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(Circulation. 1997;95:1349-1351.)
© 1997 American Heart Association, Inc.

Articles

On Variations in the Cardiac Hypertrophic Response to Pressure Overload

John Ross, Jr, MD

the Division of Cardiology, Department of Medicine, University of California San Diego School of Medicine, La Jolla, Calif.

Correspondence to John Ross, Jr, MD, UCSD School of Medicine 0613B, 9500 Gilman Dr, BSB Room 5026, La Jolla, CA 92093-0613. E-mail jross@ucsd.edu

Key Words: Editorials • hypertrophy • pressure • contractility • heart diseases • ventricles

	Introduction

 
This issue of Circulation contains an interesting and provocative study concerning the prediction of differences in cardiac hypertrophy and function in response to pressure overload. Koide et al,¹ using a canine model of controlled, progressive ascending aortic constriction over an 8-week period, report that 5 dogs having a relatively high left ventricular (LV) mass to body weight ratio (LVM/BW) before constriction (calculated by angiography) as well as a high mean normalized systolic ejection rate and low systolic wall stress developed compensatory hypertrophy and maintained normal LV function. The remaining 10 dogs with aortic constriction had a lower initial LVM/BW, developed significantly less hypertrophy, and evidenced late LV dysfunction with decreased contractility; the presence of intrinsic myocardial depression in the latter group at the end of the study also was documented by studies of function of isolated myocytes taken from these ventricles. Studies performed under anesthesia with ß-adrenergic blockade showed higher levels of afterload (mean systolic wall stress) and lower mean systolic ejection rates both before and after aortic constriction in the group developing LV dysfunction, although both groups fell within the normal range of the inverse relation between afterload and ejection rate before aortic constriction. In a subsequent group of animals, the presence of a higher wall stress (a preselected value 115 kdyne/cm²) before aortic constriction was associated with the late development of LV dysfunction in 75% of animals, whereas an initial LV wall stress below that value was associated with normal LV function at the final study in . . . [Full Text of this Article]

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