Letters to the Editor
Small atrial septal defects To The Editor: I was very interested by the article by Andersen and associates on "The natural history of small atrial septal defects: Long-term follow-up with serial heart catheterizations. ''1 It contributes much to our incomplete knowledge of the long-term hemodynamics in patients with this problem. I agree with their and others '2 appreciation of the potential inaccuracy of the pulmonary-to-systemic flow ratio and their recommendation to consider the presence or absence of diastolic flow murmurs, ECG changes, heart enlargement, and increased pulmonary vasular markings when deciding whether a patient has a large or small atrial septal defect. There is one hemodynamic measurement t h a t they did not include in their article which I would be very interested for them to examine in their 26 patients in which serial catheterizations were performed. In this type of small atrial septal defect s the mean left atrial pressure may be slightly higher, usually 1 to 3 ram. Hg, t h a n the mean right atrial pressure if the cross-sectional area of the defect is not over 2 square cm. This difference in mean atrial pressures, ff present, suggests local (at the atrial septal level) resistance to flow. I wonder whether the four patients in their series with significantly increased left-toright shunts on recatheterization lacked this pressure difference initially. If the pressures were equal, more frequent follow-up or consideration of surgery might be indicated. This small b u t significant pressure difference between the atria would appear to compliment the other prognostic factors they list and may be the most helpful. It would further extend our knowledge of the natural history of small atrial septal defects ff they would analyze this factor in their group of patients.
Richard E. Katholi, M.D. Instructor in Medicine Cardiovascular Research and Training Center School of Medicine The University of Alabama Birmingham, Ala. 35294
REFERENCES 1. Andersen, M., Lyngborg, K., M61ler, I., and Wennevold, A.: The natural history of small atrial septal defects: Long-term follow-up with serial heart catheterizations, AM. HEART J. 92:302, 1976. 2. Zaver, A, C., and Nadas, A. S.: Atrial septal defect-secundum type, Circulation 31 and 32(Suppl. III):24, 1965. 3. Dexter, L.: Atrial septal defect, Br. Heart J. 18:209, 1956.
Reply To the Editor: We wish to t h a n k Dr. Katholi for his comments on our article. At his suggestion we looked through our material in order to see if there were any differences in mean pressures between right and left atria at the initial examination. Unfortunately, our material is not relevant in t h a t respect: at the initial examination, the left atrium was not entered with
American Heart Journal
the catheter in three of the four patients with later significantly increased left-to-right shunts. In the remaining patient the catheter had to be withdrawn from the left a t r i u m before the pressure was recorded, because the patient experienced chest pain for some unknown reason. All told, in 17 of our material of 26 patients either the left atrium was not entered or the recording was technically unsatisfactory. Among the remaining nine patients there were no differences in mean pressures between the right and left atrium in three patients, a difference of 1 mm. Hg in two patients, and a difference of 2 mm. Hg in four patients. We regret t h a t we are not able to contribute to the point raised by Dr. Katholi, a point which we think is well taken.
Mogens Andersen, M.D. Kjeld Lyngborg, M.D. Inge Moller, M.D. A l l Wennevold, M.D. Cardiovascular Laboratory of Medical Department B Rigshospitalet University of Copenhagen Copenhagen, Denmark
Truncus Arteriosus Communis To the Editor: We have read the article "Truncus Arteriosus Communis: Clinical, angiocardiographic, and pathologic findings in 100 patients," by Calder and associates' which appeared in American Heart Journal in the July, 1976, issue, and also the Editorial by Jesse E. Edwards in the same issue. 2 We have analyzed 197 hearts of truncus pathologically, of which we reported 180 in The Journal of Thoracic and Cardiovascular Surgery2 We believe t h a t it is not wise to classify truncus, because of the numerous factors involved. I t is best to treat truncus in a factorial analysis in each individual case. These factors are (1) the origin of the pulmonary t r e e - t h e factor so well worked out by Collett and Edwards4; (2) the place of origin of the t r u n c u s - t h a t is, from the right ventricle, the left ventricle, or both; (3) the a m o u n t of pulmonary flow; (4) the presence or absence of t h e hypoplastic aorta type of truncus; (5) the presence or absence of truncus stenosis or insufficiency and ventricular septal defect stenosis; and (6) atypical truncus. Any one case may vary in the evaluation of each individual factor. The classification proposed by Calder and associates, 1 which divides truncus into (a) with ventricular septal defect, and (b) without ventricular septal defect, is in our opinion not wise. For in our series 99.5 per cent of cases fall into the first category. Only one member is found in the second category, a case which we have published in the American Journal of Cardiology2 To our knowledge, this is the only bona fide case of this sort in the modern literature. Even though the classification by Calder and associates 1 may be semantically
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Small atrial septal defects To The Editor: I was very interested by the article by Andersen and associates on "The natural history of small atrial septal defects: Long-term follow-up with serial heart catheterizations. ''1 It contributes much to our incomplete knowledge of the long-term hemodynamics in patients with this problem. I agree with their and others '2 appreciation of the potential inaccuracy of the pulmonary-to-systemic flow ratio and their recommendation to consider the presence or absence of diastolic flow murmurs, ECG changes, heart enlargement, and increased pulmonary vasular markings when deciding whether a patient has a large or small atrial septal defect. There is one hemodynamic measurement t h a t they did not include in their article which I would be very interested for them to examine in their 26 patients in which serial catheterizations were performed. In this type of small atrial septal defect s the mean left atrial pressure may be slightly higher, usually 1 to 3 ram. Hg, t h a n the mean right atrial pressure if the cross-sectional area of the defect is not over 2 square cm. This difference in mean atrial pressures, ff present, suggests local (at the atrial septal level) resistance to flow. I wonder whether the four patients in their series with significantly increased left-toright shunts on recatheterization lacked this pressure difference initially. If the pressures were equal, more frequent follow-up or consideration of surgery might be indicated. This small b u t significant pressure difference between the atria would appear to compliment the other prognostic factors they list and may be the most helpful. It would further extend our knowledge of the natural history of small atrial septal defects ff they would analyze this factor in their group of patients.
Richard E. Katholi, M.D. Instructor in Medicine Cardiovascular Research and Training Center School of Medicine The University of Alabama Birmingham, Ala. 35294
REFERENCES 1. Andersen, M., Lyngborg, K., M61ler, I., and Wennevold, A.: The natural history of small atrial septal defects: Long-term follow-up with serial heart catheterizations, AM. HEART J. 92:302, 1976. 2. Zaver, A, C., and Nadas, A. S.: Atrial septal defect-secundum type, Circulation 31 and 32(Suppl. III):24, 1965. 3. Dexter, L.: Atrial septal defect, Br. Heart J. 18:209, 1956.
Reply To the Editor: We wish to t h a n k Dr. Katholi for his comments on our article. At his suggestion we looked through our material in order to see if there were any differences in mean pressures between right and left atria at the initial examination. Unfortunately, our material is not relevant in t h a t respect: at the initial examination, the left atrium was not entered with
American Heart Journal
the catheter in three of the four patients with later significantly increased left-to-right shunts. In the remaining patient the catheter had to be withdrawn from the left a t r i u m before the pressure was recorded, because the patient experienced chest pain for some unknown reason. All told, in 17 of our material of 26 patients either the left atrium was not entered or the recording was technically unsatisfactory. Among the remaining nine patients there were no differences in mean pressures between the right and left atrium in three patients, a difference of 1 mm. Hg in two patients, and a difference of 2 mm. Hg in four patients. We regret t h a t we are not able to contribute to the point raised by Dr. Katholi, a point which we think is well taken.
Mogens Andersen, M.D. Kjeld Lyngborg, M.D. Inge Moller, M.D. A l l Wennevold, M.D. Cardiovascular Laboratory of Medical Department B Rigshospitalet University of Copenhagen Copenhagen, Denmark
Truncus Arteriosus Communis To the Editor: We have read the article "Truncus Arteriosus Communis: Clinical, angiocardiographic, and pathologic findings in 100 patients," by Calder and associates' which appeared in American Heart Journal in the July, 1976, issue, and also the Editorial by Jesse E. Edwards in the same issue. 2 We have analyzed 197 hearts of truncus pathologically, of which we reported 180 in The Journal of Thoracic and Cardiovascular Surgery2 We believe t h a t it is not wise to classify truncus, because of the numerous factors involved. I t is best to treat truncus in a factorial analysis in each individual case. These factors are (1) the origin of the pulmonary t r e e - t h e factor so well worked out by Collett and Edwards4; (2) the place of origin of the t r u n c u s - t h a t is, from the right ventricle, the left ventricle, or both; (3) the a m o u n t of pulmonary flow; (4) the presence or absence of t h e hypoplastic aorta type of truncus; (5) the presence or absence of truncus stenosis or insufficiency and ventricular septal defect stenosis; and (6) atypical truncus. Any one case may vary in the evaluation of each individual factor. The classification proposed by Calder and associates, 1 which divides truncus into (a) with ventricular septal defect, and (b) without ventricular septal defect, is in our opinion not wise. For in our series 99.5 per cent of cases fall into the first category. Only one member is found in the second category, a case which we have published in the American Journal of Cardiology2 To our knowledge, this is the only bona fide case of this sort in the modern literature. Even though the classification by Calder and associates 1 may be semantically
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