C-reactive protein co-expresses with tumor necrosis factor-alpha in the myocardium in human dilated cardiomyopathy

Mamoru Satoh1, Motoyuki Nakamura, Tomonari Akatsu

  • 1Second Department of Internal Medicine, Iwate Medical University School of Medicine, Uchimaru 19-1, Morioka 020-8505, Iwate, Japan. m_satoh@imu.ncvc.go.jp

Insights

C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-alpha) are elevated in dilated cardiomyopathy (DCM) patients, correlating with disease severity. Treatment with spironolactone and ACEIs/ARBs reduced these inflammatory markers.

Area of Science:

  • Cardiology
  • Immunology
  • Molecular Biology

Background:

  • C-reactive protein (CRP) is found in cardiac tissue, stimulating proinflammatory cytokines.
  • Cardiac tumor necrosis factor-alpha (TNF-alpha) is crucial in dilated cardiomyopathy (DCM) pathogenesis.

Purpose of the Study:

  • Investigate CRP and TNF-alpha co-expression in DCM myocardium.
  • Examine the association between CRP/TNF-alpha and clinical features in DCM patients.

Main Methods:

  • Real-time RT-PCR to measure CRP and TNF-alpha mRNA in endomyocardial biopsies from 41 DCM patients and 16 controls.
  • Immunohistochemistry and in situ hybridization to identify cellular sources of CRP and TNF-alpha.
  • Correlation analysis of mRNA levels with clinical parameters and treatment regimens.

Main Results:

  • Both CRP and TNF-alpha mRNA were expressed in DCM myocardium, but not in controls.
  • CRP and TNF-alpha levels positively correlated and were localized in cardiomyocytes.
  • Elevated mRNA levels correlated with reduced systolic function and increased left ventricular volume.
  • mRNA levels were lower in patients treated with spironolactone plus ACEIs or ARBs.

Conclusions:

  • Cardiac CRP and TNF-alpha may act as proinflammatory mediators in DCM, linked to clinical severity.
  • Expression of CRP and TNF-alpha decreased with spironolactone and ACEI/ARB treatment in DCM patients.
Abstract

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