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J Thorac Cardiovasc Surg 1994;107:647-0648
© 1994 Mosby, Inc.
Letters to the Editor |
Hôpital Cardiologique du Haut-Lévêque
Pessac, France
To the Editor:
We read with great interest the recent report by Vincent and colleagues
1 on the use of prostaglandin E1 combined with left atrial norepinephrine infusion to treat right ventricular failure in the postoperative period after heart transplantation. We report on a patient in whom a similar technique allowed weaning from cardiopulmonary bypass (CPB), which otherwise would have been impossible.
A 57-year-old man with end-stage cardiac failure caused by ischemic heart disease had an initial pulmonary vascular resistance of 7.4 Wood units, but this fell to 4 Wood units after intensive treatment with vasodilators and inotropic agents, indicating borderline suitability for heart transplantation. Urgent cardiac transplantation was carried out after sudden deterioration in cardiac function led to decompensation and acute renal failure. A local, morphologically compatible donor heart was implanted in standard fashion. Donor ischemic time was 105 minutes. At an attempt to discontinue CPB, there was evidence of right ventricular failure, with a right atrial pressure of as much as 28 mm Hg despite a low left atrial pressure of 4 mm Hg. Weaning from bypass proved impossible despite the use of dopamine and isoprenaline. Prostacyclin was then infused into the right atrial line, producing a drop in right atrial pressure on attempted discontinuation of CPB, but this was associated with systemic hypotension to 40 mm Hg followed by biventricular dysfunction caused by impaired coronary perfusion and the necessity to reinstitute CPB. After 3
hours and eight attempts to discontinue CPB, norepinephrine was infused into the left atrium with concomitant prostacyclin infusion into the right atrium. The patient was weaned off bypass within 3 minutes of this manipulation with a systemic systolic pressure of 95 mm Hg and right and left atrial pressures of 5 mm Hg, without the use of other inotropic agents. Treatment by biatrial infusion was gradually reduced in the postoperative period and finally stopped at 3 days after operation. During this period, serum norepinephrine concentration was serially measured in radial arterial samples and in mixed venous samples; arterial concentration was consistently 1.5 times venous concentration. Echocardiography at 1 week confirmed good biventricular function of the transplanted heart. The patient remained hemodynamically well with no evidence of right ventricular dysfunction but unfortunately died at 3 months after operation of fulminating sepsis associated with a cerebral abscess.
Fixed pulmonary vascular resistance (PVR) is normally considered a contraindication to transplantation,
2 but the extent and reversibility of elevated PVR may be difficult to determine with certainty. When patients with elevated PVR undergo cardiac transplantation with an "unconditioned" heart, severe right ventricular failure develops and may lead to death from inability to wean the patient from CPB. Although prostacyclin is effective in reducing PVR, its effect on systemic vascular resistance may be so marked as to lead to unacceptable systemic hypotension with poor coronary perfusion. It makes little sense to infuse both drugs into the venous circulation because their effects on PVR would cancel one another. Both norepinephrine and prostacyclin have a short plasma half-life and norepinephrine is removed to a large extent by systemic tissues, as confirmed in the clinical setting by our serial serum assays. This allows selective administration of each drug precisely where needed. Vincent and colleagues
1 advise the biatrial administration of prostaglandin E, and norepinephrine in patients who have postoperative evidence of right ventricular dysfunction after transplantation. The dramatic response in our patient leads us to recommend early use of this type of therapy whenever elevated PVR prevents discontinuation of CPB after heart transplantation.
References
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