T. Kono et al., Usefulness of low-dose dobutamine stress echocardiography for evaluating reversibility of brain death-induced myocardial dysfunction, AM J CARD, 84(5), 1999, pp. 578-582
Citations number
20
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Many of the myocardial wall motion abnormalities in heart donors are revers
ible after transplantation, indicating that the presence of wall motion abn
ormalities should not automatically lead to the exclusion of donor hearts.
The present study observes the natural course of brain death-induced myocar
dial dysfunction, and investigates whether low-dose dobutamine stress echoc
ardiography could identify reversible myocardial dysfunction in brain-dead
patients. We prospectively measured the serial changes of left ventricular
fractional shortening (FS) using echocardiography and cardiac troponin T fr
om admission to the time of cardiac standstill in 30 brain-dead patients. P
atients were divided into 2 groups according to FS at the time of brain dea
th; group I (FS greater than or equal to 30%) and group II (FS <30%). Dobut
amine stress echocardiography was performed in group II. Twenty-three patie
nts were in group I and 7 patients were in group II. Four patients among 7
patients in group II showed dobutamine-nonresponsive wall motion (group IIa
) and the remaining 3 patients showed dobutamine-responsive wall motion (gr
oup IIb), Troponin T at the time of brain death was markedly higher in grou
p IIa than in groups I and IIb (5.13 +/- 3.79 vs 0.23 +/- 0.20, 0.22 +/- 0.
16 ng/ml, p <0.0001, respectively). FS remained normal and troponin T was n
ot increased until cardiac standstill in group I. FS remained decreased and
troponin T remained elevated until cardiac standstill in group IIa, wherea
s FS became normal at 7 days after brain death with no change in troponin T
in group IIb. Thus, some brain death-induced myocardial dysfunction is rev
ersible and low-dose dobutamine stress echocardiography may identify revers
ible myocardial dysfunction. (C) 1999 by Excerpta Medica, Inc.