Circulation, Vol 52, 1097-1104, Copyright © 1975 by American Heart Association
RE Kerber, ML Marcus, J Ehrhardt, R Wilson and FM Abboud
In order to evaluate the relationship between regional myocardial perfusion
and segmental dyskinesis, 22 open chest dogs were studied using ultrasound
to register cardiac wall motion and radioactive labeled microspheres to
determine myocardial perfusion. In six dogs, motion and perfusion were
correlated at two levels of partial circumflex coronary artery occlusion
followed by complete occlusion. A good correlation between declining
myocardial perfusion of all the ischemic segments and development of
aneurysmal bulging (during isometric contraction) was seen: r = minus 0.80.
A similar correlation between myocardial perfusion and endocardial wall
velocity (during systolic ejection) was observed: r = 0.92. In nine dogs,
the effect of 45 minutes of complete coronary occlusion followed by 30
minutes of reperfusion was evaluated with respect to perfusion and motion.
After coronary reperfusion myocardial perfusion of the ischemic area
returned to control levels (from 32.6 +/- 3.5 to 130.3 +/- 13.3 ml/100
g/min), but aneurysmal bulging during isometric contraction persisted.
Endocardial wall velocity during systolic ejection showed a variable
response to reperfusion, achieving values ranging from 32% to 162% of the
preocclusion levels. In seven dogs the ultrasound beam was reflected off
nonischemic myocardium adjacent to areas of ischemia resulting from
coronary occlusion. Despite preservation of normal myocardial perfusion in
these nonischemic areas wall motion abnormalities were evident: endocardial
wall velocity declined from 25.8 +/- 5.8 to 14.0 +/- 4.9 mm/sec (P less
than 0.01), and aneurysmal bulging in three animals. These changes may be
due to transient undetected ischemia in the segments struck by the
ultrasound beam, or to passive alteration of the motion of the normally
perfused areas by the severe dyskinesis of the adjacent ischemic
myocardium.
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