Circulation, Vol 67, 316-323, Copyright © 1983 by American Heart Association
PD Bourdillon, BH Lorell, I Mirsky, WJ Paulus, J Wynne and W Grossman
The left ventricular diastolic pressure-volume relationship shifts upward
during angina, but why this happens is not known. To assess regional
myocardial stiffness, we studied 12 patients who had coronary artery
disease using simultaneous left ventricular micromanometer pressure
recording and M-mode echocardiography before and during angina induced by
pacing tachycardia. All patients had two- or three-vessel coronary artery
disease that involved the posterior left ventricular wall circulation and
had positive pacing stress tests, i.e., development of angina and a
postpacing rise in left ventricular end- diastolic pressure (15 +/- 3 to 31
+/- 6 mm Hg, p less than 0.001). A marked upward shift in the relationship
between the diastolic left ventricular pressure and the posterior wall
thickness (h) occurred after pacing tachycardia, but the change in left
ventricular posterior wall end-diastolic thickness was minimal (8.9 +/- 2.1
to 9.2 +/- 2.1 mm, NS). After pacing, the peak rate of left ventricular
posterior wall thinning decreased (82 +/- 37 to 48 +/- 27 mm/sec, p less
than 0.005) and the time constant of relaxation derived from the best
exponential fit to the isovolumic left ventricular pressure decay increased
(49 +/- 5 to 58 +/- 7 msec, p less than 0.001). Diastolic active left
ventricular pressure decay, extrapolated from the exponential fit, was
subtracted from the measured left ventricular pressure (which is equal in
magnitude but opposite in sign to the radial stress at the endocardium) to
calculate residual left ventricular pressure (PR) and hence residual stress
(sigma R = -PR). A radial stiffness modulus (ER) was determined by the
slope of the PR vs log h plots before and after pacing. Over the same range
of residual radial stress (sigma R), ER was always higher during
pacing-induced angina, indicating increased residual myocardial stiffness.
Increased myocardial stiffness in addition to a decreased rate of wall
thinning and slow active pressure decay contribute to the upward shift in
left ventricular pressure-wall thickness and pressure-volume relationships
during pacing-induced angina.
ARTICLES
Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man
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