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Ann Thorac Surg 1998;66:1863
© 1998 The Society of Thoracic Surgeons

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Correspondence

Reply

^a Division of Cardiothoracic Surgery, Columbia University College of Physicians and Surgeons, 177 Fort Washington Ave, Room 7-435, New York, NY 10032, USA

To the Editor

We appreciate Dr Krohn’s interest in our study and the opportunity to address his comments. Dr Krohn asserts in his letter that in our study, inhaled nitric oxide (iNO) was given to left ventricular assist device (LVAD) recipients "to dilate the pulmonary arteries, instead of removing the iatrogenic factors causing the pulmonary hypertension." He goes on to state that the pulmonary hypertension that accompanies chronic heart failure is entirely secondary to the effects of catecholamine exposure (from endogenous secretion preoperatively and "iatrogenic" administration perioperatively), and that "stopping the dopamine and dobutamine infusions promptly after insertion of the LVAD would have allowed pulmonary arterial constriction to relax, lowering pulmonary artery pressure, without help from inhaled NO."

The pathophysiologic determinants and hemodynamic sequelae of pulmonary hypertension in heart failure and after LVAD insertion are more complex than suggested by Dr Krohn, and the clinical management of these patients, including "removing the causes of the pulmonary hypertension," is not as simple and straightforward as he may believe. Although the mechanisms responsible for heart failure-induced pulmonary hypertension are not fully understood, a variety of processes have been implicated, including chronic elevations in left atrial pressure, pulmonary venous congestion, intravascular volume expansion, medial smooth muscle hypertrophy, and alterations in sympathetic tone. Interestingly, recent evidence suggests that pulmonary hypertension may in fact result from impairments in the release of NO by the pulmonary vascular endothelium [1], and that cardiopulmonary bypass-related endothelial dysfunction may be responsible for further perioperative elevations in pulmonary vascular resistance [2]. Whatever the mechanism, secondary elevations in pulmonary vascular resistance are initially reactive in nature and are usually reversible if heart failure is corrected before permanent structural changes occur. However, in contrast to Dr Krohn’s assumption, pulmonary vascular resistance does not immediately return to normal postoperatively, but in fact may remain abnormally elevated for several days to weeks [3], often resulting in temporary right ventricular dysfunction.

We also disagree with Dr Krohn’s assertion that inotropic agents should be withdrawn immediately after LVAD insertion, since as many as 20% of these patients develop right ventricular failure requiring pharmacologic support. In fact, prior to the introduction of inhaled NO at our institution, right ventricular failure refractory to inotropic agents occurred in 7% of our LVAD recipients, requiring institution of biventricular mechanical support. This post-LVAD right ventricular failure is mediated by a number of mechanisms, including volume overload due to increased venous return, reductions in right ventricular contractility due to left ventricular decompression and leftward displacement of the ventricular septum, and elevations in pulmonary vascular resistance induced by cardiopulmonary bypass and blood product transfusions.

Finally, in response to Dr Krohn’s concern about the negative inotropic effects of iNO, he is referred to our previous work in this area [4], which has demonstrated that increases in left ventricular filling pressures after iNO administration are not secondary to myocardial dysfunction but are likely a consequence of right-to-left volume redistribution induced by pulmonary vasodilation.

References

1. Dinh Zuan A.T., Higgenbottam T.W., Clelland C., Pepka-Zaba J., McGoldrick J., Wallwork J. Impairment of endothelium-dependent vasorelaxation in secondary pulmonary hypertension. Eur Respir J 1989;2:667S.
2. Komai H., Adatia I.T., Elliott M.J., de Leval M.R., Haworth S.G. Increased plasma levels of endothelin-1 after cardiopulmonary bypass in patients with pulmonary hypertension and congenital heart disease. J Thorac Cardiovasc Surg 1993;106:473-478.[Abstract]
3. Bhatia S., Kirshembaum J., Shemin R. Time course of resolution of pulmonary hypertension and right ventricular remodeling after orthotopic cardiac transplantation. Circulation 1987;76:819-826.[Abstract/Free Full Text]
4. Argenziano M., Dean D.A., Moazami N., et al. Inhaled nitric oxide is not a myocardial depressant in a porcine model of heart failure. J Thorac Cardiovasc Surg 1998;115:700-708.[Abstract/Free Full Text]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Michael Argenziano Mehmet C. Oz Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Argenziano, M. Articles by Oz, M. C. Search for Related Content PubMed Articles by Argenziano, M. Articles by Oz, M. C.