Circulation, Vol 79, 744-755, Copyright © 1989 by American Heart Association
HP Krayenbuehl, OM Hess, ES Monrad, J Schneider, G Mall and M Turina
Left ventricular biplane cineangiography, micromanometry, and
endomyocardial biopsies were performed in 27 patients with aortic stenosis
(AS) and in 17 patients with aortic insufficiency (AI). Twenty- three
patients with AS and 15 with AI were restudied at an intermediate time (18
months after successful valve replacement), and nine patients with AS and
six with AI were restudied late (70 and 62 months after surgery). Biopsy
samples were evaluated for muscle fiber diameter, percent interstitial
fibrosis, and volume fraction of myofibrils. In control biopsy samples
obtained from five donor hearts at transplantation, these morphometric
variables averaged 21.2 microns, 7.0%, and 57.2%, respectively. After
surgery, mass determined by cineangiography decreased from 186 to 115 and
94 g/m2 in patients with AS and from 201 to 131 and 93 g/m2 in patients
with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and
28.7 microns in patients with AS and was 31.4, 27.6, and 26.4 microns in
patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7%
in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left
ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2 in
patients with AS and from 42.1 to 28.9 and to 18.9 g/m2 in patients with
AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients
with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the
decrease of muscle mass determined by cineangiography at the intermediate
time after valve replacement is mediated by regression of myocardial
cellular hypertrophy in patients with AS and AI and in addition by a
decrease of fibrous content in patients with AI. Late after surgery, left
ventricular fibrous content also decreases in patients with AS. This late
decrease associated with minor changes of end-diastolic volume may be
important for improvement of increased diastolic myocardial stiffness. Even
6-7 years after valve replacement, incomplete regression of structural
abnormalities of left ventricular hypertrophy still exists compared with
the normal myocardium. The residually increased relative interstitial
fibrosis and the small late postoperative decrease of volume fraction of
myofibrils, associated with a prosthesis-related slight left ventricular
pressure increase, are at the origin of a persistent systolic overload at
the myofibrillar level.
ARTICLES
Left ventricular myocardial structure in aortic valve disease before, intermediate, and late after aortic valve replacement
Division of Cardiology, Medical Policlinic, Institute University Hospital, Zurich, Switzerland.
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J. S. Borer, S. Truter, E. M. Herrold, D. J. Falcone, M. Pena, J. N. Carter, T. F. Dumlao, J. A. Lee, and P. G. Supino Myocardial Fibrosis in Chronic Aortic Regurgitation: Molecular and Cellular Responses to Volume Overload Circulation, April 16, 2002; 105(15): 1837 - 1842. [Abstract] [Full Text] [PDF]
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