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Ann Thorac Surg 1996;61:1583-1584
© 1996 The Society of Thoracic Surgeons

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Update

Long-term Results of Mitral Valve Surgery in Patients with Severe Pulmonary Hypertension

As Originally Published in 1988:

Updated in 1996 by Alejandro Aris, MD, PhD, and Maria Luisa Cámara, MD, PhD

Cardiac Surgery Service, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain

Pulmonary hypertension has been, for many years, a limiting factor in mitral valve surgery. We believe that our original article [1] dispelled the fear of an increased risk in patients with severe pulmonary hypertension undergoing mitral valve procedures. A low operative mortality, excellent long-term survival, and the evidence of a decrease in pulmonary artery pressure after operation were the conclusions of our study. We have continued to be interested in this aspect of mitral valve disease and, as a result, we conducted a study on the hemodynamic effects of two drugs-prostaglandin E₁ and isoprotenerol-after operation for mitral stenosis in 30 patients [2]. Prostaglandin E₁ at a dose of 0.08 µg•kg^-1•min^-1 effectively decreased pulmonary vascular resistance without altering systemic arterial pressure. None of the 30 patients studied had pulmonary hypertension, but the number of patients with this problem has increased without decreasing our rate of mitral operations. In our original report, of 697 patients operated on during a 10-year period, 88 (12.6%) had a systolic pulmonary artery pressure of 70 mm Hg or greater. In the following 9 years, we have operated on 577 patients with isolated mitral pathology. However, during this period, the diagnosis of mitral disease has evolved from cardiac catheterization, with determination of right heart pressures, to echocardiography. On reviewing the records of the last 150 patients operated on for mitral disease we have found 24 (16%) with a pulmonary artery pressure of 70 mm Hg or greater as estimated by Doppler echocardiography. Considering that all these patients had some degree of tricuspid insufficiency, the percentage could be increased by patients with no tricuspid regurgitation and in whom the pulmonary artery pressure was not calculated.

The basic message of our article still holds true. In addition, methods of dealing with pulmonary hypertension and postoperative right ventricular failure have improved considerably in recent years. We found prostaglandin E₁ (0.08 µg•kg^-1•min^-1) to be an excellent drug to decrease pulmonary vascular resistance [2]. Kabbani and associates [3], who reported in 1982 an operative mortality of 15% in patients with systolic pulmonary artery pressure greater than 100 mm Hg, have used sodium nitroprusside, infused directly into the pulmonary artery, with a decrease in operative mortality to 4.2% [4]. Amrinone, a phosphodiesterase inhibitor, decreases the afterload of the right ventricle [5] and has been used to reduce pulmonary artery pressure and pulmonary vascular resistance [6]. The same effects can be obtained with intervention through the airways. Inhaled nitric oxide significantly decreases both, without affecting systemic arterial pressure [7]. More recently, the role of hypercapnia on pulmonary vascular resistance in patients undergoing mitral valve replacement has been shown [8].

We continue to support the role of surgery in patients with mitral valve disease and severe pulmonary hypertension. With all these methods at hand, the operation can be performed more safely than 10 years ago.

Footnotes

Address reprint requests to Dr Aris, Cardiac Surgery Service, Hospital de la Santa Creu i Sant Pau, San A. M. Claret 167, 08025 Barcelona, Spain.

References

1. Cámara ML, Aris A, Padró JM, Caralps JM. Long-term results of mitral valve surgery in patients with severe pulmonary hypertension. Ann Thorac Surg 1988;45:133–6.[Abstract]
2. Cámara ML, Aris A, Alvarez J, Padró JM, Caralps JM. Hemodynamic effects of prostaglandin E₁ and isoprotenerol early after cardiac operations for mitral stenosis. J Thorac Cardiovasc Surg 1992;103:1177–85.[Abstract]
3. Kabbani SS, Bashour T, Dunlap R, Hanna ES. Mitral stenosis with severe pulmonary hypertension. Tex Heart Inst J 1982;9:307–10.
4. Kabbani SS, Jamal H, Abdun F, Jokhadar M. Management of patients with mitral disease and extreme degrees of pulmonary hypertension. Cardiovasc Surg 1995;3(Suppl 1):16.
5. Konstam MA, Cohen SR, Salem DN, Das D, Aronovitz MJ, Brockway BA. Effect of amrinone on right ventricular function: predominance of afterload reduction. Circulation 1986;74:359–66.[Abstract/Free Full Text]
6. Hess W, Arnold B, Viet S. The haemodynamic effects of amrinone in patients with mitral stenosis and pulmonary hypertension. Eur Heart J 1986;7:800–7.[Abstract/Free Full Text]
7. Girard C, Lehot JJ, Pannetier JC, Filley S, French P, Estanove S. Inhaled nitric oxide after mitral valve replacement in patients with chronic pulmonary artery hypertension. Anesthesiology 1992;77:880–3.[Medline]
8. Fullerton DA, McIntyre RC Jr, Kirson LE, St. Cyr JA, Whitman GJR, Grover FL. Impact of respiratory acid-base status in patients with pulmonary hypertension. Ann Thorac Surg (in press).

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