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J Thorac Cardiovasc Surg 1996;111:284-285
© 1996 Mosby, Inc.
LETTERS TO THE EDITOR |
Harefield, United Kingdom
To the Editor:
We were interested to read of the experience of Mertes and associates,
1 because we have had similar experience with the use of inhaled nitric oxide for the implantation of the HeartMate 1000P left ventricular assist system (LVAS) (Thermo Cardiosystems, Inc., Woburn, Mass.). Our patient, similar to theirs, was 54 years old with end-stage idiopathic dilated cardiomyopathy but with additional renal and hepatic failure. We also had difficulty weaning the patient from cardiopulmonary bypass (CPB), being unable to increase the LVAS flows to more than 2 L/min because of poor right ventricular function. The introduction of inhaled nitric oxide at a rate of 80 ppm resulted in immediate improvement of LVAS flow rates to more than 4 L/min and improvement in oxygenation, and CPB was subsequently successfully terminated. The effect of nitric oxide was demonstrated by a significant fall in LVAS flows (to 2.5 L/min) when inhaled nitric oxide was temporarily withdrawn (for change of cylinder and transport to the intensive care unit). Despite a subsequent promising 48-hour period when nitric oxide was able to be withdrawn, and despite LVAS flow rates of more than 5 L/min, progressive hepatic and multiple organ failure developed, from which the patient died 2 weeks later.
We are enthusiastic about the role of nitric oxide in this situation for a number of theoretical reasons. First, inhaled nitric oxide is specific to the pulmonary vasculature, giving rise to decreased pulmonary vascular resistance. 2 This reduction in right ventricular afterload is likely to be of benefit in the management of postimplantation right heart failure provided that one can expect the pulmonary vascular resistance to decrease with time; this one would expect if the elevated resistance is caused by left ventricular dysfunction or if the resistance has been transiently exacerbated by perioperative blood transfusion. However, if the postimplantation right ventricular failure is due to poor preoperative right ventricular function or if there has been a perioperative decline in right ventricular function (i.e., poor myocardial protection), then the outlook for these patients may be poor and they may require the addition of a right ventricular assist device with all of its attendant risks. Additionally, in this situation of right ventricular failure, tricuspid regurgitation is almost inevitable, and the reduced impedance to forward flow ensures a smaller tricuspid regurgitant fraction and more efficient output from the dilated right ventricle. Second, unlike other vasodilators, nitric oxide has minimal systemic action because of rapid inactivation by hemoglobin. 3 Third, the use of inhaled nitric oxide, in contrast to intravenous pulmonary vasodilators, improves perfusion of ventilated alveoli and decreases the shunt fraction. 4 Last, unlike prostacyclin, inhaled nitric oxide has no demonstrable effect on hemostasis in vivo. In cases in which anticoagulation is unnecessary (as in the HeartMate LVAS), the lack of antihemostatic activity is an advantage.
Having expressed our enthusiasm for inhaled nitric oxide on anecdotal and theoretical grounds, we argue that the case presented by Mertes and associates 1 has insufficient support for the conclusion that improvement was due to the use of inhaled nitric oxide. We are surprised to read that improvement occurred only after 30 minutes of nitric oxide administration at a rate of 50 ppm. From our experience, as well as other reports 5 of the use of inhaled nitric oxide in this and other situations (after transplantation and after mitral valve operations), we would have expected an almost immediate response. No further data to support the proposed effect of nitric oxide are offered, such as the effect of termination or interruption of nitric oxide. To the critical observer, the improvement may have been due to a spontaneous recovery in right ventricular function while the patient was supported by a further period of normothermic CPB, quite apart from delayed effects of concomitant treatment (e.g., diuretics, inodilators) that may have been additionally used.
In summary, we share the enthusiasm for the use of inhaled nitric oxide in the management of right ventricular failure after the insertion of a totally implantable LVAS. However, we do not accept the conclusion, on the data presented for this case, that inhaled nitric oxide was responsible for the improvement seen. In addition, although nitric oxide is extremely valuable in rapidly lowering pulmonary vascular resistance, unless the increased resistance is due to a reversible cause, the prospects for successful bridge to transplantation with an implantable LVAS alone may be poor.
References
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