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Left ventricular systolic series elastic properties in aortic stenosis before and after valve replacement


Ritter, M; Hess, O M; Murakami, T; Jenni, R; Egloff, L; Nonogi, H; Schneider, J; Krayenbuehl, H P (1988). Left ventricular systolic series elastic properties in aortic stenosis before and after valve replacement. Cardiovascular Research, 22(11):759-767.

Abstract

In seven patients with aortic valve disease the time course of an auxotonic beat was compared with that of an isovolumetric beat produced by aortic cross clamping during open heart surgery. The rate of systolic stress rise (dS/dt; g·cm−2) of the isovolumetric beat at peak meridional wall stress (Sp; g·cm−2) of the auxotonic beat was determined by tipmanometry and simultaneous sonomicrometry and was found to be 87% of maximum dS/dt. In the second part of the study the stiffness index (k) was calculated in patients undergoing cardiac catheterisation according to: k = 0.87·(max·dS/dt)/Sp·Vcf, where Vcf = normalised midwall circumferential fibre shortening velocity (circ·s−1). In 22 patients, 10 controls and 12 patients with aortic stenosis before (pre) and after (post) valve replacement the systolic stiffness index k (circ−1) was determined using tipmanometry and frame by frame angiocardiography. Muscle fibre diameter and interstitial fibrosis were assessed from left ventricular endomyocardial biopsies. The systolic stiffness index k was 15 circ−1 in controls, 14 in preoperative patients with aortic stenosis and 12 (p<0.01 v controls) in postoperative patients. There was a significant correlation between k and muscle fibre diameter (r = 0.55; p<0.01) but not between k and interstitial fibrosis or ejection fraction. We conclude that systolic stiffness index k is normal despite marked left ventricular hypertrophy in preoperative patients with aortic stenosis. Following successful valve replacement systolic stiffness index decreased and was significantly lower than in controls. Series elasticity appears to be determined by structures related to the muscle cell rather than to interstitial fibrosis

Abstract

In seven patients with aortic valve disease the time course of an auxotonic beat was compared with that of an isovolumetric beat produced by aortic cross clamping during open heart surgery. The rate of systolic stress rise (dS/dt; g·cm−2) of the isovolumetric beat at peak meridional wall stress (Sp; g·cm−2) of the auxotonic beat was determined by tipmanometry and simultaneous sonomicrometry and was found to be 87% of maximum dS/dt. In the second part of the study the stiffness index (k) was calculated in patients undergoing cardiac catheterisation according to: k = 0.87·(max·dS/dt)/Sp·Vcf, where Vcf = normalised midwall circumferential fibre shortening velocity (circ·s−1). In 22 patients, 10 controls and 12 patients with aortic stenosis before (pre) and after (post) valve replacement the systolic stiffness index k (circ−1) was determined using tipmanometry and frame by frame angiocardiography. Muscle fibre diameter and interstitial fibrosis were assessed from left ventricular endomyocardial biopsies. The systolic stiffness index k was 15 circ−1 in controls, 14 in preoperative patients with aortic stenosis and 12 (p<0.01 v controls) in postoperative patients. There was a significant correlation between k and muscle fibre diameter (r = 0.55; p<0.01) but not between k and interstitial fibrosis or ejection fraction. We conclude that systolic stiffness index k is normal despite marked left ventricular hypertrophy in preoperative patients with aortic stenosis. Following successful valve replacement systolic stiffness index decreased and was significantly lower than in controls. Series elasticity appears to be determined by structures related to the muscle cell rather than to interstitial fibrosis

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Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:1 November 1988
Deposited On:18 Oct 2018 06:12
Last Modified:24 Nov 2018 02:59
Publisher:Oxford University Press
ISSN:0008-6363
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1093/cvr/22.11.759
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicenceoxford101093cvr2211759 (Library Catalogue)

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