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      Serum C-reactive protein elevation in left ventricular remodeling after acute myocardial infarction—role of neurohormones and cytokines

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          Abstract

          We previously reported that increased peak serum C-reactive protein (CRP) level after acute myocardial infarction (AMI) was a major predictor of cardiac rupture and long-term outcome. The aim of this study was to clarify the role of serum CRP elevation as a possible marker of left ventricular (LV) remodeling after AMI. We prospectively studied 31 patients who underwent primary angioplasty for a first anterior Q-wave AMI. Peak serum CRP level was determined by serial measurements after admission. LV volume and the plasma levels of various neurohormones and cytokines were measured on admission, and 2 weeks and 6 months after AMI. Patients with higher peak CRP levels (above the median) had a greater increase in LV end-diastolic volume during 2 weeks after AMI (+21+/-14 vs. +5+/-6 ml/m(2), P=0.001) and a lower ejection fraction (45+/-11 vs. 53+/-7%, P=0.02) than those with lower CRP levels, associated with a higher incidence of pump failure, atrial fibrillation, and LV aneurysm. Plasma levels of norepinephrine, brain natriuretic peptide, and interleukin-6 2 weeks after AMI were higher in the high CRP group than in the low CRP group. Increased peak serum CRP level was associated with a greater increase in LV volume after anterior AMI. Plasma norepinephrine and interleukin-6 levels were increased in patients with higher CRP levels, suggesting a possible role of sympathetic activation and enhanced immune response in the development of LV remodeling after AMI.

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          Author and article information

          Journal
          International Journal of Cardiology
          International Journal of Cardiology
          Elsevier BV
          01675273
          April 2003
          April 2003
          : 88
          : 2-3
          : 257-265
          Article
          10.1016/S0167-5273(02)00416-3
          12714206
          bf695a54-d457-4725-ae63-be631c2dbe8e
          © 2003

          https://www.elsevier.com/tdm/userlicense/1.0/

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