Circulation, Vol 87, 247-260, Copyright © 1993 by American Heart Association
A Gomez, H Unruh and SN Mink
BACKGROUND. In chronic obstructive lung disease, a right to left
ventricular septal shift that occurs as a consequence of right ventricular
pressure overload is the usual mechanism given to explain a decrease in
left ventricular (LV) diastolic performance. The purpose of the present
study was to examine the extent to which this mechanism could account for a
decrease in LV diastolic function in a canine model in which pulmonary
artery pressure was elevated to a level found in human disease. METHODS AND
RESULTS. Severe emphysema was produced in dogs by repeated instillations of
the enzyme papain into the lung. To assess LV diastolic function, we used
sonomicrometry, in which three pairs of subendocardial crystal transducers
were implanted along the three orthogonal axes of the LV. LV end-diastolic
dimensions and pressure-strain relations along the three axes, as well as
the time constant of LV isovolumic relaxation (T), were measured before
(baseline) and after 1 year of emphysema (post-1-year study). The results
showed that after 1 year of pulmonary hypertension, LV pressure- strain
relations were decreased along the septal-lateral and anterior- posterior
axes, but a right to left ventricular septal shift was not detected. The
relation of average midwall circumferential stress to midwall
circumferential strain was used to describe the intrinsic compliance of the
LV. The results showed that myocardial stiffness increased in emphysema but
that chamber volume was not reduced. At the post-1-year study, T was
abnormally increased in the emphysema group in response to augmented
preload and afterload compared with preemphysema measurements. CONCLUSIONS.
We conclude that mechanisms other than ventricular interdependence may be
operative in leading to altered LV diastolic filling in chronic emphysema.
ARTICLES
Altered left ventricular chamber stiffness and isovolumic relaxation in dogs with chronic pulmonary hypertension caused by emphysema
Department of Medicine, University of Manitoba, Winnipeg, Canada.
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