Characterization of a Model to Independently Study Regression of Ventricular Hypertrophy

William E. Stansfield, Mauricio Rojas, Drew Corn, Monte Willis, Cam Patterson, Susan S. Smyth, Craig H. Selzman

Research output: Contribution to journalArticlepeer-review

42 Scopus citations


Background: Although a host of studies catalogue changes that occur with the development of left ventricular hypertrophy (LVH), there is little information about features related solely to LVH regression. This is due, in part, to a lack of animal models to study this question. While traditional models of aortic banding have provided useful information regarding the development of LVH, a similarly effective model is necessary to study mechanisms associated with LVH regression. Materials and methods: Minimally invasive transverse arch banding was performed in C57BL6 mice using a slipknot technique. Twenty-eight days later, the band was removed. Carotid Doppler velocity gradients were serially measured to assess the degree of aortic constriction. Echocardiography, histology, electron microscopy, and real-time polymerase chain reaction were used to assess functional, structural, and genetic aspects of hypertrophy. Results: Banding of the transverse arch created the expected increase in aortic velocity and gradient between the left and right carotid artery, which normalized with relief of the constriction. Pressure overload resulted in a robust hypertrophic response as assessed by heart weight/body weight ratios, gross and microscopic histology, transthoracic echocardiography, electron microscopy, and hypertrophy gene expression. These markers were reversed within 1 week following debanding and were maintained for up to 4 weeks. Mortality rate for the cumulative procedure was 5% over a 2-month period. Conclusions: These results demonstrate a safe, effective, and reproducible method of promoting LVH regression-avoiding the need for endotracheal intubation, mechanical ventilation, and a second invasive surgery to remove the constriction. The simplicity of this technique combined with the well-known advantages of using the mouse species makes this model both unique and relevant. Ultimately, this model will facilitate focused study of independent mechanisms involved with LVH regression.

Original languageEnglish
Pages (from-to)387-393
Number of pages7
JournalJournal of Surgical Research
Issue number2
StatePublished - Oct 2007

Bibliographical note

Funding Information:
This research was supported by grants from the American College of Surgeons (C.H.S.), Thoracic Surgery Foundation for Research And Education (W.E.S., C.H.S.), and National Institutes of Health (C.P., S.S.). We thank Robert Bagnell, Vicky Madden, and Elena Davis in the Microscopy Services Laboratory, Department of Pathology and Laboratory Medicine at UNC–Chapel Hill, for assistance with electron microscopy experiments; Jackie Kylander of UNC’s Carolina Cardiovascular Biology Center for help with echocardiography studies; Margaret Cloud of the UNC Division of Cardiothoracic Surgery for editorial assistance; and Jianping Jin of the UNC Center for Bioinformatics for statistical review.


  • aortic stenosis
  • heart failure
  • hypertension
  • hypertrophy
  • model
  • murine
  • regression

ASJC Scopus subject areas

  • Surgery


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