Circulation, Vol 69, 855-865, Copyright © 1984 by American Heart Association
OM Hess, M Ritter, J Schneider, J Grimm, M Turina and HP Krayenbuehl
Passive diastolic properties were determined in 10 control patients and 21
patients with aortic valve disease before and 17.5 months after successful
valve replacement. Ten patients had severe aortic stenoses (AS), five had
combined aortic valve lesions (AS + aortic insufficiency [AI]), and six
patients had severe AI. Left ventricular endomyocardial biopsies were
obtained before and after surgery in patients with AS, AS + AI, and AI.
Simultaneous echocardiographic and high-fidelity pressure measurements were
made in all patients, and left ventricular chamber stiffness was calculated
from a viscoelastic pressure-circumference relationship and left
ventricular myocardial stiffness from a viscoelastic stress-strain
relationship. The constant of chamber stiffness, beta', was slightly
although not significantly increased in patients with AS (0.27 before and
0.24 after surgery), but was normal in those with AS + AI (0.22 before and
0.17 after surgery) and slightly decreased in those with AI (0.18 before
and 0.16 after surgery) when compared with in control subjects (0.21). The
constant of myocardial stiffness beta was normal in patients with AS
(13.2), AS + AI (11.5), and AI (11.7) before surgery compared with in the
control group (12.5). beta increased, however, significantly in those with
AS (25.2; p less than .02), but not in those with AS + AI (16.3; NS) and AI
(12.8; NS) after surgery. Myocardial morphologic characteristics showed a
significant decrease in muscle fiber diameter in patients with AS, AS + AI,
and AI, as well as a significant increase in interstitial fibrosis from 15%
to 26% (p less than .05) in those with AS and a slight increase from 15% to
22% (NS) in those with AS + AI and from 19% to 24% (NS) in those with AI.
Left ventricular fibrous content (left ventricular muscle mass index
multiplied by interstitial fibrosis) remained, however, unchanged in all
three groups after aortic valve replacement. In conclusion, left
ventricular chamber stiffness is increased in AS but decreased in AI,
whereas LV myocardial stiffness is normal in patients with aortic valve
disease before surgery. After surgery, left ventricular myocardial
stiffness increased significantly in AS patients but remained unchanged in
those with AI. Postoperative changes in myocardial structure were
characterized by a decrease in muscle fiber diameter and a relative
increase in interstitial fibrosis, whereas fibrous content remained
unchanged. Thus, regression of myocardial hypertrophy in aortic valve
disease is accompanied by an increase of myocardial stiffness in concentric
hypertrophy that is not seen in eccentric hypertrophy.
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Diastolic stiffness and myocardial structure in aortic valve disease before and after valve replacement
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