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Contrast-induced acute kidney injury (CI-AKI) after primary percutaneous coronary intervention (PCI) in ST-segment elevation myocardial infarction (STEMI) patients independently predicts worse short- and long-term adverse events, including mortality, according to a HORIZONS-AMI substudy published online March 6, 2014, ahead of print in the European Heart Journal.

Investigators led by Roxana Mehran, MD, of Mount Sinai Medical Center (New York, NY), analyzed CI-AKI data from 2,968 STEMI patients from the HORIZONS-AMI (Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction) trial. CI-AKI, defined as an increase in serum creatinine of ≥ 0.5 mg/dL or a 25% relative rise in creatinine within 48 hours after contrast exposure, occurred in 16.1% of patients (n = 479).

In the prospective HORIZONS-AMI trial, 3,602 STEMI patients were randomized to bivalirudin (n = 1,800) or heparin plus a glycoprotein IIb/IIIa inhibitor (n = 1,802) and later to a paclitaxel-eluting stent or an otherwise identical bare-metal stent.

In the current substudy, patients who developed CI-AKI were more likely to have diabetes, history of congestive heart failure, anemia, and to be older at baseline. Procedurally, they were more likely to have the LAD as the infarct-related artery, LVEF < 40%, cardiogenic shock, and received an IABP. Furthermore, the median volume of contrast used in patients who developed CI-AKI was 245 cc (IQR, 190-320 cc), rather than the 225 cc (IQR, 180-290 cc) used in the group that did not develop CI-AKI (P = 0.0003).

Multivariate analysis identified contrast volume, white blood cell count, LAD infarct-related artery, age, anemia, creatinine clearance < 60 mL/min, and history of congestive heart failure as independent predictors of CI-AKI.

There were no differences between rates of CI-AKI by type of contrast used (low-osmolar vs iso-osmolar; 15.6% vs 15.3%; P = 0.87).

Dreary Long-Term Outcomes

Patients who developed CI-AKI compared with those who did not had increased 30-day rates of net adverse clinical events (co-primary endpoint; defined as major bleeding not related to CABG or a composite of MACE; 22% vs 9.3%), MACE (defined as death, reinfarction, TVR for ischemia, or stroke; 11.7% vs 3.9%), and non-CABG-related major bleeding (co-primary endpoint; 14.6% vs 6.3%). Results were maintained at 3-year follow-up (table 1).

Table 1. Unadjusted Outcomes at 3 Years

a Abbreviation: NACE, net adverse clinical events

Trends were later confirmed in propensity-matched pairs.

Multivariable analysis demonstrated that the 3-year risk of net adverse clinical events, MACE, non-CABG major bleeding, and mortality all were independently predicted by CI-AKI (table 2).

Table 2. Event Risk at 3 Years: CI-AKI vs No Contrast Related Kidney Injury

Although patients who received low-osmolar contrast had lower 30-day rates of net adverse clinical events (P = 0.01), MACE (P = 0.0003), and stent thrombosis (P = 0.04) compared to those treated using iso-osmolar contrast, differences were not maintained at 3-year follow-up.

Kidney Protection Could Improve Outcomes

Interestingly, data from this study suggest that rates of CI-AKI in STEMI patients are similar to those of other acute coronary syndromes, including NSTEMI, Dr. Mehran and colleagues note.

“It has been thought that this form of acute kidney injury selects patients with increased comorbidities and that the increased rate of adverse outcomes is reflective of those comorbidities,” explain the authors. However, they say the results of this study and others suggest that CI-AKI could be directly responsible for long-term events.

In a telephone interview with TCTMD, Peter McCullough, MD, of the Baylor University Medical Center (Dallas, TX), agreed: “The P values are so small, the differences so great [in this study], that there is probably a renal component contributing to these events.… This HORIZON-AMI trial substudy supports the effort [to improve outcomes by protecting the kidneys].”

Even in patients without kidney disease at baseline, Dr. McCullough explained, “there were still predictors of who would develop acute CI-AKI such as contrast volume, CHF, BMI, age, and LAD infarct-related artery.” Based on this observation, the study authors posit, “Of the modifiable risk factors, careful attention to contrast volume needs to be a key focus, especially in patients at a higher risk of CI-AKI.”

 Dr. McCullough said that it is important to protect both heart cells and the kidneys. “I’m hopeful that if we can come up with new products or approaches that drop rates of acute kidney injury, we can start to significantly influence at least the 30-day rates of [net adverse clinical events] and MACE,” he concluded.

Note: Several study coauthors are faculty members of the Cardiovascular Research Foundation (CRF), which owns and operates TCTMD.

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