HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Millner, R. W. Articles by Pepper, J. R. Search for Related Content PubMed PubMed Citation Articles by Millner, R. W. Articles by Pepper, J. R.

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.

This article has been cited by other articles:

				A.K. Hasnat, E. T. van der Velde, J. K.F. Hon, and M. H. Yacoub Reproducible model of post-infarction left ventricular dysfunction: haemodynamic characterization by conductance catheter Eur. J. Cardiothorac. Surg., July 1, 2003; 24(1): 98 - 104. [Abstract] [Full Text] [PDF]

				G. Sakaguchi, Y. Sakakibara, K. Tambara, F. Lu, G. Premaratne, K. Nishimura, and M. Komeda A pig model of chronic heart failure by intracoronary embolization with gelatin sponge Ann. Thorac. Surg., June 1, 2003; 75(6): 1942 - 1947. [Abstract] [Full Text] [PDF]

				M. T. Rademaker, V. A. Cameron, C. J. Charles, E. A. Espiner, M. G. Nicholls, C. J. Pemberton, and A. M. Richards Neurohormones in an ovine model of compensated postinfarction left ventricular dysfunction Am J Physiol Heart Circ Physiol, March 1, 2000; 278(3): H731 - H740. [Abstract] [Full Text] [PDF]

				Y. Toyoda, M. Okada, and M. A. Kashem A canine model of dilated cardiomyopathy induced by repetitive intracoronary doxorubicin administration J. Thorac. Cardiovasc. Surg., June 1, 1998; 115(6): 1367 - 1374. [Abstract] [Full Text] [PDF]

				R. R. Waterford, J. R. Van Camp, M. A. Gallagher, M. T. Anderson, S. F. Bolling, and L. A. Brunsting III Adjustable Model of Chronic Left Ventricular Dysfunction Ann. Thorac. Surg., December 1, 1997; 64(6): 1682 - 1685. [Abstract] [Full Text]

				A. A. Hagege, M. Desnos, F. Fernandez, B. Besse, N. Mirochnik, M. Castaldo, J. C. Chachques, A. Carpentier, and C. Guerot Clinical Study of the Effects of Latissimus Dorsi Muscle Flap Stimulation After Cardiomyoplasty Circulation, November 1, 1995; 92(9): 210 - 215. [Abstract] [Full Text]