| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J Thorac Cardiovasc Surg 2002;124:641-642
© 2002 The American Association for Thoracic Surgery
Letters to the Editor |
Department of Cardiothoracic Surgery and Anaesthesiology, Karolinska Institute, Huddinge University Hospital, SE-141 86 Stockholm, Sweden
To the Editor:
Extracorporeal membrane oxygenation (ECMO) has been suggested as a successful rescue intervention in primary allograft failure.
1 Taghavi and coworkers reported their experience of 6 patients supported by ECMO because of right or biventricular failure after cardiac transplantation. Five patients were successfully weaned from ECMO, but 2 of these died of sepsis-induced multiorgan failure. All patients were in cardiac failure before initiation of ECMO despite maximal drug treatment, which in their institution included high doses of norepinephrine and suprarenin. They also discussed the possibilities of using nitric oxide and alprostadil (prostaglandin E1) to reduce pulmonary vascular resistance.
However, a number of additional supporting options should be considered before ECMO. 2 These include phosphodiesterase III inhibitors (milrinone), inhalation of pure oxygen, and the use of the intra-aortic balloon pump (IABP).
We report our recent experience with biventricular failure early after cardiac transplantation. A 60-year-old woman weighing 68 kg had a dilated cardiomyopathy (left ventricular end-diastolic diameter 76 mm), an ejection fraction of 15%, a cardiac index of 1.7 L/m2, moderate mitral regurgitation, and a pulmonary vascular resistance of 2.6 Wood units. The patient received a donor heart with an ischemic time of 256 minutes. She was easily weaned from cardiopulmonary bypass with normal doses of milrinone (a bolus of 50 µg/kg and an infusion of 0.50 µg · kg-1 · min-1), dopamine, and epinephrine. Two hours later, biventricular failure developed rapidly, with the cardiac index dropping below 1.3 L/m2, despite increasing doses of epinephrine and ventilation with pure oxygen. We initially inserted an IABP with only moderate improvement of hemodynamics and considered the use of ECMO. However, we tried a megadose of milrinone (14 mg) followed by a high-dose infusion of milrinone (0.75 µg · kg-1 · min-1) as well as norepinephrine to counteract the induced systemic hypotension. The patient experienced a quick and lasting improvement in cardiac index to above 2.5 L/m2, and ECMO was not necessary. Repeated postoperative transthoracic echocardiographic examinations have shown normal right and left ventricular function.
We believe that this dramatic improvement was due to the aggressive use of milrinone and suggest that a megadose of milrinone is an attractive option in the treatment of cardiac failure after cardiac transplantation. Unlike most other inotropic agents, milrinone does not increase myocardial oxygen demand and can be synergistically combined with beta agonists to improve hemodynamics. In surviving animals, milrinone infusion led to significant increases in right ventricular function, which occurred in association with significant improvements in pulmonary vascular impedance and transpulmonary efficiency. 3
12/8/125483
doi:10.1067/mtc.2002.125483
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
