期刊
JOURNAL OF CARDIAC FAILURE
卷 16, 期 5, 页码 381-389出版社
CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
DOI: 10.1016/j.cardfail.2009.12.020
关键词
Kidney; heart failure; inflammation; oxidative stress
资金
- Medical School Faculty and Alumni
- Keio University Medical Science Fund
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. (J. Cardiac Fail 2010:16:381-389)
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