Circulation, Vol 74, 815-825, Copyright © 1986 by American Heart Association
JD Carroll, RM Lang, AL Neumann, KM Borow and SI Rajfer
Symptoms of congestive heart failure frequently reflect abnormalities in
both systolic and diastolic performance. While much work has been reported
regarding the mechanisms by which positive inotropic and vasodilator
therapy affect systolic performance, little is known about their effect on
diastolic function. In 12 patients with diffuse congestive cardiomyopathy
micromanometer left ventricular and aortic pressure measurements were
recorded simultaneously with two- dimensionally targeted M mode
echocardiograms and thermodilution- determined cardiac output. Each patient
received dopamine (2, 4, and 6 micrograms/kg/min), and dobutamine (2, 6,
and 10 micrograms/kg/min), and 10 received nitroprusside (0.125 to 2.0
micrograms/kg/min). Baseline hemodynamics were characterized by low cardiac
index (2.1 +/- 0.7 liter/min/m2, mean +/- SD), high left ventricular
end-diastolic pressure (24 +/- 10 mm Hg), and increased end-diastolic (6.8
+/- 1.0 cm) and end-systolic dimensions (6.0 +/- 1.0 cm). All patients had
abnormal left ventricular pressure decay with a prolonged time constant (67
+/- 20 msec) and reduced peak diastolic lengthening rates. Dopamine and
dobutamine decreased the time constant of relaxation and increased the peak
lengthening rate. Dobutamine also reduced the minimum diastolic pressure
from 14 +/- 7 to 10 +/- 9 mm Hg (p less than .01); neither drug reduced
end-diastolic pressure. In fact, dopamine elevated end-diastolic pressures
in seven patients, despite more rapid pressure decay. Diastolic
pressure-dimension relations after dopamine and dobutamine showed a
leftward shift with a reduced end-systolic chamber size, but no significant
changes in passive chamber stiffness. Nitroprusside decreased left
ventricular minimum diastolic pressure by 4 +/- 2 mm Hg and end-diastolic
pressure by 7 +/- 4 mm Hg (p less than .01). It did not consistently
accelerate left ventricular pressure decay at the doses tested. The
decreased end-diastolic pressure with nitroprusside was due to a reduced
end-diastolic dimension in five patients. In the other patients, all of
whom had elevated right atrial pressures, diastolic pressure-dimension
relations showed a parallel downward shift after nitroprusside. Thus,
positive inotropic therapy with beta 1-adrenoceptor agonists enhances early
diastolic distensibility by accelerating relaxation, augmenting filling,
and reducing end-systolic chamber size. Vasodilator therapy is much more
effective in lowering diastolic pressures.(ABSTRACT TRUNCATED AT 400 WORDS)
ARTICLES
The differential effects of positive inotropic and vasodilator therapy on diastolic properties in patients with congestive cardiomyopathy
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