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Usefulness of low-dose dobutamine stress echocardiography for evaluating reversibility of brain death-induced
1Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan.
Insights
Brain death can cause reversible myocardial dysfunction. Low-dose dobutamine stress echocardiography can identify this reversible dysfunction in brain-dead patients, potentially improving donor heart utilization.
Area of Science:
- Cardiology
- Transplantation Medicine
- Critical Care Medicine
Background:
- Myocardial dysfunction is common in brain-dead organ donors.
- Reversible myocardial dysfunction may not preclude donor heart transplantation.
- Brain death can induce myocardial dysfunction, impacting donor organ viability.
Purpose of the Study:
- To observe the natural course of brain death-induced myocardial dysfunction.
- To investigate if low-dose dobutamine stress echocardiography can identify reversible myocardial dysfunction in brain-dead patients.
Main Methods:
- Prospective measurement of left ventricular fractional shortening (FS) and cardiac troponin T in 30 brain-dead patients.
- Division of patients into two groups based on FS at brain death (Group I: FS ≥30%, Group II: FS <30%).
- Dobutamine stress echocardiography performed in Group II patients to assess myocardial response.
Main Results:
- Four of seven Group II patients showed dobutamine-nonresponsive dysfunction (Group IIa), with markedly elevated troponin T.
- Three of seven Group II patients showed dobutamine-responsive dysfunction (Group IIb), with normalized FS and stable troponin T after 7 days.
- Group I patients maintained normal FS and troponin T until cardiac standstill.
Conclusions:
- Brain death-induced myocardial dysfunction can be reversible.
- Low-dose dobutamine stress echocardiography is a potential tool for identifying reversible myocardial dysfunction in brain-dead donors.
- These findings suggest that myocardial dysfunction should not automatically exclude donor hearts.
Abstract:
Many of the myocardial wall motion abnormalities in heart donors are reversible after transplantation, indicating that the presence of wall motion abnormalities should not automatically lead to the exclusion of donor hearts. The present study observes the natural course of brain death-induced myocardial dysfunction, and investigates whether low-dose dobutamine stress echocardiography 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 from admission to the time of cardiac standstill in 30 brain-dead patients. Patients were divided into 2 groups according to FS at the time of brain death; group I (FS > or =30%) and group II (FS <30%). Dobutamine stress echocardiography was performed in group II. Twenty-three patients 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 (group IIb). Troponin T at the time of brain death was markedly higher in group 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 not increased until cardiac standstill in group I. FS remained decreased and troponin T remained elevated until cardiac standstill in group IIa, whereas 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 reversible and low-dose dobutamine stress echocardiography may identify reversible myocardial dysfunction.