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Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
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Published on: April 17, 2021

Decreased myocardial chromogranin a expression and colocalization with brain natriuretic peptide during reverse

Jeremias Wohlschlaeger1, Moritz von Winterfeld, Hendrik Milting

  • 1Department of Pathology and Neuropathology, University Hospital Essen, University of Duisburg-Essen, Germany.

The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation
|April 1, 2008
PubMed

Insights

Left ventricular assist device (LVAD) treatment decreases chromogranin A expression, but not neural cell adhesion molecule (NCAM)/CD56, in heart failure patients. Neither marker correlates with cardiac hypertrophy, and plasma chromogranin A is not a reliable biomarker for reverse remodeling.

Area of Science:

  • Cardiology
  • Biomarkers
  • Heart Failure Research

Background:

  • Chronic heart failure elevates natriuretic peptides and chromogranin A, markers of cardiac hypertrophy and disease severity.
  • Left ventricular assist device (LVAD) treatment has been shown to reduce natriuretic peptides and hypertrophy.

Purpose of the Study:

  • To investigate the association of chromogranin A and neural cell adhesion molecule (NCAM)/CD56 with cardiac hypertrophy.
  • To determine if LVAD treatment regulates chromogranin A and NCAM/CD56 expression and their relation to reverse cardiac remodeling.

Main Methods:

  • Immunohistochemistry and morphometric quantification of atrial and brain natriuretic peptide, chromogranin A, and NCAM/CD56 in paired myocardial samples before and after LVAD.
  • Evaluation of plasma chromogranin A levels.
  • Immunofluorescence double staining to visualize cardiomyocyte colocalization of brain natriuretic peptide and chromogranin A.

Main Results:

  • LVAD treatment significantly decreased natriuretic peptide and chromogranin A protein expression (p < 0.05), while NCAM/CD56 remained unchanged.
  • Chromogranin A and NCAM/CD56 expression did not correlate with cardiomyocyte diameters, unlike natriuretic peptides.
  • Plasma chromogranin A levels showed no significant difference before and after LVAD, and sarcoplasmic colocalization of chromogranin A and brain natriuretic peptide decreased post-LVAD.

Conclusions:

  • Chromogranin A and CD56 are not associated with cardiac hypertrophy in heart failure.
  • Ventricular support via LVAD significantly reduces chromogranin A expression and its colocalization with brain natriuretic peptide.
  • Plasma chromogranin A is not a suitable biomarker for assessing reverse cardiac remodeling after LVAD due to low expression and lack of correlation with ventricular unloading.
Abstract

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