Circulation, Vol 74, 126-134, Copyright © 1986 by American Heart Association
PB Kurnik, MR Courtois and PA Ludbrook
To determine whether alteration of intrinsic myocardial stiffness is
responsible for the reduction of left ventricular filling pressure and
volume by nifedipine in patients with impaired baseline ventricular
function, we evaluated the hemodynamic responses in 32 patients undergoing
diagnostic cardiac catheterization. Micromanometric pressure and
ventriculographic dimensional data were acquired before and 30 min after
randomly assigned administration of nifedipine (20 mg sublingual) or
placebo. A mathematical model requiring no assumptions about the
stress-radius relationship or direct measurement of strain was used. No
hemodynamic variables were changed after placebo. Left ventricular end-
diastolic volume and pressure declined and cardiac output increased after
nifedipine, particularly in subjects with impaired ventricular performance.
Despite these salutary effects, intrinsic myocardial stiffness, elastic
stiffness at a common level of stress, chamber stiffness, and rate of
isovolumic relaxation were unchanged after nifedipine, even in patients
with abnormal baseline ventricular function. The potent peripheral
arteriodilator effect of nifedipine, rather than any direct myocardial or
ventricular effects, appears to be responsible for the improved systolic
and diastolic performance.
ARTICLES
Effects of nifedipine on intrinsic myocardial stiffness in man
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