Background: Acute kidney injury (AKI) after myocardial infarction is associated with poor clinical outcome. However, mechanisms of the adverse effect of AKI on clinical outcome after reperfused ST-elevation myocardial infarction (STEMI) have not been fully elucidated. Methods and Results: We examined 141 consecutive patients with reperfused first anterior STEMI. AKI was defined as an increase in serum creatinine of ≥0.3 mg/dL within 48 hours after admission. Patients with AKI had higher incidence of in-hospital cardiac death (P = .0004) and major adverse cardiac events (MACE, P = .020) during a mean of 39 ± 40 (range, 1 to 96) months than those without, in association with adverse left ventricular (LV) remodeling. White blood cell count on admission and peak C-reactive protein were higher in patients with than those without AKI. Plasma norepinephrine on admission, interleukin-6, brain natriuretic peptide, and malondialdehyde-modified low-density lipoprotein 2 weeks after STEMI were higher in patients with AKI than those without AKI. Cox proportional hazards model analysis revealed AKI was an independent predictor of MACE (hazard ratio = 2.38, P = .019). Conclusions: AKI was a strong predictor of MACE in association with adverse LV remodeling. Enhanced inflammatory response, oxidative stress, and neurohormonal activation may synergistically accelerate renal dysfunction and LV remodeling after STEMI.
- heart failure
- oxidative stress
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine