Prognostic Significance of Acute Kidney Injury After Reperfused ST-Elevation Myocardial Infarction

Synergistic Acceleration of Renal Dysfunction and Left Ventricular Remodeling

Atsushi Anzai, Toshihisa Anzai, Kotaro Naito, Hidehiro Kaneko, Yoshinori Mano, Yusuke Jo, Yuji Nagatomo, Yuichiro Maekawa, Akio Kawamura, Tsutomu Yoshikawa, Satoshi Ogawa

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)381-389
Number of pages9
JournalJournal of Cardiac Failure
Volume16
Issue number5
DOIs
Publication statusPublished - 2010 May

Fingerprint

Ventricular Remodeling
Acute Kidney Injury
Kidney
ST Elevation Myocardial Infarction
Brain Natriuretic Peptide
Malondialdehyde
Leukocyte Count
LDL Lipoproteins
Proportional Hazards Models
C-Reactive Protein
Interleukin-6
Creatinine
Norepinephrine
Oxidative Stress
Myocardial Infarction
Incidence

Keywords

  • heart failure
  • inflammation
  • Kidney
  • oxidative stress

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Prognostic Significance of Acute Kidney Injury After Reperfused ST-Elevation Myocardial Infarction : Synergistic Acceleration of Renal Dysfunction and Left Ventricular Remodeling. / Anzai, Atsushi; Anzai, Toshihisa; Naito, Kotaro; Kaneko, Hidehiro; Mano, Yoshinori; Jo, Yusuke; Nagatomo, Yuji; Maekawa, Yuichiro; Kawamura, Akio; Yoshikawa, Tsutomu; Ogawa, Satoshi.

In: Journal of Cardiac Failure, Vol. 16, No. 5, 05.2010, p. 381-389.

Research output: Contribution to journalArticle

Anzai, Atsushi ; Anzai, Toshihisa ; Naito, Kotaro ; Kaneko, Hidehiro ; Mano, Yoshinori ; Jo, Yusuke ; Nagatomo, Yuji ; Maekawa, Yuichiro ; Kawamura, Akio ; Yoshikawa, Tsutomu ; Ogawa, Satoshi. / Prognostic Significance of Acute Kidney Injury After Reperfused ST-Elevation Myocardial Infarction : Synergistic Acceleration of Renal Dysfunction and Left Ventricular Remodeling. In: Journal of Cardiac Failure. 2010 ; Vol. 16, No. 5. pp. 381-389.
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AB - 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.

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