Abstract 5822: Interaction Between Acute Kidney Injury and Left Ventricular Remodeling After Myocardial Infarction: Possible Role of Inflammation, Oxidative Stress and Neurohormonal Activation
Background: Acute kidney injury (AKI) after MI is associated with poor clinical outcome. However, the mechanisms of the adverse effect of AKI on clinical outcome after STEMI have not been fully elucidated.
Methods: We examined 141 consecutive patients with reperfused first anterior STEMI. Patients were divided into 2 groups according to presence or absence of AKI, defined as an increase in serum creatinine of ≥0.3 mg/dl within 48 hours after admission (AKI group; n=31, non-AKI group; n=110). Peripheral WBC count, serum CK and CRP levels were serially measured. Left ventriculography and measurements of plasma IL-6, malondialdehyde-modified low density lipoprotein (MDA-LDL) and neurohormones were performed on admission and 2 weeks after MI.
Results: AKI group was older and had lower estimated GFR (eGFR) on admission compared with non-AKI group. Other variables, including coronary risk factors, medications, coronary angiographic findings and dose of contrast medium used for PCI, were similar between the 2 groups. AKI group had higher incidence of in-hospital cardiac death (P=0.0004) and major adverse cardiac events (MACE, P=0.020) during the follow-up compared with non-AKI group. AKI was associated with greater LV end-diastolic (P=0.006) and end-systolic volumes (P=0.007) and lower ejection fraction (P=0.012) 2 weeks after MI, although these parameters on admission were similar between the 2 groups. WBC count on admission (P=0.004) and peak CRP (P=0.0009) were higher in AKI group than in non-AKI group, despite no significant difference in peak CK. Plasma norepinephrine on admission, IL-6 and MDA-LDL 2 weeks after MI were higher in AKI group than non-AKI group. Multiple logistic regression analysis revealed that significant determinants of AKI on admission were WBC count ≥13,000/mm3, age ≥70 years and eGFR< 60 ml/min/1.73m2 . Cox proportional hazards model analysis revealed that AKI was an independent predictor of MACE (HR=2.38, P=0.019).
Conclusions: AKI after reperfused STEMI was a strong predictor of short- and long-term clinical outcomes in association with exaggerated LV remodeling. Enhanced inflammatory response, oxidative stress and neurohormonal activation may synergistically accelerate renal dysfunction and LV remodeling after STEMI.