Wohlschlaeger, Jeremias and von Winterfeld, Moritz and Milting, Hendrik and El Banayosy, Aly and Schmitz, Klaus Juergen and Takeda, Atsushi and Takeda, Nobuakira and Azhari, Petra and Schmid, Christof and August, Christian and Schmid, Kurt Werner and Baba, Hideo Andreas (2008) Decreased myocardial chromogranin A expression and colocalization with brain natriuretic peptide during reverse cardiac remodeling after ventricular unloading. JOURNAL OF HEART AND LUNG TRANSPLANTATION, 27 (4). pp. 442-449. ISSN 1053-2498,
Full text not available from this repository. (Request a copy)Abstract
Aims: In chronic heart failure, atrial and brain natriuretic peptide expression is increased and serves as a clinical marker of cardiac hypertrophy. Chromogranin A is also up-regulated during chronic heart failure and associated with disease severity and prognosis. Significant decrease of both natriuretic peptide and hypertrophy after left ventricular assist device (LVAD) treatment was reported. This study investigated whether chromogranin A and neural cell adhesion molecule (NCAM)/CD56 are associated with cardiac hypertrophy and regulated by LVAD. Methods: Expression of atrial and brain natriuretic peptide, chromogranin A, and NCAM/CD56 were investigated by immunohistochemistry and morphometricatly quantified in 33 paired myocardial samples before and after LVAD. In a different set of patients, chromogranin A was evaluated in the plasma. Cardiomyocyte colocalization of brain natriuretic peptide and chromogranin A was visualized by immunofluorescence doublestaining. Results: Natriuretic peptide and chromogranin A protein expression is significantly decreased after LVAD (P < 0.05). NCAM/CD56 expression remains unaltered by unloading. In contrast with natriuretic peptide, chromogranin A and NCAM/CD56 expression is not correlated with cardiomyocyte diameters. Although increased compared with controls, no significant differences for chromogranin A plasma levels were found before and after LVAD. Sarcoplasmic colocalization of chromogranin A and brain natriuretic peptide is considerably decreased after LVAD. Conclusions: Neither chromogranin A nor CD56 is associated with cardiac hypertrophy. Chromogranin A is significantly decreased by ventricular support. Sarcoplasmic colocalization of brain natriuretic peptide and chromogranin A is diminished after unloading. However, owing to its low expression, the negative regulation of chromogranin A is not reflected by plasma levels and thus does not appear to be an appropriate biomarker of reverse cardiac remodeling after unloading.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ASSIST DEVICE SUPPORT; HEART-FAILURE; WORKING HEART; PLASMA; VASOSTATINS; MORTALITY; FRAGMENT; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Herz-, Thorax- und herznahe Gefäßchirurgie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 05 Nov 2020 06:25 |
| Last Modified: | 05 Nov 2020 06:25 |
| URI: | https://pred.uni-regensburg.de/id/eprint/31115 |
Actions (login required)
 |
View Item |
