Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after coronary angiography and percutaneous coronary intervention (PCI). The aim of the present study was to assess the clinical features and in-hospital outcomes of CIN after emergency PCI. The serum creatinine (SCr) concentration was measured from days 0 to 30 in 338 consecutive patients with acute coronary syndrome undergoing emergency PCI. CIN was defined as an increase in SCr of >25% or >0.5 mg/dl within 2 days after PCI. Overall, 94 patients (28%) developed CIN. The mean SCr on admission was not significantly different between patients with CIN and those without CIN. The CIN group had significantly greater SCr at days 1, 2, and 30 than did the no CIN group. Multivariate analysis showed female gender (odds ratio [OR] 2.38, 95% confidence interval [CI] 1.12 to 5.07, p = 0.025), a culprit lesion in the left anterior descending artery (OR 2.37, 95% CI 1.31 to 4.27, p = 0.0042), contrast agent volume >200 ml (OR 3.60, 95% CI 1.96 to 6.62, p <0.001) and end-diastolic pulmonary arterial pressure >15 mm Hg (OR 2.03, 95% CI 1.02 to 4.04, p <0.01) to all correlate independently with CIN. The in-hospital mortality rate was greater in the CIN group than in the no CIN group (9.6% vs 3.3%, respectively; p = 0.025). In conclusion, CIN is a frequent complication of emergency PCI for acute coronary syndrome and is associated with a greater mortality rate and persistent renal dysfunction.
The growing number of coronary angiographic procedures requiring contrast media has triggered a parallel increase of contrast-induced nephropathy (CIN). CIN remains an important cause of hospital-acquired renal function decline and implies a grim short- and long-term prognosis. Recent randomized trials have shown that emergency percutaneous coronary intervention (PCI) increases myocardial salvage and improves the survival rate of patients with acute myocardial infarction. Other studies have shown that among high-risk patients with unstable angina, early PCI significantly reduces the incidence of major cardiac events. However, CIN can occur after emergency PCI for multiple reasons. Only one study has recently demonstrated that CIN is frequent complication in the era of emergency PCI for acute myocardial infarction. The importance of CIN after emergency PCI in patients with acute coronary syndrome (ACS) has not yet been well examined. The purpose of the present study was to determine the incidence, clinical predictors, and prognostic implications of CIN in patients undergoing emergency PCI.
Methods
The present study included patients with acute ST-segment elevation myocardial infarction or unstable angina/non–ST-segment elevation myocardial infarction undergoing emergency PCI from January 2000 to June 2007. The patients were eligible for inclusion if they had been admitted within 24 hours of the onset of chest pain that had lasted for ≥30 minutes with ST-segment elevation of ≥0.2 mV in ≥2 contiguous leads and creatinine kinase elevation or its MB isozyme to ≥2 times normal. Patients were also enrolled if they had had an episode of ischemic chest pain of ≥10 minutes with transient or persistent ST-segment depression (>0.5 mm), T-wave inversion (>1 mm), and/or elevation of troponin T greater than the upper limit of normal, thus presenting with refractory angina or hemodynamic instability despite maximum drug therapy within ≤24 hours of admission. Patients were excluded if the coronary anatomy was not suitable for PCI or if emergency bypass grafting was required. In addition, patients requiring chronic peritoneal or hemodialysis treatment and cardiogenic shock at admission were excluded. The ethical committee of our institution approved the present study, and all patients provided written informed consent.
After contrast medium exposure, physiologic (0.45%) saline was given intravenously at a rate of 1 ml/kg/hour for 12 hours. In patients with left ventricular dysfunction (ejection fraction <40%) or overt heart failure, the hydration rate was reduced to 0.5 ml/kg/hour. Supportive pharmacologic therapies or mechanical support was left to the discretion of the interventionists and cardiologists of the coronary care unit, according to our institute’s clinical protocols and international experience guidelines. An echocardiographic evaluation was performed in all patients at admission. Serum creatinine (SCr) was measured at admission (baseline) and on days 1, 2, 7, and 30 after contrast medium exposure.
Emergency PCI was performed by a 24-hour, on-call, interventional team, according to standard clinical practice, using the femoral approach and 6F guiding catheters. We used nonionic low-osmolality contrast medium for all patients. The patients received aspirin (100 mg) and ticlopidine (100 mg) in the coronary care unit and continued to take low-dose aspirin (100 mg/day) and ticlopidine (200 mg/day) after the procedure. In addition, the patients received a bolus of 5,000 U heparin in the coronary care unit, followed by a bolus of 5,000 U heparin just before the procedure. Target lesions were predilated using conventional angioplasty balloons followed by stent implantation. After PCI, right heart catheterization was performed, and the right atrium pressure, pulmonary arterial blood pressure, and pulmonary arterial wedge pressure were measured using the DS-3000 system (Fukuda Denshi, Tokyo, Japan). The cardiac output was also examined by thermodilution, using the method described by Ganz et al.
CIN was defined as a 25% increase in SCr from baseline or an absolute increase of ≥0.5 mg/dl that appeared within 2 days after emergency PCI. According to our clinical protocol, emergency renal replacement therapy (hemofiltration or hemodialysis) was performed if oligoanuria lasting >24 hours was observed.
Continuous data are presented as the mean ± SD and categorical data as frequencies. Continuous variables were compared using a paired or unpaired Student’s t test. Categorical variables were compared using chi-square statistics and Fisher’s exact test.
A 2-step analysis was used to identify the independent predictors of CIN. First, a univariate analysis was used to select the clinical, angiographic, or procedural risk factors of CIN. Continuous variables were transformed to binary data with 1 indicating the presence of assumed risk factors and 0 otherwise. Second, the univariate predictors with p <0.05 were entered into a stepwise multivariate logistic regression model. The odds ratio (OR) and 95% confidence intervals (CI) were presented in the final multivariate model. The data are expressed as the percentage for discrete factors and the mean value ± SD for continuous factors. Statistical significance was accepted for all p values <0.05.
Results
Of 373 patients with ACS, 35 were excluded (no indication for PCI in 7, coronary bypass surgery because of coronary anatomy not suitable for PCI in 8, chronic dialysis in 10, and cardiogenic shock at admission in 10). Thus, 338 consecutive patients (254 men and 84 women, mean age 66 ± 11 years) were included in the present study. Of these 338 patients, 94 (28%) developed CIN and 244 did not. The baseline patient characteristics are listed in Table 1 . The patients in the CIN group were older, more often women, less likely to have a history of hyperlipidemia, less likely to smoke, more likely to have congestive heart failure on admission, and more likely to have a greater enzymatic peak. The baseline SCr value was similar in the 2 groups. In 47 (14%) of 338 patients, an abnormal SCr level (>1.1 mg/dl) was present at hospital admission. Of these 47 patients, only 12 (25%) developed CIN.
| Characteristic | CIN | p Value | |
|---|---|---|---|
| No (n = 244) | Yes (n = 94) | ||
| Age (years) | 65 ± 10 | 67 ± 11 | 0.048 |
| Age >75 years | 47 (19%) | 29 (31%) | 0.022 |
| Men | 192 (79%) | 62 (66%) | 0.015 |
| Body mass index (kg/m 2 ) | 23.7 ± 3.2 | 24.0 ± 3.6 | 0.461 |
| Hypertension | 146 (60%) | 62 (66%) | 0.221 |
| Dyslipidemia | 184 (75%) | 60 (64%) | 0.030 |
| Diabetes mellitus | 74 (30%) | 38 (40%) | 0.081 |
| Smoking | 152 (62%) | 46 (49%) | 0.018 |
| Complicated congestive heart failure | 67 (27%) | 40 (43%) | 0.008 |
| Serum creatinine >1.1 mg/dl | 35 (14%) | 12 (13%) | 0.707 |
| Serum creatinine (mg/dl) | 0.90 ± 0.47 | 0.83 ± 0.49 | 0.209 |
| Total cholesterol (mg/dl) | 186 ± 43 | 183 ± 45 | 0.554 |
| Triglycerides (mg/dl) | 118 ± 81 | 104 ± 70 | 0.137 |
| Low-density lipoprotein (mg/dl) | 118 ± 46 | 119 ± 48 | 0.961 |
| High-density lipoprotein (mg/dl) | 44 ± 16 | 45 ± 16 | 0.887 |
| Hemoglobin A1c (%) | 5.7 ± 1.4 | 5.9 ± 1.5 | 0.303 |
| Glucose (mg/dl) | 185 ± 82 | 185 ± 73 | 0.994 |
| Peak creatine kinase (U/L) | 3,097 ± 2,909 | 4,052 ± 3,642 | 0.012 |
| Peak creatine kinase >3,000 IU/L | 97 (40%) | 52 (55%) | 0.010 |
Table 2 lists the procedural characteristics of the patients in the 2 groups. The culprit lesion was more frequently seen in the left anterior descending artery in the CIN group. The contrast volume was not significantly different between the 2 groups. Of the 338 patients, 181 (54%) had received a contrast volume >200 ml. Significantly more patients in the CIN group (72%) were exposed to a contrast volume >200 ml than those without CIN (46%, p <0.001). Mechanical circulatory assistance with right ventricular pacing was used more frequently in those without CIN. Overall, 13 patients received hemodialysis after contrast medium exposure, 6 patients with CIN (6%) and 7 patients without CIN (3%). No patient developed end-stage renal disease requiring permanent hemodialysis.
| Variable | CIN | p Value | |
|---|---|---|---|
| No (n = 244) | Yes (n = 94) | ||
| Unstable angina/NSTEMI | 16 (7%) | 4 (4%) | |
| AMI | 228 (93%) | 90 (96%) | 0.422 |
| Culprit lesion | |||
| Left main trunk | 2 (1%) | 2 (2%) | 0.310 |
| LAD | 115 (47%) | 62 (66%) | 0.002 |
| Left circumflex artery | 18 (7%) | 9 (10%) | 0.657 |
| Right coronary artery | 107 (44%) | 21 (22%) | <0.001 |
| Contrast volume (ml) | 210 ± 93 | 229 ± 77 | 0.090 |
| Stent type | |||
| Multilink | 126 (52%) | 53 (56%) | 0.433 |
| NIR | 29 (12%) | 14 (16%) | 0.463 |
| Bx Velocity | 6 (2%) | 4 (4%) | 0.474 |
| Driver | 65 (27%) | 19 (20%) | 0.221 |
| Express II | 18 (7%) | 4 (4%) | 0.297 |
| IABP supported | 34 (14%) | 16 (17%) | 0.474 |
| Pacemaker | 33 (14%) | 5 (5%) | 0.051 |
| Ventilator | 23 (9%) | 13 (14%) | 0.240 |
| Need for hemodialysis | 7 (3%) | 6 (6%) | 0.234 |
The patients in the CIN group had greater systolic and end-diastolic pulmonary arterial blood pressure and greater pulmonary arterial wedge pressure after PCI ( Table 3 ). All patients were classified into 4 hemodynamic subsets, as described by Forrester et al. The number of patients in the Forrester III subgroup (reduced cardiac output and normal pulmonary arterial wedge pressure) showed no differences between the 2 groups. However, patients in the Forrester class IV subgroup (reduced cardiac output and elevated pulmonary arterial wedge pressure) more frequently developed CIN (9%) than did not (3%; p = 0.036).
| Variable | CIN | p Value | |
|---|---|---|---|
| No (n = 244) | Yes (n = 94) | ||
| Blood pressure (mm Hg) | |||
| Systole | 120 ± 28 | 116 ± 25 | 0.284 |
| Diastole | 71 ± 16 | 69 ± 15 | 0.305 |
| Pulmonary artery pressure (mm Hg) | |||
| Systole | 26 ± 8 | 29 ± 11 | 0.006 |
| Diastole | 12 ± 5 | 15 ± 7 | 0.0002 |
| Right atrium pressure (mm Hg) | 7 ± 4 | 7 ± 4 | 0.271 |
| PCWP (mm Hg) | 12 ± 6 | 14 ± 8 | 0.011 |
| Cardiac output (L/min) | 5.09 ± 1.72 | 4.95 ± 1.83 | 0.488 |
| Forrester class | |||
| II | 34 | 18 | |
| III | 24 | 7 | |
| IV | 7 | 8 | |
The SCr value at baseline and from baseline to day 30 is shown in Figure 1 . The SCr value at baseline was not significantly different between the 2 groups (0.83 ± 0.47 mg/dl vs 0.90 ± 0.49 mg/dl, respectively; p = NS). Although the SCr at day 14 was not significantly different between the 2 groups (0.96 ± 0.47 vs 0.90 ± 0.49 mg/dl, p = NS), the concentration at day 1 (1.13 ± 0.66 vs 0.85 ± 0.34 mg/dl, p <0.001), day 2 (1.16 ± 0.83 vs 0.88 ± 0.38 mg/dl, p <0.001), day 7 (1.06 ± 0.62 vs 0.91 ± 0.34 mg/dl, p = 0.004), and day 30 (1.27 ± 1.21 vs 0.96 ± 0.30 mg/dl, p = 0.032) were significantly greater in the CIN group.
