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Bone Resorption in Progressive Systemic Sclerosis
To the Editor: We diHerentiated between bone erosion or bone defects (Of' partial loss of bone substance) and bone resorption or destruction (or complete dissolution of a bony segment). Because of this, when we searched the literature (including a Medline search), the articles by Sargent et al and by Keats were not discovered. We apologize for this oversight but would suggest that what we have shown is a much more advanced stage of bone resorption in progressive systemic sclerosis which does not appear to have begun with the superior marginal rib 'defects described by Sargent et al. This suggests that there may be more than one type of either bone erosion or bone resqrption occurring in progressive systemic sclerosis. James C. Steigerwald, M.D. Associate Professor of Medicine and Acting Head, Division of Rheumatic Diseases University of Colorado Medical Center, Denver
Echoes from Swan-G·anz Catheter To the Editor: In their article entitled "Echocardiographic Manifestations of Postinfarction Ventricular Septal Rupture" (Chest 68:778-780, 1975), Silverman et al report interesting cases with ventricular septal rupture. I disagree with them on their interpretation of the echoes in the right ventricle in Figures 1 and 3. Those echoes are produced by the Swan-Ganz catheter. In Figure 1, the catheter echoes resemble a tricuspid valve; however, they are stronger and multiple, and the excursion is large, as was noted by the authors. In Figure 3, the catheter is seen in the outflow tract of the right ventricle, quite removed from the tricuspid area. It is my experience that Swan-Ganz catheters will almost invariably produce echoes; they may resemble tricuspid or pulmonic valves, but they are usually more intense and multiple. Jorge A. Levisman, M.D.. Assistant Professor, Division of Cardiology Department of Medicine, School of Medicine University of C alifomia, Los Angeles
To the Editor: The letter by Dr. Levisman raises an excellent question concerning the origin of the strong echo in the right ventricular outflow tract in the patients we saw with postinfarctional ventricular septal rupture. We have previously recognized echoes in this area which we believed were produced by the Swan-Ganz catheter in the outflow tract. In these patients, we had not noted the extensive opening motion present (25 mm in case 1 and 19 mm in case 2). To evaluate this point, we recently recorded echocardiograms for several patients with Swan-Ganz catheters in the pulmonary artery. We could not record a motion similar to that seen in the echo of patient 1; however, we did record an echo in a patient
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who had a motion similar to that seen in case 3 with an excursion of approximately 18 mm. We have studied a subsequent patient with postinfarctional ventricular septal rupture who had undergone echocardiographic studies prior to insertion of a Swan-Ganz catheter. In this patient the prominent echo of the tricuspid valve was recorded in the right ventricular outflow tract. I feel certain that the echoes seen in case 1 do not represent the Swan-Ganz catheter; however, the motion and the position recorded in case 3 are similar to some patients with a Swan-Ganz catheter in place. The excessive motion may be due to the presence of a left-to-right shunt. We believe that the prominent motion of the tricuspid valve is still an important clue to postinfarctional ruptured ventricular septum. In evaluating patients with new systolic murmurs in our coronary care unit, we have seen this only with a ruptured ventricular septum. Barry D. Silverman, M.D. Emory-Northside Assistant Professor of Medicine Northside Hospital, Atlanta
Dextran 40 and Noncardiogenic Pulmonary Edema To the Editor: An article by Kaplan and Sabin l in the September 1975 issue of Chest suggests I possible etiologic relationship between dextran 40 ( Rheomacrodex ) and noncardiogenic pulmonary edema. Although most of their arguments are valid and the drug may be a cause of pulmonary capillary damage, the absence of data regarding central venous and, particularly, pulmonary arterial wedge pressures makes a definitive conclusion impossible. Unger et al 2 have shown that left ventricular failure may be the cause of progressive pu!monary consolidation, even without clinical or radiologic evidence of cardiomegaly. In their study, four of 14 patients suspected of having pulmonary edema of noncardiac origin (based on chest x-ray films and clinical presentation) did, in fact, have elevations in pulmonary arterial wedge pressure. The cardiac silhouette in Figure 1 in the article by Kaplan and Sabin 1 is borderline j.n size. Although the observation that dextran 40 causes noncardiogenic pulmonary edema may be valid, the absence of data regarding left ventricular filling pressure makes a definitive statement regarding this relationship only speculative'. Dennis M. Greenbaum, M.D. Associate Director, Medical Intensive Care Unit St. Vincent's Hospital and Medical Center New York REFERENCES .
1 Kaplan AI, Sabin S: Dextran 40: Another cause of druginduced noncardiogenic pulmonary edema. Chest 68:376377,1975. 2 Unger KM, Shibel EM, Moser KM: Detection of left ventricular failure in patients with adult respiratory distress syndrome. Chest 67:8-13, 1975
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Echoes from Swan-G·anz Catheter To the Editor: In their article entitled "Echocardiographic Manifestations of Postinfarction Ventricular Septal Rupture" (Chest 68:778-780, 1975), Silverman et al report interesting cases with ventricular septal rupture. I disagree with them on their interpretation of the echoes in the right ventricle in Figures 1 and 3. Those echoes are produced by the Swan-Ganz catheter. In Figure 1, the catheter echoes resemble a tricuspid valve; however, they are stronger and multiple, and the excursion is large, as was noted by the authors. In Figure 3, the catheter is seen in the outflow tract of the right ventricle, quite removed from the tricuspid area. It is my experience that Swan-Ganz catheters will almost invariably produce echoes; they may resemble tricuspid or pulmonic valves, but they are usually more intense and multiple. Jorge A. Levisman, M.D.. Assistant Professor, Division of Cardiology Department of Medicine, School of Medicine University of C alifomia, Los Angeles
To the Editor: The letter by Dr. Levisman raises an excellent question concerning the origin of the strong echo in the right ventricular outflow tract in the patients we saw with postinfarctional ventricular septal rupture. We have previously recognized echoes in this area which we believed were produced by the Swan-Ganz catheter in the outflow tract. In these patients, we had not noted the extensive opening motion present (25 mm in case 1 and 19 mm in case 2). To evaluate this point, we recently recorded echocardiograms for several patients with Swan-Ganz catheters in the pulmonary artery. We could not record a motion similar to that seen in the echo of patient 1; however, we did record an echo in a patient
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who had a motion similar to that seen in case 3 with an excursion of approximately 18 mm. We have studied a subsequent patient with postinfarctional ventricular septal rupture who had undergone echocardiographic studies prior to insertion of a Swan-Ganz catheter. In this patient the prominent echo of the tricuspid valve was recorded in the right ventricular outflow tract. I feel certain that the echoes seen in case 1 do not represent the Swan-Ganz catheter; however, the motion and the position recorded in case 3 are similar to some patients with a Swan-Ganz catheter in place. The excessive motion may be due to the presence of a left-to-right shunt. We believe that the prominent motion of the tricuspid valve is still an important clue to postinfarctional ruptured ventricular septum. In evaluating patients with new systolic murmurs in our coronary care unit, we have seen this only with a ruptured ventricular septum. Barry D. Silverman, M.D. Emory-Northside Assistant Professor of Medicine Northside Hospital, Atlanta
Dextran 40 and Noncardiogenic Pulmonary Edema To the Editor: An article by Kaplan and Sabin l in the September 1975 issue of Chest suggests I possible etiologic relationship between dextran 40 ( Rheomacrodex ) and noncardiogenic pulmonary edema. Although most of their arguments are valid and the drug may be a cause of pulmonary capillary damage, the absence of data regarding central venous and, particularly, pulmonary arterial wedge pressures makes a definitive conclusion impossible. Unger et al 2 have shown that left ventricular failure may be the cause of progressive pu!monary consolidation, even without clinical or radiologic evidence of cardiomegaly. In their study, four of 14 patients suspected of having pulmonary edema of noncardiac origin (based on chest x-ray films and clinical presentation) did, in fact, have elevations in pulmonary arterial wedge pressure. The cardiac silhouette in Figure 1 in the article by Kaplan and Sabin 1 is borderline j.n size. Although the observation that dextran 40 causes noncardiogenic pulmonary edema may be valid, the absence of data regarding left ventricular filling pressure makes a definitive statement regarding this relationship only speculative'. Dennis M. Greenbaum, M.D. Associate Director, Medical Intensive Care Unit St. Vincent's Hospital and Medical Center New York REFERENCES .
1 Kaplan AI, Sabin S: Dextran 40: Another cause of druginduced noncardiogenic pulmonary edema. Chest 68:376377,1975. 2 Unger KM, Shibel EM, Moser KM: Detection of left ventricular failure in patients with adult respiratory distress syndrome. Chest 67:8-13, 1975
CHEST, 70: 1, JULY,
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