidney disease (CKD) patients. We evaluated 126 asymptomatic CKD patients (mean estimated glomerular filtration rate: 36.1 ± 14.1 mL/min/1.73 m, mean age 70.3 ± 10.1 years). A non-contrast computed tomography scan was used to determine the abdominal aortic calcification index (ACI) and CAC score, and this relationship was investigated. Among the subjects, AAC was present in 109 patients (86.5 %) as defined by ACI >0 and median ACI was 11.7 %. ACI increased in accordance with advances in CAC score grades (3.0, 5.2, 17.2, and 32.8 % for CAC score 0, 1-100, 101-400, and 401 or more, respectively, p < 0.001). Even after multivariate adjustment, ACI was independently associated with severe CAC score as defined by CAC score >400 [odds ratio 1.08, 95 % confidence interval (CI) 1.04-1.12, p < 0.001]. Receiver-operating curve analysis showed that the ACI optimal cut-off value predicting severe CAC score was 16.5 % (area under the curve = 0.79, 95 % CI 0.69-0.90, p < 0.001). The C statics for predicting CAC score was significantly increased by adding ACI values to the model including other risk factors (0.853 versus 0.737, p = 0.023). In conclusion, the ACI value of 16.5 % allows us to predict the presence of severe CAC in CKD patients, and that the addition of ACI to the model with traditional risk factors significantly improves the predictive ability of severe CAC score. These data reinforce the utility of ACI as a screening tool in clinical practice. [ABSTRACT FROM AUTHOR]

Background: The clinical usefulness of physiological and radiological examinations for cardiovascular disease (CVD) risk stratification has not been fully demonstrated in chronic kidney disease (CKD) patients. In the present study, predictive values of CVD were investigated among asymptomatic CKD patients by comprehensive and non-invasive CVD screening programs. Methods: We prospectively evaluated 139 asymptomatic CKD patients. All patients were examined by comprehensive and non-invasive CVD risk screening programs that included carotid ultrasonography, coronary artery calcification score (CACS), pulse wave velocity, and flow-mediated vasodilation, and their associations with major adverse cardiovascular events (MACEs) were analyzed. Results: During the median follow-up of 32.3 months, 13 MACEs were observed. Among all CVD screening examinations, severity of the carotid plaque score (PS) and CACS was significantly higher in the MACE group than in the MACE-free group (11.3 ± 5.8 versus 6.1 ± 5.3, P = 0.001 and 657 versus 74, P = 0.020, respectively). Kaplan-Meier curves for the incidences of MACEs classified according to the combination of carotid PS and CACS showed that severe carotid PS and severe CACS groups had the highest event rate in comparison with the groups without any of these (29.9, 11.9, and 3.6 %, respectively, P < 0.001). Conclusions: In this long-term follow-up analysis, the combination of carotid atherosclerosis and CACS was a useful and non-invasive screening tool for predicting cardiovascular events among asymptomatic CKD patients. [ABSTRACT FROM AUTHOR]

Background and purpose: Metabolic syndrome (MetS) and chronic kidney disease (CKD) have both been reported as risk factors for cardiovascular events. The aim of this study was to assess the synergistic effect of MetS and CKD on atherosclerotic plaque and cardiovascular outcomes. Methods and subjects: A total of 545 consecutive patients who underwent percutaneous coronary inter-vention (PCI) were divided into 4 groups based on the presence or absence of MetS and CKD. MetS was defined using the criteria of the Adult Treatment Panel III of the US National Cholesterol Education Pro-gram. CKD was defined as an estimated glomerular filtration rate of <60ml/min/1.73m². We analyzed the incidence of major adverse cardiac events (MACE), including cardiovascular death, nonfatal myocar-dial infarction, target lesion revascularization, and revascularization for new lesions. We also assessed coronary plaque characteristics of 204 patients using integrated backscatter intravascular ultrasound (IB-IVUS). Results: MACE occurred more frequently in patients with both MetS and CKD (51.4%) than in the other groups, during the follow-up period (log-rankp < 0.001). In the IB-IVUS analyses, patients with both MetS and CKD exhibited greater plaque burden (p = 0.003) with higher lipid content (p = 0.048) compared to the other groups. In Cox analysis, both MetS and CKD proved to be independent predictors of MACE even after adjustment for confounding factors (p = 0.018). Conclusions: Comorbidity of MetS and CKD is an independent predictor of adverse cardiovascular out-comes in patients undergoing coronary intervention, an effect that may be attributed to coronary plaque instability. [ABSTRACT FROM AUTHOR]

Background. It is well known that chronic kidney disease is a strong independent predictor of adverse outcomes after percutaneous coronary intervention in patients with ischemic heart disease. Recently, peri-procedural myocardial injury has been associated with adverse cardiac events. The aim of this study was to investigate the relationship between renal function and peri-procedural myocardial injury in patients undergoing elective stent implantation. Methods. This study comprised 273 consecutive patients who underwent elective stent implantation. They were divided into two groups: estimated glomerular filtration rate (eGFR) <60 mL/min/1.73m2 and eGFR ≥60 mL/min/1.73m2. Peri-procedural TnT levels higher than three times the normal limit were defined as peri-procedural myocardial injury. Results. Patients with eGFR <60 mL/min/1.73m2 showed a higher incidence of peri-procedural myocardial injury compared to patients with eGFR ≥60 mL/min/1.73m2 (4.3 versus 20.9%, P < 0.0001). Even after a multivariate adjustment, the eGFR level predicted peri-procedural myocardial injury [odds ratio 0.92, 95% confidence interval (CI): 0.89–0.95, P < 0.0001]. Total stent length was also an independent predictor of peri-procedural myocardial injury (odds ratio 1.09, 95% CI: 1.02–1.16, P = 0.009). Using a receiver-operating curve analysis, eGFR level of 62.1 mL/min/1.73m2 (sensitivity 93.3%, specificity 57.2%) was the best value (area under the curve = 0.803) to maximize the power of eGFR levels in predicting peri-procedural myocardial injury. Conclusions. Patients with eGFR <60 mL/min/1.73m2 were strongly associated with peri-procedural myocardial injury after elective stent implantation. Therefore, eGFR may be a simple and convenient predictor of peri-procedural myocardial injury. [ABSTRACT FROM PUBLISHER]

Background: An increase in cystatin C (CyC) of ≥10% for 24 hours may predict contrast-induced nephropathy and worse outcomes in patients with renal dysfunction undergoing invasive coronary angiography. Objective: We investigated the changes in CyC in patients with preserved renal function referred for contrast-enhanced coronary computed tomography angiography (CTA). Methods: We studied 151 patients undergoing CTA with 70 mL of iopamidol. Serum creatinine and CyC, a sensitive measure of renal dysfunction, shown to be associated with adverse outcomes, were measured 1 day and 1 week after CTA, respectively. The percentage change in CyC (%CyC) was determined and evaluated in comparison to fluid intake. Results: The patients were dichotomized into 2 groups: 47 patients had ≥10% increase in CyC 1 day after CTA (group A) and 104 did not (group B). The percentage of diabetic patients, hemoglobin A1c (HbA1c), and the CyC levels at 1 week were significantly greater, and the oral fluid volume was significantly lower in group A than in group B. The %CyC inversely correlated with oral fluid volume (r = −0.80, P < 0.0001) and positively with HbA1c (r = 0.38, P < 0.001). Multiple regression analysis showed that oral fluid intake (β = −0.796, P < 0.0001) and HbA1c (β = 0.128, P = 0.007) are independent predictors for %CyC of ≥10%. Conclusion: Frequency of CyC elevation was strongly related to hydration after the study and also weakly related to HbA1c. Sufficient oral fluid intake (oral fluid volume/kg ≥ 20 mL/kg) is crucial, particularly for poorly controlled diabetic patients referred for CTA even though they show preserved renal function. [Copyright &y& Elsevier]

Background. Recent studies have demonstrated that patients with chronic kidney disease are at high risk of atherosclerosis. Recently it has been found that coronary plaque components can be evaluated by integrated backscatter intravascular ultrasound (IB-IVUS), and lipid-rich plaque is associated with vulnerable plaque. The aim of the study was to investigate the relationship between renal function and tissue characterization of coronary plaque composition at the target stenotic site for percutaneous coronary intervention (PCI). [ABSTRACT FROM PUBLISHER]

Background and aims Abdominal aortic calcification (AAC) is an important predictor of cardiovascular mortality in patients with chronic kidney disease (CKD). However, little is known regarding AAC progression in these patients. This study aimed to identify risk factors associated with AAC progression in patients with CKD without hemodialysis. Methods We recruited 141 asymptomatic patients with CKD without hemodialysis [median estimated glomerular filtration rate (eGFR), 40.3 mL/min/1.73 m 2 ] and evaluated the progression of the abdominal aortic calcification index (ACI) over 3 years. To identify risk factors contributing to the rate of ACI progression, the associations between baseline clinical characteristics and annual change in ACI for each CKD category were analyzed. The annual change of ACI (ΔACI/year) was calculated as follows: (second ACI − first ACI)/duration between the two evaluations. Results Median ΔACI/year values significantly increased in advanced CKD stages (0.73%, 0.87%, and 2.24%/year for CKD stages G1-2, G3, and G4-5, respectively; p for trend = 0.041). The only independent risk factor for AAC progression in mild to moderate CKD (G1-3, eGFR ≥ 30 mL/min/1.73 m 2 ) was pulse pressure level (β = 0.258, p = 0.012). In contrast, parathyroid hormone (PTH) level was significantly correlated with ΔACI/year (β = 0.426, p = 0.007) among patients with advanced CKD (G4-5, eGFR < 30 mL/min/1.73 m 2 ). Conclusions This study suggests that the AAC progression rate was significantly accelerated in patients with advanced CKD. In addition, measuring PTH is useful to evaluate both bone turnover and AAC progression in patients with advanced CKD. [ABSTRACT FROM AUTHOR]

The prognosis of patients with diastolic heart failure (HF) is as poor as that of patients with systolic HF. Greater chronic kidney disease-associated mortality occurs in patients with left ventricular (LV) diastolic HF than in those with systolic HF. Indoxyl sulfate (IS), a uremic toxin, directly affects cardiac cells adversely in in vitro experiments. We investigated the association of IS, a uremic toxin, and chronic kidney disease with LV diastolic dysfunction in the clinical setting. The present study included 204 consecutive patients with preserved LV systolic function. To evaluate LV function, all patients underwent echocardiography. To measure the plasma IS levels and estimated glomerular filtration rate (eGFR), blood samples were obtained. Of the 204 patients, 75 (37%) had LV diastolic dysfunction. A significantly lower prevalence of LV diastolic dysfunction was present in patients with lower plasma IS levels (≤1.0 μg/ml) than those with greater plasma IS levels (38 [29%] vs 37 [51%], p <0.001). Furthermore, a significantly lower prevalence of LV diastolic dysfunction was present in patients with lower plasma IS levels and preserved eGFR than those with greater plasma IS levels and preserved eGFR, those with lower plasma IS levels and a reduced eGFR, or those with greater plasma IS levels and reduced eGFR (20 [21%] vs 18 [53%], p = 0.001; 20 [21%] vs 18 [46%], p = 0.004; and 20 [21%] vs 19 [56%], p <0.001, respectively). In conclusion, greater plasma IS levels or a reduced eGFR, or both, represent an increased risk of LV diastolic dysfunction. [ABSTRACT FROM AUTHOR]

It is well known that chronic kidney disease is a risk factor for atherosclerosis. The present study was conducted to identify any relation between the estimated glomerular filtration rate (eGFR) and coronary plaque characteristics using integrated backscatter intravascular ultrasound (IB–IVUS), which can detect coronary plaque composition. We performed IB–IVUS for 201 consecutive patients undergoing percutaneous coronary intervention, and they were divided into 3 groups according to the eGFR values (group 1 [n = 20], ≥90 ml/min/1.73 m2; group 2 [n = 123], 60 to 90 ml/min/1.73 m2; and group 3 [n = 58], <60 ml/min/1.73 m2). Coronary plaques in nonculprit lesions on 3-dimensional analysis were evaluated using IB–IVUS. The baseline characteristics were similar, except for older age and a greater prevalence of men in group 3. IB–IVUS showed a percentage of lipid volume of 44.7 ± 5.0% in group 1, 53.6 ± 6.2% in group 2, and 63.5 ± 6.2% in group 3 (p <0.01), with a corresponding percentage of fibrous volume of 53.9 ± 4.9%, 45.1 ± 6.0%, and 35.3 ± 6.1%, respectively (p <0.01). The eGFR correlated significantly with both parameters (r = −0.68, p <0.001 and r = 0.68, p <0.001, respectively). In conclusion, lower eGFR levels were associated with greater lipid and lower fibrous contents, contributing to coronary plaque vulnerability. [Copyright &y& Elsevier]

Introduction: The incidence of contrast-induced nephropathy (CIN) increases with the progression of renal dysfunction. Therefore, percutaneous coronary intervention (PCI) are frequently avoided in patients with advanced renal dysfunction due to fear of CIN, which may result in poor outcomes. On the other hand, recent reports have shown that PCI can be safely performed even in patients with advanced renal dysfunction by instituting appropriate CIN-prevention strategies. However, data are limited regarding the occurrence and prognostic influence of CIN in patients with advanced renal dysfunction. Methods: We examined the data obtained from 323 consecutive patients with advanced renal dysfunction (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m2) who underwent PCI at 5 hospitals between 2011 and 2016. CIN was defined as a ≥25% increase in baseline serum creatinine levels and/or a ≥0.5 mg/dL increase in absolute serum creatinine levels within 72 h after PCI. Incidence of all-cause death and the initiation of permanent dialysis were examined during follow-up. Results: The prevalence of emergency/urgent PCI was 53.3%. Intravascular ultrasound was used in 266 patients (82.4%), and the volume of contrast used was 71.7±57.2 mL. CIN was observed in 31 patients (9.7%). Patients who developed CIN more commonly presented with shock and pulmonary congestion and received emergency/urgent PCI and had received a greater volume of contrast agent. The median follow-up duration was 656 days (interquartile range 257-1143 days). The cumulative rates of all-cause death or the initiation of permanent dialysis, all-cause death, and the initiation of permanent dialysis were 38.1%, 25.9%, and 18.2%, respectively at 2 years. A comparison between patients with and without CIN showed no significant intergroup differences in the occurrence of the aforementioned events. Conclusions: The development of CIN was not a common occurrence if PCI was performed by instituting appropriate CIN-prevention strategies even in patients with advanced renal dysfunction. The long-term prognosis following PCI is observed to be poor in this studied population. [ABSTRACT FROM AUTHOR]

Background The presence of abdominal aortic calcification (AAC) can predict cardiovascular (CV) outcomes in hemodialysis patients. However, little is known about the predictive value of AAC for CV outcomes in chronic kidney disease (CKD) patients without hemodialysis. The aim of this study was to investigate the prevalence and the predictive value of AAC in asymptomatic CKD patients. Methods We prospectively evaluated 347 asymptomatic CKD patients without hemodialysis [median estimated glomerular filtration rate (eGFR): 43.2 mL/min/1.73 m 2 ]. A non-contrast computed tomography scan was used to determine the abdominal aortic calcification index (ACI) as a semi-quantitative measure of AAC. The patients were divided into three groups according to the tertiles of ACI. Results Among the subjects, AAC was found (ACI > 0) in 296 patients (86.3%), and the median ACI was 11.4%. During the median follow-up of 41.5 months, a total of 33 CV events were observed. Patients with the highest tertile of ACI had the highest risk of CV outcomes compared with the other two groups (96.5%, 93.0%, and 74.3%, respectively; p < 0.001). The Cox proportional hazard models showed that ACI was an independent predictor of CV outcomes (hazard ratio 1.36, 95% confidence interval 1.17–1.60, p < 0.001). The C-index was also significantly increased by adding eGFR and ACI values to the model along with the other conventional risk factors (0.79 versus 0.66, p = 0.043). Conclusion Evaluation of the AAC provides useful information for predicting adverse clinical outcomes among asymptomatic CKD patients without hemodialysis. [ABSTRACT FROM AUTHOR]

Circulating CD34-positive (CD34+) cells, a population that includes endothelial progenitor cells, are believed to contribute to vascular homeostasis. Here we determine the prognostic value of CD34+ cell measurements in 216 chronic hemodialysis patients. A total of 43 cardiovascular events and 13 deaths occurred over an average 23 months follow-up in this cohort. A cutoff number for circulating CD34+ cells was determined by receiver operating characteristic curve analysis to maximize the power of the CD34+ cell count in predicting future cardiovascular events. Based on this, 93 patients were categorized as having low and 123 patients as having high numbers of CD34+ cells, determined by flow cytometry at the time of enrollment. Both cumulative cardiovascular event-free survival and all-cause survival were significantly less in the group of patients with low numbers of CD34+ cells. By multivariate analyses, a low level of circulating CD34+ cells was an independent and significant predictor for both cardiovascular events and all-cause mortality. Our study shows that a reduced number of circulating CD34+ cells is significantly associated with vascular risks and all-cause mortality in patients on chronic hemodialysis. These cells may be a useful biomarker.Kidney International (2008) 74, 1603–1609; doi:10.1038/ki.2008.495; published online 8 October 2008 [ABSTRACT FROM AUTHOR]