Clinical Implications of Contrast-Induced Nephropathy in Patients Without Baseline Renal Dysfunction Undergoing Coronary Angiography.

BACKGROUND: The clinical implications of different definitions of contrast-induced nephropathy (CIN) in patients without baseline renal dysfunction are not well defined. METHODS: Consecutive patients at a single centre without baseline renal dysfunction (estimated glomerular filtration rate, eGFR≥60ml/min/1.73m2) undergoing coronary angiography or percutaneous coronary intervention (PCI), were systematically evaluated for long-term risk of mortality following CIN using two broad definitions: an absolute increase from baseline in serum creatinine (SCr) ≥0.3mg/dl (mild to severe absolute CIN) and a relative increase from baseline of 25% (mild to severe relative CIN) within 72hours. RESULT: Of 2,823 subjects alive before discharge following coronary angiography there were 320 episodes of mild to severe relative CIN (11.3%) and 125 of mild to severe absolute CIN (4.4%). During a median follow-up of 2.3years, 73 patients (3.2%) died. After adjustment for confounders, mild to severe absolute CIN was associated with an adjusted hazard ratio (HR) (95% confidence interval) for all-cause mortality of 3.31 (1.74-6.30) (p<0.0001) and relative CIN with an adjusted HR of 1.92 (1.09, 3.38) (p=0.024). The risk of mortality rose with severity of CIN. Two commonly used definitions of CIN combining absolute and relative terms (increase ≥ 0.3mg/dl or 50%, and ≥ 0.5mg/dl or 25% from the baseline) confirmed these results. CONCLUSION: Among patients without baseline renal dysfunction undergoing coronary angiography, the incidence of CIN can range widely depending on definition. Absolute CIN is less common than relative CIN. Regardless of definition, CIN is associated with a markedly increased risk of long-term mortality. This finding requires confirmation in multicentre studies.

Safe Hydration to Prevent Contrast-Induced Acute Kidney Injury and Worsening Heart Failure in Patients with Renal Insufficiency and Heart Failure Undergoing Coronary Angiography or Percutaneous Coronary Intervention.

An optimal hydration volume (HV) that prevents contrast-induced acute kidney injury (CI-AKI) in patients with renal insufficiency and heart failure (HF) at a high risk of worsening HF (WHF) has not been determined. We aimed to determine a safe HV that prevents CI-AKI and WHF following coronary angiography (CAG) or percutaneous coronary intervention (PCI) in patients with renal insufficiency and HF. We recruited 1,307 patients with renal insufficiency and HF and investigated the relationships between the peri-procedural HV/weight (HV/W) ratio, and the risks of CI-AKI and WHF following CAG or PCI. Higher HV/W quartiles were associated with higher CI-AKI rates (Q1: 6.2%, Q2: 9.1%, Q3: 12.5%, and Q4: 18.7%; P < 0.001) and a greater likelihood of WHF (Q1: 2.2%, Q2: 2.7%, Q3: 4.9%, and Q4: 11.7%; P < 0.001). The multivariate analyses indicated that excessively high HV/W ratios were associated with moderately increased risks of CI-AKI (Q4 versus Q1: adjusted odds ratio [OR] 2.16, 95% confidence interval [CI] 1.17-4.00) and WHF (Q4 versus Q1: adjusted OR 3.09, 95% CI 1.21-7.88). The multivariate Cox regression analysis indicated that a higher HV/W ratio was associated with significantly increased long-term mortality (Q2 versus Q1: adjusted hazard ratio [HR] 2.36; Q3 versus Q1: adjusted HR 2.85; Q4 versus Q1: adjusted HR 2.94; all P < 0.05). In conclusion, an excessively high HV/W might be associated with a moderately increased risk of CI-AKI, WHF, and long-term mortality in patients with renal insufficiency and HF.

Safe Hydration Volume to Prevent Contrast-induced Acute Kidney Injury and Worsening Heart Failure in Patients With Heart Failure and Preserved Ejection Fraction After Cardiac Catheterization.

Few studies have investigated the efficacy and safety of hydration to prevent contrast-induced acute kidney injury (CI-AKI) and worsening heart failure (WHF) after cardiac catheterization in heart failure and preserved ejection fraction (HFpEF; HF and EF ≥50%) patients. We recruited 1206 patients with HFpEF undergoing cardiac catheterization with periprocedural hydration volume/weight (HV/W) ratio data and investigated the relationship between hydration volumes and risk of CI-AKI and WHF. Incidence of CI-AKI was not significantly reduced in individuals with higher HV/W [quartile (Q) 1, Q2, Q3, and Q4: 9.7%, 10.2%, 12.7%, and 12.2%, respectively; P = 0.219]. Multivariate analysis indicated that higher HV/W ratios were not associated with decreased CI-AKI risks [Q2 vs. Q1: odds ratio (OR), 0.95; Q3 vs. Q1: OR, 1.07; Q4 vs. Q1: OR, 0.92; all P > 0.05]. According to multivariate analysis, higher HV/W significantly increased the WHF risk (Q4 vs. Q1: adjusted OR, 8.13 and 95% confidence interval, 1.03-64.02; P = 0.047). CI-AKI and WHF were associated with a significantly increased risk of long-term mortality (mean follow-up, 2.33 years). For HFpEF patients, an excessively high hydration volume might not be associated with lower risk of CI-AKI but may increase the risk of postprocedure WHF.

Pre-Procedural Risk Score of Contrast-Induced Nephropathy in Elderly Patients Undergoing Elective Coronary Angiography.

To establish a scoring model to predict the risk of contrast-induced nephropathy (CIN) in elderly patients undergoing elective coronary angiography (CAG).A total of 1286 patients aged > 65 years who had undergone elective CAG between August 2009 and February 2013 were enrolled in this study. They were randomly (3:2) assigned to a development (n = 756) or validation dataset (n = 530). Independent predictors of CIN were identified by using logistic regression and were assigned a weighted integer, which was used to establish a score model.CIN incidence in the development set was 6.3%. The risk score model contained 3 variables (with the weighted integer): age > 75 years (1.5), creatinine clearance (CrCl) < 60 mL/minute (1), and congestive heart failure (CHF) (1.5). CIN incidence was 3.1%, 9.1%, and 29.0% in the low-risk group (≤ 1), moderate risk group (1 - 3), and high-risk group (≥ 3), respectively. The risk model demonstrated good prediction value in the development (c-statistic = 0.727) and validation (c-statistic = 0.695) datasets. Compared to the non-CIN group, the CIN group had a significantly higher rate of inhospital major adverse cardiac events (P < 0.01).The risk score model with 3 variables, namely age > 75 years, CrCl < 60 mL/minute, and CHF, is a clinical prediction tool for CIN in elderly patients before elective CAG. CIN is one of the independent risk factors of major adverse cardiac events (MACE).

Contrast-induced nephropathy following chronic total occlusion percutaneous coronary intervention in patients with chronic kidney disease.

OBJECTIVES: Contrast-induced nephropathy (CIN) has not been systematically studied in high-risk patients with chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI) for chronic total occlusion (CTO). METHODS: We prospectively observed 515 consecutive patients with CKD undergoing PCI. Patients were divided into three groups: patients who underwent attempted PCI for CTO (group A, n = 85), patients who did not receive PCI for CTO (group B, n = 45) and patients without CTO (group C, n = 385). RESULTS: CIN developed in 55 patients (10.68 %). Group A patients received a larger CM dose than group B or group C (p = 0.024). The intravenous hydration volume, age and CIN Mehran score were not significantly different between the three groups. The incidence of CIN was 9.4 % for group A, 6.7 % for group B and 11.4 % for group C (p = 0.344). In-hospital mortality and required renal replacement therapy (p = 0.325) were not significantly different between the groups. Multivariate analysis showed that after adjusting for potential confounding factors, the odds ratio for CIN was 1.03 (p = 0.944) for group A and 0.64 for group B (p = 0.489) compared to group C. CONCLUSIONS: Attempts to achieve recanalization of CTO in patients with CKD might not increase the risk of CIN if appropriate preventative measures are taken. KEY POINTS: • Contrast-induced nephropathy can increase morbidity and mortality • Chronic kidney disease patients are at the greatest risk of CIN • Patients with CKD undergoing CTO-PCI are common • Incidence of CIN has not been reported in CKD patients • CTO-PCI in CKD patients might not increase the risk of CIN.

A Quantum Dot Fluorescence Sensor System Design for Hg²âº Trace Detection.

The detection of Hg²âº ions usually requires large laboratory equipment, which encounters difficulties for rapid field test in most applications. In this paper, we design a reflective sensor for trace Hg²âº analysis based on the fluorescent quenching of Quantum dots, which contains two major modules, i. e. the fluorescent sensing module and the signal processing module. The fluorescence sensing module is composed of a laser source, a light collimated system and a photo-detector, which enables the realization of the fluorescence excitation as well as its detection. The signal processing module realized the further amplification of the detected signal and hereafter the filtering of noises. Furthermore, the Hg²âº concentration will displayed on the QT interface using a Linux embedded system. The sensor system is low cost and small, which makes it available for rapid field test or portable applications. Experimental results show that the sensor has a good linear relationship for the Hg²âº concentration range from 15.0 x 10⁻9 to 1.8 x 10⁻6 mol · L⁻¹. The regression equation is V0/V = 1.309 13 + 3.37c, where c is Hg²âº concentration, and V0 is the voltage value for the blank case. In our work, the linearity is determined as 0. 989 26. The experiments exhibit that Ca²âº, Mn²âº and Pb²âº ions have small influence on the Hg²âº detection, and the interfere of other common ions can be neglected, which indicates a good selectivity of the sensor. Finally, it shows that our sensor has a rapid response time of 35 s and a good repeatability, thus it is potential for field test of trace Hg²âº.

[Expression and significance of RhoA and NF-ΚB in human gastric carcinoma].

OBJECTIVE: To investigate the expression of RhoA and NF-κB in gastric carcinoma and their correlation with clinicopathological fearures. To determine the effective prognostic factors of long-term suivival of gastric carcinoma patients. METHODS: The role of RhoA and NF-κB in gastric carcinoma was assessed by tissue array technology and the levels of RhoA and NF-κB expression in paraffin-embedded tissues was quantified by immunohistochemistry from 189 cases of gastric carcinoma, 54 cases of their adjacent tissues, and 32 cases of normal gastric mucosa. The prognosis of gastric carcinoma was evaluated by Kaplan-Meier survival analysis and Cox multivariate regression analysis. RESULTS: The positive rates of RhoA expression were 84.7%, 68.5% and 65.6% in gastric carcinoma, adjacent tissues and normal mucosa, respectively. The expression of RhoA in gasric carcinoma was significantly higher than that in adjacent tissues and normal mucosa (P < 0.05). The positive rates of NF-κB expression were 75.1%, 42.6% and 15.6%% in gastric carcinoma, adjacent tissues and normal mucosa, respectively. The expression of NF-κB in gasric carcinoma was significantly higher than that in adjacent tissues and normal mucosa (P < 0.05). RhoA was positively linked with NF-κB (r = 0.203, P = 0.005). In gastric carcinoma, the expression of RhoA was related with depth of invasion (P < 0.05), and the expression of NF-κB was related with depth of invasion and lymph node metastasis (P < 0.05). The Kaplan-Meier survival analysis showed that the tumor size, lymph node metastasis, depth of invasion, expression of RhoA and NF-κB can shorten the cumulative survival rate. With these paramaters entering the Cox multivariate regression analysis mode, it was revealed that expression of NF-κB, lymph node metastasis and depth of invasion are independent prognostic factors. CONCLUSIONS: The overexpression of RhoA and NF-κB is involved in the occurrence and development of gastric carcinoma. RhoA is positively linked with NF-κB. They are correlated with the invasion and metastasis of gastric carcinoma. The expression of NF-κB, lymph node metastasis, depth of invasion are independent prognostic factors playing an important role in prediction of the clinical outcome after radical resection of gastric carcinoma.

Therapeutic effects of myocardin-related transcription factor A (MRTF-A) knockout on experimental mice with nonalcoholic steatohepatitis induced by high-fat diet.

OBJECTIVE: To explore the effects of myocardin-related transcription factor A (MRTF-A) knockout on mice with nonalcoholic steatohepatitis (NASH) induced by high-fat diet (HFD). METHODS: Normal-fat diet (NFD) or HFD was fed to MRTF-A-knockout (MRTF-A-/-) and wild-type (WT) mice for 16 weeks. Liver histopathological status was observed using Hematoxylin and Eosin (HE) staining, Oil Red O staining, Sirius Red staining, and Immunohistochemical staining. The mRNA and protein levels in liver tissues were measured through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot. RESULTS: Compared with WT + HFD group, mice in MRTF-A-/- + HFD group were decreased in body weight, blood glucose, plasma insulin, liver TG and NAFLD activity score (NAS), with liver function recovery. Besides, compared with HFD-fed WT mice, HFD-fed MRTF-A-/- mice were improved in hepatic fibrosis, accompanied by decreased collagen content (%) and down-regulated expressions of α-SMA, COL1A2, TGFß1, and SMAD3. In mice fed with HFD, the expression of MCP-1, CCR2, F4/80 and CD68 declined in liver tissues of MRTF-A-/- mice as compared with WT mice. Besides, in hepatic macrophages isolated from HFD-fed mice, the observed increased expression of TNF-α, IL-1ß, MCP-1, as well as decreased expression of CCR2. Compared with WT + HFD group, MRTF-A-/- + HFD group mice were decreased regarding NF-κB p65 in liver tissues. CONCLUSION: MRTF-A knockout reduced macrophage infiltration, down-regulated NF-κB p65 expression, and ameliorated inflammation and fibrosis of liver tissues in mice, thereby becoming a potential therapeutic target for NASH treatment.

Correction: Predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury and mortality following coronary angiography or intervention.

[This corrects the article DOI: 10.18632/oncotarget.19034.].

Comparing common doses (double-dose vs usual-dose) of atorvastatin for preventing contrast-induced acute kidney injury and mortality after coronary angiography.

High-dose atorvastatin pretreatment was proved reducing the risk of contrast-induced acute kidney injury (CI-AKI), especially in patients with high C-reactive protein (CRP) levels. We evaluated the effects of common atorvastatin doses (double vs usual) on the risk of CI-AKI and mortality.We recorded outcomes from 1319 patients who were administered periprocedural common doses of atorvastatin. The risks of CI-AKI and mortality between double-dose (40 mg/d) and usual-dose atorvastatin (20 mg/d) were compared using multivariable regression models in all patients or CRP tertile subgroups.Seventy-six (5.8%) patients developed CI-AKI. Double-dose atorvastatin compared with usual-dose did not further reduce the risk of CI-AKI (adjusted odds ratio [OR]: 2.28, 95% confidence interval [CI]: 0.92-5.62, P = .074), even for patients in the highest CRP tertile (>8.33 mg/L; adjusted OR: 3.76, 95% CI: 0.83-17.05, P = .086). Similar results were observed in reducing mortality in all patients (adjusted hazard ratio: 0.47, 95% CI: 0.10-2.18; P = .339) and in the highest CRP tertiles (P = .424). In the subgroup analysis, double-dose atorvastatin increased risk of CI-AKI in patients with creatinine clearance (CrCl) < 60 mL/min, anemia, contrast volume > 200 mL and > 2 stents implanted (P = .046, .009, .024, and .026, respectively).Daily periprocedural double-dose atorvastatin was not associated with a reduced risk of CI-AKI compared with usual-dose, and did not provide an improved long-term prognosis, even in patients with high CRP levels. However, it increased the risk of CI-AKI in patients with a high contrast volume/CrCl.

miR­21 attenuates contrast­induced renal cell apoptosis by targeting PDCD4.

Contrast medium (CM) is widely used in cardiac catheterization; however, it may induce acute kidney injury or renal failure, although the underlying mechanism remains to be elucidated. MicroRNA­21 (miR­21) is involved in renal disease and has been indicated to regulate cellular apoptosis and fibrosis, although its role in CM­induced renal cell injury is unknown. The present study examined the expression and potential targets of miR­21 in human renal proximal tubular epithelial (HK­2) cells following CM treatment. CM induced renal cell apoptosis and decreased miR­21 expression. The expression level of the apoptosis regulator protein, B­cell lymphoma 2 (Bcl­2) was upregulated, whereas that of the apoptosis regulator, Bcl­2­associated X protein (Bax) was downregulated upon transfection of miR­21 mimics; miR­21 overexpression additionally directly inhibited the expression of programmed cell death protein 4 (PDCD4), as determined by a dual luciferase reporter assay, and PDCD4 silencing reduced the rate of HK­2 cell apoptosis. The results of the present study indicated that miR­21 protected renal cells against CM­induced apoptosis by regulating PDCD4 expression.

Association of post-procedural early (within 24h) increases in serum creatinine with all-cause mortality after coronary angiography.

BACKGROUND: The majority of patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI) are discharged early, with only early (within 24h) serum creatinine (SCr) data available without evidence of clinical prognosis. We aimed to systemically evaluate the association between post-procedural early increase in SCr and all-cause mortality following CAG. METHODS: We performed a retrospective sub-study analysis within a prospective observational study including 3091 consecutive patients with baseline and post-procedural early (within 24h) SCr data. The degree (mild, moderate, or large) of absolute and relative increases in SCr from baseline. The mean follow-up time was 2.49years. RESULT: Moderate or large early increases in SCr were relatively rare (large increase: >1.0mg/dl [0.5%], >100% [0.4%]), whereas mild absolute and relative increases in SCr were more common (mild increase: 0.25 to 0.50mg/dl [4.5%], 25% to 50% [5.9%]). During the follow-up period, there were 136 post-procedural deaths (5.6%). After adjustment for confounders, mild absolute and relative increases in SCr were associated with increased mortality (hazard ratio [HR]: 1.9 and 1.8, respectively, both P<0.05). Moderate or large increases in SCr were associated with higher mortality, even higher than with pre-existing renal dysfunction (HR: 5.36 and 4.12 for moderate increase [0.5 to 1.0mg/dl] and estimated glomerular filtration rate<60ml/min). CONCLUSION: Post-procedural mild, moderate, or large early increase in SCr, is associated with significantly increased long-term mortality. Although moderate or large increase in SCr following CAG was relatively rare, the prognosis is more serious, and is worse than that of pre-existing renal dysfunction. CLINICAL TRIAL REGISTRATION: Predictive Value of Contrast Volume to Creatinine Clearance Ratio (PRECOMIN, ClinicalTrials.govNCT01400295).

Association of left ventricular ejection fraction with contrast-induced nephropathy and mortality following coronary angiography or intervention in patients with heart failure.

BACKGROUND: Left ventricular ejection fraction (LVEF) is the most widely used parameter to evaluate the cardiac function in patients with heart failure (HF). However, the association between LVEF and contrast-induced nephropathy (CIN) is still controversial. Therefore, the aim of this study is to evaluate the association of LVEF with CIN and long-term mortality following coronary angiography (CAG) or intervention in patients with HF. METHODS: We analyzed 1,647 patients with HF (New York Heart Association [NYHA] or Killip class >1) undergoing CAG or intervention, including 207 (12.57%) patients with reduced LVEF (HFrEF), 238 (14.45%) with mid-range LVEF (HFmrEF) and 1,202 (72.98%) with preserved LVEF (HFpEF). CIN was defined as an absolute increase of ≥0.5 mg/dL or a relative increase of ≥25% from baseline serum creatinine within 48-72 h after contrast medium exposure. Multivariable logistic regression and Cox proportional hazards regression analyses were performed to identify the association between LVEF, CIN and long-term mortality, respectively. RESULTS: Overall, 225 patients (13.7%) developed CIN. Individuals with lower LVEF were more likely to develop CIN (HFrEF, HFmrEF and HFpEF: 18.4%, 21.8% and 11.2%, respectively; P<0.001), but without a significant trend after adjusting for the confounding factors (HFrEF vs HFpEF: odds ratio [OR] =1.01; HFmrEF vs HFpEF: OR =1.31; all P>0.05). However, advanced HF (NYHA class >2 or Killip class >1) was an independent predictor of CIN (adjusted OR =1.54, 95% confidence interval [CI], 1.07-2.22; P=0.019). During the mean follow-up of 2.3 years, reduced LVEF (HFrEF group) was significantly associated with increased mortality (HFrEF vs HFpEF: adjusted hazard ratio =2.88, 95% CI, 1.77-4.69; P<0.001). CONCLUSION: In patients with HF undergoing CAG or intervention, not worsened LVEF but advanced HF was associated with an increased risk of CIN. In addition, reduced LVEF was an independent predictor of long-term mortality following cardiac catheterization.

Intensity of hydration changes the role of renin-angiotensin-aldosterone system blockers in contrast-induced nephropathy risk after coronary catheterisation in patients with chronic kidney disease.

OBJECTIVE: This study evaluated the potential effect of hydration intensity on the role of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) on contrast-induced nephropathy in patients with renal insufficiency. METHODS: All eligible patients were included and stratified according to hydration intensity defined as saline hydration volume to body weight tertiles: <10.21 mL/kg, 10.21 to <17.86 mL/kg, and ⩾17.86 mL/kg. RESULTS: In total, 84 (6.7%) of 1254 patients developed contrast-induced nephropathy: 6.2% in the ACEI/ARB group versus 10.8% in the non-ACEI/ARB group ( P=0.029), with an adjusted odds ratio (OR) of 0.89 (95% confidence interval (CI) 0.46-1.73, P=0.735). The incidence of contrast-induced nephropathy was lower in the ACEI/ARB group than in the non-ACEI/ARB group in the second tertile ( P=0.031), while not significantly different in the first ( P=0.701) and third ( P=0.254) tertiles. ACEIs/ARBs were independently associated with a lower contrast-induced nephropathy risk (OR 0.26, 95% CI 0.09-0.74, P=0.012) and long-term all-cause death (hazard ratio 0.461, 95% CI 0.282-0.755, P=0.002) only in the second hydration volume to body weight tertile. CONCLUSION: The effects of ACEIs/ARBs on contrast-induced nephropathy risk vary according to saline hydration intensity in chronic kidney disease patients, and may further reduce contrast-induced nephropathy risk in patients administered moderate saline hydration.

Could late measurement of serum creatinine be missed for patients without early increase in serum creatinine following coronary angiography?

Most patients are discharged early (within 24 hours) after coronary angiography (CAG) and may miss identification the late (24-48 hours) increase in serum creatinine (SCr), whose characteristics and prognosis have been less intensively investigated.We prospectively recruited 3065 consecutive patients with SCr measurement, including only1344 patients with twice SCr measurement (both early and late). The late contrast-induced acute kidney injury (CI-AKI) was defined as significantly increase in SCr (≥0.3 mg/dL or ≥50%) not in early phase, but only in late phase after the procedure, and the early CI-AKI experienced a significantly increase in early phase.Overall, CI-AKI developed in 134 patients (10%), and the incidence of late and early CI-AKI were 3.6% and 6.4%, respectively. There were no difference in age, renal, and heart function, contrast volume among patients with late and early CI-AKI. With mean follow-up period of 2.45 years, long-term mortality (3 years, 29.7% and 35.6%, respectively, P = .553) was similar for patients with late and early CI-AKI. Cox analysis showed that both late (adjusted HR 2.05; 95% CI, 1.02-4.15) and early (adjusted HR 2.68; 95% CI, 1.57-4.59) CI-AKI was significantly associated with long-term mortality (all P < .001).Only late increase in SCr, as late CI-AKI, accounted for about one-third of CI-AKI incidence and has similar good predictive value for long-term mortality with that of an early increase, early CI-AKI, among patients with SCr measured twice, supporting the importance of late repeating SCr measurement after CAG, even without an early significant increase in SCr.

Association of lipoprotein(a) with long-term mortality following coronary angiography or percutaneous coronary intervention.

BACKGROUND: There is no consistent evidence to suggest the association of plasma lipoprotein(a) (Lp[a]) with long-term mortality in patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI). HYPOTHESIS: Level of Lp(a) is associated with long-term mortality following CAG or PCI. METHODS: We enrolled 1684 patients with plasma Lp(a) data undergoing CAG or PCI between April 2009 and December 2013. The patients were divided into 2 groups: a low-Lp(a) group (Lp[a] <16.0 mg/dL; n = 842) and a high-Lp(a) group (Lp[a] ≥16.0 mg/dL; n = 842). RESULTS: In-hospital mortality was not significantly different between the high and low Lp(a) groups (0.8% vs 0.5%, respectively; P = 0.364). During the median follow-up period of 1.95 years, the high-Lp(a) group had a higher long-term mortality than did the low-Lp(a) group (5.8% vs 2.5%, respectively; P = 0.003). After adjustment of confounders, multivariate Cox regression analysis revealed that a higher Lp(a) level was an independent predictor of long-term mortality (hazard ratio: 1.96, 95% confidence interval: 1.07-3.59, P = 0.029). CONCLUSIONS: Our data suggested that an elevated Lp(a) level was significantly associated with long-term mortality following CAG or PCI. However, additional larger multicenter studies will be required to investigate the predictive value of Lp(a) levels and evaluate the benefit of controlling Lp(a) levels for patients undergoing CAG or PCI.

Predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury and mortality following coronary angiography or intervention.

OBJECTIVE: To investigate the predictive value of post-procedural early (within 24 h) increase in cystatin C for contrast-induced acute kidney injury (CI-AKI) and all-cause mortality following coronary angiography or intervention. METHODS: We prospectively investigated 1042 consecutive patients with both baseline and early post-procedural cystatin C measurement undergoing coronary angiography or intervention. CI-AKI was defined as an increase ≥0.3 mg/dL or >50% in serum creatinine from baseline within 48 h post-procedure. Mean follow-up was 2.26 years. RESULTS: Overall, the patients had a CI-AKI incidence was 3.6% (38/1042), mean serum creatinine of 87 µmol/L. Compared with Mehran risk score, post-procedural early absolute increase (AUC: 0.584 vs. 0.706, P = 0.060) and relative increase (AUC: 0.585 vs. 0.706, P = 0.058) in cystatin C had poorer predictive value for CI-AKI. According to multivariate analysis, post-procedural significant early increase (≥0.3 mg/dL or ≥10%) in cystatin C developed in 231 patients (22.2%), was not independent predictor of CI-AKI (adjusted OR: 1.23, 95% CI, 0.56-2.69, P = 0.612), and long-term mortality (adjusted HR: 0.90; P = 0.838). CONCLUSIONS: Our data suggested post-procedural early increase (within 24 h) in cystatin C was not effective for predicting CI-AKI or all-cause mortality following coronary angiography or intervention among patients at relative low risk of CI-AKI, the negative finding of poor predictive value should be further evaluated in larger multicenter trials.

Preprocedural High-Sensitivity C-Reactive Protein Predicts Contrast-Induced Nephropathy and Long-Term Outcome After Coronary Angiography.

We investigated whether high-sensitivity C-reactive protein (hsCRP) levels were associated with contrast-induced nephropathy (CIN) and long-term mortality after coronary angiography (CAG). Patients (N = 2133) undergoing CAG with preprocedural hsCRP were consecutively enrolled. High-sensitivity C-reactive protein was measured before angiography. Median follow-up was 2.3 years. The overall incidence of CIN was 2.77% (59 of 2133). There was a positive trend of hsCRP quartiles (Q) with rates of CIN: 0.9% for Q1 (<1.6 mg/L), 0.9% for Q2 (1.6-3.9 mg/L), 2.4% for Q3 (4.0-11.3mg/L), and 6.8% for Q4 (>11.3 mg/L; P < .05). The receiver operating characteristic (ROC) analysis showed that the cutoff point of hsCRP was 7.3 mg/L for predicting CIN with a 72.7% sensitivity and a 67.0% specificity (area under the curve [AUC] = 0.742, 95% confidence interval [CI] 0.672-0.810; P < .05). The predictive value of hsCRP was similar to the Mehran score for CIN (AUChsCRP = 0.742 vs AUCMehran = 0.801; P = .228). After adjustment for other potential risk factors, hsCRP >7.3 mg/L still was an independent predictor of CIN (odds ratio [OR] = 2.83, 95% CI: 1.44-5.58; P = .003). Furthermore, hsCRP >7.3 mg/L was associated with higher mortality (OR = 2.04, 95% CI: 1.30-3.19; P = .002).

Association of N-terminal pro-brain natriuretic peptide with contrast-induced acute kidney injury and long-term mortality in patients with heart failure and mid-range ejection fraction: An observation study.

The potential value of N-terminal pro-brain natriuretic peptide (NT-proBNP) for contrast-induced acute kidney injury (CI-AKI) in patients with heart failure and mid-range ejection fraction (HFmrEF) is unclear. We investigated whether NT-proBNP is associated with CI-AKI and long-term mortality following elective cardiac catheterization in patients with HFmrEF.A total of 174 consecutive patients with HFmrEF undergoing elective coronary angiography or intervention were enrolled. The primary endpoint was the development of CI-AKI, defined as an absolute increase of ≥0.3 mg/dL or ≥ 50% from baseline serum creatinine with 48 hours after contrast medium exposure. Receiver-operating characteristic curve analysis was conducted, and Youden index was used to determine the best cutoff NT-proBNP value. Multivariable logistic regression and Cox proportional hazards regression analyses were performed to identify the independent risk factors for CI-AKI and long-term mortality, respectively.The incidence of CI-AKI was 12.1%. Patients with CI-AKI had higher NT-proBNP values than those without (4373[1561.9-7470.5] vs 1303[625.2-2482.3], P = 0.003). Receiver-operating characteristic curve revealed that NT-proBNP was not significantly different from the Mehran risk score in predicting CI-AKI (area under the curve [AUC] = 0.723 vs 0.767, P = 0.516). The best cutoff NT-proBNP value for CI-AKI was 3299 pg/mL, with 70.6% sensitivity and 83.1% specificity. Multivariable analysis demonstrated that NT-proBNP ≥3299 pg/mL is significantly related to CI-AKI (odds ratio = 12.79; 95% confidence interval, 3.18-51.49; P < 0.001). Cox regression analysis showed that NT-proBNP ≥3299 pg/mL is associated with long-term mortality (adjusted hazard ratio = 11.91; 95%CI, 2.16-65.70; P = 0.004) during follow-up.In patients with HFmrEF, NT-proBNP ≥3299 pg/mL is associated with CI-AKI and long-term mortality following elective coronary angiography or intervention.

Hyperuricemia Is an Independent Predictor of Contrast-Induced Acute Kidney Injury and Mortality in Patients Undergoing Percutaneous Coronary Intervention.

We investigated whether hyperuricemia is an independent predictor of contrast-induced acute kidney injury (CI-AKI) and mortality in patients undergoing percutaneous coronary intervention (PCI). In a single-center study of 1772 patients undergoing PCI, the development of CI-AKI and mortality during a 2.8-year median follow-up period was assessed. The incidence of CI-AKI was significantly higher in the hyperuricemic group than in the normouricemic group (5.78% vs 1.76%, P < .001). According to multivariate analysis (after adjusting for potential confounding factors), hyperuricemia predicted CI-AKI (odds ratio: 1.962; 95% confidence interval [CI]: 1.014-3.798; P = .045). The other risk factors for CI-AKI were >75 years, emergent PCI, chronic kidney disease (CKD), and anemia. Hyperuricemia with a tendency toward significantly independently predicted long-term mortality, after adjusting for CI-AKI, CKD, and emergent PCI (hazard ratio: 1.571; 95% CI: 1.006-2.452; P = .047). In patients undergoing PCI, hyperuricemia is associated with a risk of CI-AKI. Furthermore, after adjusting for other variables, including CI-AKI and CKD, long-term mortality after PCI was higher in those with hyperuricemia than with normouricemia.