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Ann Thorac Surg 1997;64:586-587
© 1997 The Society of Thoracic Surgeons

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Correspondence

Aneurysm of Pulmonary Trunk

Second Department of Surgery, Kagoshima University Faculty of Medicine, 8-35-1 Sakuragaoka, Kagoshima, 890 Japan

To the Editor:

The recent article by Chen and associates [1] reporting a giant aneurysm of main pulmonary artery leads us to present a similar case of our patient as the eighth.

A 67-year-old man was first admitted to the Kagoshima University Hospital with the diagnosis of mitral and tricuspid regurgitation 4 years earlier. Cardiac catheterization showed mild pulmonary hypertension of 47/16 mm Hg. Angiography revealed moderate to severe mitral and tricuspid regurgitation, and enlarged pulmonary trunk with mild pulmonary valve regurgitation. No congenital cardiac lesion was found. Mitral valve replacement with a 31-mm Björk-Shiley valve and tricuspid valve annuloplasty were performed. Aneurysmal dilatation of the pulmonary trunk, 6 cm in diameter, was left untreated after biopsy of its wall. The ascending aorta showed no dilatation. The pathologic specimen showed marked infiltration of acute and chronic inflammatory cells mainly in the tunica media with destruction and defect of elastic tissue, loss of muscular tissue, and increase in collagen fibers. His postoperative course was uneventful.

He attended the outpatient clinic for regular check-ups for 4 years. With time, both pulmonary valve regurgitation and the dilatation of the pulmonary trunk gradually increased. Preoperative investigation showed mild tricuspid regurgitation, moderate pulmonary valve regurgitation, and marked dilatation of the pulmonary trunk with no pulmonary hypertension (31/4 mm Hg). He underwent a second operation. A giant aneurysm of the pulmonary trunk with considerable thinning of its wall, 10 cm in maximal diameter, extended from just above the pulmonary annulus to bifurcation of both main pulmonary arteries. The aneurysm was incised longitudinally. Macroscopically no evidence of dissection or atherosclerotic change was found. The pulmonary valve was tricuspid and had no organic change on the leaflets. The pulmonary annular dilatation apparently caused the pulmonary valve regurgitation. Pulmonary valve annuloplasty by double sutures with 3-0 polypropylene was performed. A large portion of the anterior aneurysm wall was excised. The walls were approximated with a continuous suture of 2-0 polypropylene. He had no difficulty on cessation of cardiopulmonary bypass. The pathologic specimen showed the same findings as previous ones. His postoperative course was uneventful. Postoperative examination showed mild dilatation of the pulmonary trunk with no pulmonary valve regurgitation.

In the present case, the leading cause of the aneurysm is unclear, as in the case reported by Chen and associates [1]. Pulmonary valve regurgitation was left untreated in previous reports [2], but we performed pulmonary valve annuloplasty. Regular follow-up at 2 years 3 months showed a satisfactory condition.

References

1. Chen Y-F, Chiu C-C, Lee C-S. Giant aneurysm of main pulmonary artery. Ann Thorac Surg 1996;62:272–4.[Abstract/Free Full Text]
2. Williams TE Jr, Schiller M, Craenen J, Hosier DM, Sirak HD. Pulmonary artery aneurysm. Successful excision and replacement of the main pulmonary artery. J Thorac Cardiovasc Surg 1971;62:63–7.[Medline]

Divisions of Cardiovascular Surgery and Cardiology, Kaohsiung Medical College, 100 Shih-Chuan 1st Rd, Kaohsiung, Taiwan

Reply To the Editor:

We thank Dr Shimokawa and associates for their interest in our article. Doctor Shimokawa and his colleagues should be congratulated for having successful surgical treatment of such a rare case. In view of the maximal diameter of the aneurysm of the main pulmonary artery of 10 cm and considerable wall thinning, surgical intervention had to be considered because of the possible fatal outcome if the aneurysm was left untreated. Giant aneurysms are inherently unstable because any dilatation in turn increases the dilating force. This sequence is in accord with the law of Laplace, which states that the wall tension is directly proportional to intravascular pressure and radius of the vessel and is inversely relatedly to the wall thickness, so that the thinner the vessel wall becomes, the more wall tension increases, and the vessel dilates more or even ruptures [1].

We agree with Shimokawa and colleagues that the leading cause of the aneurysm is not clear. Mild pulmonary hypertension cannot be the cause of the aneurysm. Moreover, none of the usual factors was present in their reported case. As in our case, the aneurysm could be considered idiopathic.

Reference

1. Butto F, Lucas RV, Edwards JE. Pulmonary arterial aneurysm—a pathologic study of five cases. Chest 1987;92:237–41. [Abstract/Free Full Text]

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This Article Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Akira Taira Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shimokawa, S. Articles by Lee, C.-S. Search for Related Content PubMed PubMed Citation Articles by Shimokawa, S. Articles by Lee, C.-S.