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The Annals of Thoracic Surgery, Vol 52, 78-83, Copyright © 1991 by The Society of Thoracic Surgeons


ARTICLES

Experimental model of left ventricular failure

RW Millner, JM Mann, I Pearson and JR Pepper
Department of Cardiothoracic Surgery, St. George's Hospital, London, United Kingdom.

A model of chronic cardiac failure has undergone extensive hemodynamic investigation. Under anesthesia the homonymous and second diagonal coronary arteries of sheep have been ligated. The resulting myocardial infarction caused significant acute hemodynamic impairment (paired two- tailed t tests), mean pulmonary artery pressure increasing from 7.31 +/- 0.94 to 13.80 +/- 1.19 mm Hg (p less than 0.001), pulmonary artery diastolic pressure increasing from 4.94 +/- 1.03 to 11.13 +/- 1.27 mm Hg (p less than 0.001), and directly measured left ventricular end- diastolic pressure increasing from 9.31 +/- 1.52 to 17.42 +/- 1.82 mm Hg (p less than 0.001) after infarction documented with invasive monitoring. There was a hemodynamically significant left ventricular aneurysm (paired two-tailed t tests) in animals studied 3 months later, with increased mean pulmonary artery pressure from 7.20 +/- 1.15 to 13.80 +/- 2.00 mm Hg (p = 0.009), an increase in pulmonary artery diastolic pressure from 4.60 +/- 1.30 to 12.10 +/- 2.06 mm Hg (p = 0.006), and an increase in left ventricular end-diastolic pressure from 11.00 +/- 1.94 mm Hg before infarction to 17.00 +/- 2.69 mm Hg (p = 0.038). We conclude that this is a useful model of chronic left ventricular failure that is reproducible and applicable to investigations of therapeutic options in chronic heart failure.


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