S. Yamaki et al., MICROATELECTASIS IN PATIENTS WITH SECUNDUM ATRIAL SEPTAL-DEFECT AND ITS RELATION TO PULMONARY-HYPERTENSION, Japanese Circulation Journal, 61(5), 1997, pp. 384-389
In patients with secundum atrial septal defect, pulmonary hypertension
appears to be attributable to microatelectasis of the lung. To confir
m this hypothesis, pulmonary arteries in surgical biopsy specimens fro
m 72 patients with atrial septal defect and pulmonary hypertension wer
e subjected to morphometric examination. Thirty eight of the 72 patien
ts (53%) were found to have microatelectasis of the lung, which sugges
ts that an even higher frequency would have been found if the entire o
rgan had been examined. Atelectatic changes were found in 21 of 39 pat
ients with plexogenic pulmonary arteriopathy (54%), 8 of 15 with muscu
loelastosis (53%), and 9 of 13 with both of these lesions (69%). No su
ch changes were observed in 5 patients with atrial septal defect who s
howed thromboembolism-type lesions of the pulmonary arteries. On the o
ther hand, microatelectasis was not observed in another 5 patients wit
h atrial septal defect who did not exhibit pulmonary hypertension. The
medial smooth muscles of pulmonary arteries in ateletatic areas were
thicker (16.4+/-4.0 mu m) than those in non-atelectatic areas (10.3+/-
3.3 mu m). The index of pulmonary vascular disease was not significant
ly different between atelectatic (2.0+/-0.6) and non-atelectatic areas
(1.9+/-0.5). We conclude that in microatelectatic areas, which may te
nd to develop after respiratory infections in patients with atrial sep
tal defect, hypoxic vasoconstriction of the small pulmonary arteries i
s liable to occur, which causes hypertrophy of the media. This is like
ly to lead to the elevation of pulmonary arterial pressure and sustain
ed pulmonary hypertension.