Ann Thorac Surg 1996;61:236-237
© 1996 The Society of Thoracic Surgeons
Invited Commentary
Invited Commentary
Margaret D. Allen, MD
Cardiothoracic Surgery University of Washington 1959 NE Pacific St, Box 356310 Seattle, WA 98195
See also page 234.
In practice, one often learns more from bad experiences than good ones. In spite of this, we tend to report only the good results for publishing. Therefore, I commend DeLeon and associates for sharing their clinical dilemmas as a learning experience for all readers. This article puts into print what many surgeons have noted on the operating table: distal pulmonary hypertension can cause distention of pulmonary homografts. Yet, it is interesting to speculate on the relationship between pulmonary root distention and valvular incompetence and raise some further questions to be answered. Certainly, in cardiac transplantation, donor pulmonary roots and valves are frequently subject to high recipient pulmonary artery pressures or high pulmonary vascular resistances, but pulmonic valvular incompetence is not the rule. And, in pulmonary autografts placed suddenly under systemic pressure as aortic valve replacements, torrential pulmonary valvular incompetence is not the standard result. Is it the cryopreservation of the pulmonary homograft that makes the difference? This would seem unlikely because, in experimental models, cryopreserved pulmonary homograft roots placed in the systemic circulation do not necessarily become incompetent even though the root and annulus become visibly distended.
It is possible that the size of the pulmonary annulus and extent of leaflet surface available for coaptation could make a difference. Perhaps, in pulmonary valve reconstructions in which postoperative pulmonary hypertension is expected, rather than sizing a homograft root to fit exactly, it may be prudent to oversize the pulmonary conduit slightly, forcing the leaflets to be more redundant and, therefore, likely to still have an adequate surface of coaptation when the annulus becomes distended. Also, the felt or pericardial strip around the homograft annulus placed at the time of implantation, as advocated by Ross for his homograft roots, might be a reasonable routine measure to prevent annular dilatation in the face of persistent pulmonary hypertension.
No doubt, geometry plays a greater role than we realize and may be as important as the hemodynamics we all monitor and measure. Again, in cardiac transplantation, just a small amount of torque on the donor pulmonary root can produce leaflet prolapse, and kinking of the donor pulmonary artery can produce a distal stenotic gradient and right ventricular failure, potentially resulting in pulmonary valvular incompetence, analogous to this case. We are only beginning to appreciate the role that diastolic eddy currents in the valve sinuses play in closing both aortic and pulmonary leaflets. Recreating these diastolic leaflet closing forces has become a major consideration in the new ascending aortic graft replacement procedures for Marfan's syndrome in which the aortic valve is spared (the David procedure). Is there a significant difference between diastolic flow patterns in the sinuses of Valsalva depending on whether pulmonary hypertension is caused by an immediately distal anatomic stenosis, as in the pulmonary atresia variants or distal anastomotic stenoses, versus the more distal nonanatomic ``obstruction'' of elevated pulmonary vascular resistance in the lung parenchyma? One might suppose that the eddy currents in the sinuses responsible for valve leaflet closure and coaptation would be significantly altered by a distal anatomic stenosis, especially one close to the valve, but be unaffected in the case of diffuse elevated pulmonary vascular resistance, as in primary pulmonary hypertension. I suspect that this may have been the true problem in the presented case rather than the systolic pressures. These questions are ones that may be better answered in the future by ``virtual reality'' computer-modeling techniques being developed through advanced bioengineering rather than by bitter experience.
Related Article
-
Early Pulmonary Homograft Failure From Dilatation Due to Distal Pulmonary Artery Stenosis
- Serafin Y. DeLeon, J. Michael Tuchek, Timothy J. Bell, Joanne Hofstra, Dolores A. Vitullo, Jose A. Quinones, and Elizabeth A. Fisher
Ann. Thorac. Surg. 1996 61: 234-237.
[Abstract]
[Full Text]
