Key result
Contrast-induced nephropathy affects ~19% of primary PCI patients and is linked to significantly higher mortality.
Why the study?
Patients undergoing primary PCI for AMI may be at higher risk of contrast-induced nephropathy due to hemodynamic instability and the unfeasibility of adequate prophylaxis.
What are the incidence, predictors, and outcomes of contrast-induced nephropathy in patients undergoing primary PCI for acute myocardial infarction?
Observational (n=208)
What are the incidence, predictors, and outcomes of contrast-induced nephropathy in patients undergoing primary PCI for acute myocardial infarction?
Contrast-induced nephropathy frequently complicates primary PCI for AMI, is associated with higher mortality, and is predicted by older age, longer time-to-reperfusion, higher contrast volume, and IABP use.
CIN identification may aid risk stratification in primary PCI; leaves open whether targeted prevention reduces associated mortality.
OBJECTIVES: The aim of this research was to assess the incidence, clinical predictors, and outcome of contrast-induced nephropathy (CIN) after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). BACKGROUND: Contrast-induced nephropathy is associated with significant morbidity and mortality after PCI. Patients undergoing primary PCI may be at higher risk of CIN because of hemodynamic instability and unfeasibility of adequate prophylaxis. METHODS: In 208 consecutive AMI patients undergoing primary PCI, we measured serum creatinine concentration (Cr) at baseline and each day for the following three days. Contrast-induced nephropathy was defined as a rise in Cr >0.5 mg/dl. RESULTS: Overall, CIN occurred in 40 (19%) patients. Of the 160 patients with baseline Cr clearance >/=60 ml/min, only 21 (13%) developed CIN, whereas it occurred in 19 (40%) of those with Cr clearance <60 ml/min (p < 0.0001). In multivariate analysis, age >75 years (odds ratio [OR] 5.28, 95% confidence interval [CI] 1.98 to 14.05; p = 0.0009), anterior infarction (OR 2.17, 95% CI 0.88 to 5.34; p = 0.09), time-to-reperfusion >6 h (OR 2.51, 95% CI 1.01 to 6.16; p = 0.04), contrast agent volume >300 ml (OR 2.80, 95% CI 1.17 to 6.68; p = 0.02) and use of intraaortic balloon (OR 15.51, 95% CI 4.65 to 51.64; p < 0.0001) were independent correlates of CIN. Patients developing CIN had longer hospital stay (13 +/- 7 days vs. 8 +/- 3 days; p < 0.001), more complicated clinical course, and significantly higher mortality rate (31% vs. 0.6%; p < 0.001). CONCLUSIONS: Contrast-induced nephropathy frequently complicates primary PCI, even in patients with normal renal function. It is associated with higher in-hospital complication rate and mortality. Thus, preventive strategies are needed, particularly in high-risk patients.
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Marenzi et al. (2004) conducted an observational in Acute myocardial infarction (n=208). Primary percutaneous coronary intervention was evaluated on Contrast-induced nephropathy (rise in serum creatinine >0.5 mg/dl). Contrast-induced nephropathy occurred in 19% of patients undergoing primary PCI for AMI and was associated with significantly higher mortality compared to those without CIN (31% vs. 0.6%; P<0.001).
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