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Front Pediatr. 2013 Oct 28;1:33. doi: 10.3389/fped.2013.00033. eCollection 2013.

Congestive heart failure: experimental model.

Frontiers in pediatrics

Antonio Francesco Corno, Xue Cai, Caroline B Jones, Giuseppina Mondani, Mark R Boyett, Jonathan Charles Jarvis, George Hart

Affiliations

  1. School of Medical Sciences, Health Campus, University Sains Malaysia , Kubang Kerian, Kelantan , Malaysia.
  2. Core Technology Facility, University of Manchester , Manchester , UK.
  3. Core Technology Facility, University of Manchester , Manchester , UK ; Alder Hey Children NHS Foundation Trust , Liverpool , UK.
  4. John Moores University , Liverpool , UK.

PMID: 24400279 PMCID: PMC3864258 DOI: 10.3389/fped.2013.00033

Abstract

INTRODUCTION: Surgically induced, combined volume and pressure overload has been used in rabbits to create a simplified and reproducible model of acute left ventricular (LV) failure.

MATERIALS AND METHODS: New Zealand white male rabbits (n = 24, mean weight 3.1 ± 0.2 kg) were randomly assigned to either the Control group (n = 10) or to the Heart Failure group (HF, n = 14). Animals in the Control group underwent "sham" procedures. Animals in the HF group underwent procedures to induce LV volume overload by inducing severe aortic valve regurgitation with aortic cusp disruption and pressure overload using an occlusive silver clip positioned around the pre-renal abdominal aorta.

RESULTS: Following Procedure-1 (volume overload) echocardiography confirmed severe aortic regurgitation in all animals in the HF group, with increased mean pulse pressure difference from 18 ± 3 to 38 ± 3 mmHg (P < 0.0001). After Procedure-2 (pressure overload) all animals in the HF group showed clinical and echocardiographic signs of constriction of the abdominal aorta and echocardiography confirmed progressively declining LV function. At the end of the protocol there was a significant increase of the heart/body weight ratio in the HF group vs. Control group (4.6 ± 0.2 vs. 2.9 ± 0.1 g/kg, P < 0.05), and echocardiography showed in HF group significant increase of the LV end-diastolic diameter (2.15 ± 0.09 vs. 1.49 ± 0.03 cm, P < 0.001) and reduction of the LV shortening fraction (26.3 ± 3.8 vs. 41.3 ± 1.6%, P < 0.001).

CONCLUSION: This experimental model: (a) consistently produces LV hypertrophy/dilatation and subsequent congestive heart failure, (b) provides new data on the time course of LV dilatation, hypertrophy and failure, (c) allows study of the progress and evolution of LV systolic and diastolic dysfunction in the presence of induced LV failure, (d) is suitable to study intervention or pharmacological administration to reduce the negative effects of acute LV failure.

Keywords: congestive heart failure; experimental research; left heart failure; ventricular dilatation; ventricular hyprtrophy

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