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.

The relationship between pre-procedural elevated arterial lactate and contrast-induced nephropathy following primary percutaneous coronary intervention.

BACKGROUND: Risk stratification has been one of the main steps in preventing contrast-induced nephropathy (CIN), which is a common complication after percutaneous coronary intervention (PCI). Elevated arterial lactate is a biomarker indicating severe disease condition and post-intervention complications. The relationship between lactate and CIN has not been established. This study is performed to investigate the relationship between elevated arterial lactate level and contrast-induced nephropathy (CIN). METHODS: Patients diagnosed with ST-segment elevated myocardial infarction (STEMI) were prospectively enrolled, with lactate measured within 0.5-1 hours before primary percutaneous coronary intervention (PCI). Patients with cardiopulmonary resuscitation, any forms of severe anaerobic condition, or end-stage renal disease undergoing dialysis were excluded. CIN was defined as an increase in serum creatinine ≥0.5 mg/dL or 25% within 72 hours after PCI. The Mehran Risk Score (MRS) is widely regarded as a classic risk model for CIN and the risk factors of MRS were applied in our multivariate regression analysis. RESULTS: Of the 227 enrolled patients, 47 (20.7%) developed CIN according to the definition. The mean lactate level was higher in the CIN group than in the non-CIN group (2.68±2.27 vs. 1.74±1.94, P<0.001). The arterial lactate level ≥2.0 mmol/L had 57.5% sensitivity and 75.6% specificity in predicting CIN. The performance of the lactate level in discriminating CIN was similar to that of the MRS (AUClac =0.707 vs. AUCMRS =0.697, P=0.86). After adjusting for other risk factors, lactate ≥2.0 mmol/L still significantly predicted CIN (odds ratio =3.77, 95% CI, 1.77-7.99, P=0.001). CONCLUSIONS: An arterial lactate level of ≥2.0 mmol/L is associated with CIN in STEMI patients after primary PCI.

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.].

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.

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.

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.