Circulation, Vol 81, 1688-1696, Copyright © 1990 by American Heart Association
M Courtois, SJ Kovacs and PA Ludbrook
A consistent pattern of intraventricular regional pressure gradients exists
under physiological conditions during the rapid filling phase of diastole
in the normal dog left ventricle. We hypothesized that this pressure
gradient pattern is caused, in part, by early diastolic recoil of the left
ventricular walls in conjunction with release of elastic potential energy
stored during systole, generating suction and thus contributing to
diastolic filling. If so, any condition that interferes with normal
regional systolic function might be expected to modify the pattern of the
normal early diastolic intraventricular pressure gradients. Accordingly,
the present study was designed to determine whether acutely induced
regional systolic left ventricular mechanical dysfunction is accompanied by
changes in the pattern of the early diastolic intraventricular pressure
gradients. Acute myocardial ischemia was induced by balloon occlusion of
the left anterior descending coronary artery (LAD) in nine anesthetized
closed-chest dogs. The maximum early diastolic intraventricular pressure
gradient (MIVP) was measured between the mid-left ventricle and apex with a
dual- sensor micromanometer (3-cm spacing between the sensors) before and
20 minutes after LAD occlusion. Ejection fraction (EF) and number of
dyskinetic chords (DChords) were measured from left ventricular contrast
ventriculograms. Twenty minutes after LAD occlusion, the nine dogs
evidenced significant changes in EF (56 +/- 10% to 37 +/- 8%), DChords (0
+/- 0 to 17 +/- 16 chords), left ventricular minimum pressure (-1.7 +/- 0.5
to 0.0 +/- 1.5 mm Hg), left ventricular end- diastolic pressure (4.2 +/-
1.2 to 5.9 +/- 2.2 mm Hg), and heart rate (90 +/- 17 to 103 +/- 18
beats/min).(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Physiological early diastolic intraventricular pressure gradient is lost during acute myocardial ischemia
Washington University School of Medicine, Cardiovascular Division, St. Louis, MO 63110.
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