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Author Notes:

Correspondence: Yanggan Wang, Email: yanggan.wang@emory.edu

Subject:

Research Funding:

This work was supported by grants awarded to Yanggan Wang from the NIH (R21HL-088168, R01HL-083271), American Health Assistant Foundation (H2007-019), and Emory University (seed grant 280263, pilot grant 33059), as well as support from Children's Healthcare of Atlanta.

Yibing Nong is a fellow also supported by Beijing New Star Project of Science and Technology (2008A058).

Keywords:

  • Echocardiography
  • Heart failure
  • Hypertrophy
  • Murine

A Juvenile Murine Heart Failure Model of Pressure Overload

Tools:

Journal Title:

Pediatric Cardiology

Volume:

Volume 32, Number 2

Publisher:

, Pages 145-153

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Persistent pressure overload can cause cardiac hypertrophy and progressive heart failure (HF). The authors developed a pressure-overload HF model of juvenile mice to study the cardiac response to pressure overload that may be applicable to clinical processes in children. Severe thoracic aortic banding (sTAB) was performed using a 28-gauge needle for 40 juvenile (age, 3 weeks) and 47 adult (age, 6 weeks) C57BL/6 male mice. To monitor the structural and functional changes, M-mode echocardiography was performed for conscious mice that had undergone sTAB and sham operation. Cardiac hypertrophy, dilation, and HF occurred in both juvenile and adult mice after sTAB. Compared with adults, juvenile HF is characterized by greater impairment of ventricular contractility and less hypertrophy. In addition, juvenile mice had significantly higher rates of survival than adult mice during the early postoperative weeks. Consistent with clinical HF seen in children, juvenile banded mice demonstrated a lower growth rate than either adult banded mice or juvenile control mice that had sham operations. The authors first developed a juvenile murine model of pressure-overload HF. Learning the unique characteristics of pressure-overload HF in juveniles should aid in understanding age-specific pathologic changes for HF development in children.

Copyright information:

© Springer Science+Business Media, LLC 2010

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