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Ann Thorac Surg 1991;52:78-83
© 1991 The Society of Thoracic Surgeons

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Articles

Experimental model of left ventricular failure

Department of Cardiothoracic Surgery, St. George's Hospital, London, United Kingdom

Accepted for publication March 1, 1991.

^_* Address reprint requests to Dr Millner, Department of Cardiothoracic Surgery, St. George's Hospital, Blackshaw Rd, London SW17 0QT, UK.

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 < 0.001), pulmonary artery diastolic pressure increasing from 4.94 ± 1.03 to 11.13 ± 1.27 mm Hg (p < 0.001), and directly measured left ventricular enddiastolic pressure increasing from 9.31 ± 1.52 to 17.42 ± 1.82 mm Hg (p < 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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