Volume 16 Number 4 October 1992
L&ten
to the Editors
665
prevented in a most direct and logical manner. Extensive dissection, mobilization and anastomosis of the LRV are avoided as is the risk of venous thrombosis. The retroperitoneal approach in aorta and left renal vessel surgery allows direct accessto the critical anatomy without manipulation of intraperitoneal structures. Peter N. Thmpon, MD R C&t Darling II& MD Bcnjmh B. Chang, MD Dbiraj M. Shah, MD Robert P. Lcadwy, MD Albany Medical College Vascular Surgery Section 47 New Scotland Ave., A-61 Albany, NY 12208
\ Fig. 2. Diagram illustrates ing “nutcracker” anatomy.
\ I\ transposition
of SMA, reliev-
depend on a previous understanding of this syndrome; for example, an excretory urogram often shows vascular impressions, or “notching”, of the renal pelvis and ureters. Renal angography may reveal varices and delayed washout of contrast medium on venous phase. Angiography should precede venography in the work-up of hematuria to eliminate other more common vascular abnormalities fi-om the diagnosis (e.g., hemangiomas and arteriovenous malformations) . Direct imaging by retrograde phlebography is the gold standard test and permits pressure recordings, which are mandatory in current practice. Typically, LRV-IVC gradients have been recorded in the range of 5 to 7 mm Hg4y5 With understanding of the anatomic causes of NCS, treatment has centered on relieving venous outtlow obstruction. Previous surgical corrections have focused on venous manipulation.4~5 In this case the SMA was reimplanted inferior to the LRV by use of a retroperitoneal approach, thus removing the “clamp” from the renal vein. Several advantages are offered. By permanently eliminating “nutcracker’ anatomy, the cause is treated and recurrence may be
REFERENCES 1. de Schepper A. “Nutcracker” fenomeen van de vena renalis en veneuze pathologic van de linker nier. J Belge Radio1 1972; 55:507-11. 2. Barnes RW, Fleisher HI, III, Redman JF, Smith JW, Harshfield DL, Ferris EJ. Mesoaortic compression of the left renal vein (the so-called nutcracker syndrome): repair by a new stenting procedure. J VASC SURG 1988;8:415-21. 3. Coolsaet BL. Ureteric pathology in relation to right and left gonadal veins. Urology 1978;12:40-9. 4. Beinart C, Sniderman KW, Tamura S, Vaughan ED Jr, SOSTA. Left renal vein to inferior vena cava pressure relationship in humans. J Ural 1982;127:1070-1. 5. Stewart BH, Reiman G. Left renal venous hypertension “nutcracker” syndrome managed by direct renocaval reimplantation. Urology 1982;20:365-9. 24141139931
Aneurysms and experimental atherosckrosis To the Ed&m: I draw attention to the paper by Zarins et al.’ on “aneurysms” in cholesterol-fed cynomolgus monkeys. 1. The authors are unaware that an aneurysm is a
persistent localized dilation of a blood vesseland is distinct from diffuse dilation or ectasia. For example, left ventricular dilation is not aneurysmal dilation. The authors did not demonstrate aneurysmal dilation in any animal. They reported an increase in the cross-sectional area of the abdominal
aortic lumen at one specific site in the regression
group compared to animals in the other two groups on a high-cholesterol, high-fat diet in which the cross-sectional area of the lumen was reduced by the fat storage in the aortic intima and media. No indication of the extent of the dilation was provided. 2. The lumen of the regression monkeys would have heen reduced initially hecause of the high-cholesterol, high-fat diet and then would have increased after lipid depletion of the thickened intima in the regression phase. This group should have been compared with a true control
666
Letters to the Editors
group on a stock diet. The authors may have revealed some mild ectasia, but the failure to use an adequate control and their comparisons with aortic lumina reduced by cholesterol feeding give a false impression of the degree of ectasia produced by regression. Grossly overloading animals with cholesterol and fat cannot be assumed to be harmless to the vesselwall so at&ted becausemany of the smooth muscle cells will be laden with lipids and the interstitium will be heavily infiltrated with fat. The gross morphologic changes during induction must affect the function of the cellular components of the wall, and the calcification that ensues during regression2 indicates mural damage. 3. The weight of the monkeys varied from 3 to 5 kg, but no information was provided regarding the sizeand age distribution of the animals in each group. It is to be expected that the aortic diameters will also vary considerably as a consequence of such significant differences in animal size. The absence of this information when so few animals are in the groups invalidates the conclusions. 4. Contrary to the authors’ allegations, a highcholesterol, high-fat diet in experimental animals does not reproduce atherosclerosis as it occurs in man.3,4 Their previous paper on aneurysms in cholesterol-fed animals, which they cite as supportive evidence, cannot be regarded asscientific evidenceof aneurysm formation in monkeys on a high-cholesterol diet, as has been indicated.5 Some ectasia of the aortas of cholesterol-fed animals after cessation of the diet may be found, but Zarins et al. fail to provide satisfactory evidence for even that claim and certainly have not established any association between aortic aneurysm and cholesterol feeding. William
E. Stebbens, MD,
Dphil
Malaghan Institute of Medical Research Wellington School of Medicine PO Box 7060 Wellington South New Zealand REFERENCES 1. Zarins CK, Xu C, Glagov S. Aneurysmal enlargement of the aorta during regression of experimental atherosclerosis. J VASC SURG 1992;15:90-101. 2. St. Clair RW. Atherosclerosis regression in animal models: current concepts of cellular and biochemical mechanisms. Prog Cardiovasc Dis 1983;26: 109-32. 3. Stehbens WE. An appraisal of cholesterol-feeding in experimental atherogenesis. Prog Cardiovasc Dis 1986;29: 107-28. 4. Stehbens WE. Vascular complications in experimental atherosclerosis. Prog Cardiovasc Dis 1986;29:221-37. 5. Stehbens WE. Aneurysms in atherosclerosis. J VASC SURG 1991;13:766-7. 24/41/40225
Reply To the Editors:
Dr. Stehbens statesthat we are unaware that aneurysms are distinct from diffuse dilation and ectasia.Indeed we are
Journal of VASCULAR SURGERY
well aware of the distinction between ectasiaand aneurysm formation, and we carefully controlled for the possibility that diffuse ectasia may have occurred in our experiment. As stated in our article, we reported not only abdominal and thoracic aortic dimensions but also the relative size of the abdominal and thoracic aortas in each animal. We calculated the abdominal/thoracic (A/T) ratio for the lumen area as well as the A/r ratio for the internal elastic lamina (IEL) area. With difli.tse enlargement, or ectasia,the ratios would be unchanged. In the two diet induction groups (6 months and 12 months) the A/T lumen area ratios were 0.45 + 0.13 and 0.42 c 0.12, respectively, and this is the same ratio as is found in normal-diet control animals (unpublished observation). For the regression animals the lumen area ratio was increased to 0.64 -C 0.30 @ < 0.05), indicating aortic enlargement localized in the abdominal aorta. There was no enlargement of the thoracic aorta. Dr. Stehbens further alleges that we did not demonstrate aneurysmal dilation in any animal and that we did not indicate the extent of the dilation. On the contrary, we clearly demonstrated in the text and in Fig. 2 the extent of dilation for each animal in each of the three groups. In four of the six regression animals, the lumen area and IEL area were more than 1 SD greater than the mean of the same measuremenfi in the two dietary groups. In two regression animals, both lumen area and IEL area were more than 2 SD above the mean for both dietary groups and might be considered aneurysmal. We chose an even stricter definition of aneurysm. In one regression animal, both lumen area and IEL area were more than 4 SD greater than the mean for both dietary groups. This animal alsohad an m lumen area ratio more than 4 SD above the mean. This marked localized dilation of the abdominal aorta, more than twice the diameter of the normal aorta and more than 1.2 times larger than the thoracic aorta, can be appropriately classified as a true aneurysm by every criterion for the definition of aneurysms. Although it is true that intimal plaque deposition would tend to reduce lumen caliber, the true measure of aortic size is the area encompassed by the IEL, which would not be altered by intimal plaque deposition. We therefore used the IEL area to assessaortic size. We reported no difference in IEL area between 6-month and 12-month diet induction animals. Thoracic and abdominal aortic size in these diet-fed animals was no different from that in normal-diet control animals (unpublished observations). Although it is true that a 2% cholesterol/25% peanut oil diet affects the arterial wall, administration of this diet alone for a 12-month period did not result in aneurysmal dilation in our experiment. Yet, aswe indicated in our article, animals on a 6-month regression regimen after 6 months of atherogenic diet had a twofold enlargement of abdominal aortic IEL area during the same period (p c 0.05). We assessedthe relation of animal size and weight to aortic dimensions. There was no correlation between gross body weight and aortic size, although the numbers of animals studied were small. We also searchedfor relationships among body size, serum cholesterol, plaque forma-
L&ten
to the Editors
665
prevented in a most direct and logical manner. Extensive dissection, mobilization and anastomosis of the LRV are avoided as is the risk of venous thrombosis. The retroperitoneal approach in aorta and left renal vessel surgery allows direct accessto the critical anatomy without manipulation of intraperitoneal structures. Peter N. Thmpon, MD R C&t Darling II& MD Bcnjmh B. Chang, MD Dbiraj M. Shah, MD Robert P. Lcadwy, MD Albany Medical College Vascular Surgery Section 47 New Scotland Ave., A-61 Albany, NY 12208
\ Fig. 2. Diagram illustrates ing “nutcracker” anatomy.
\ I\ transposition
of SMA, reliev-
depend on a previous understanding of this syndrome; for example, an excretory urogram often shows vascular impressions, or “notching”, of the renal pelvis and ureters. Renal angography may reveal varices and delayed washout of contrast medium on venous phase. Angiography should precede venography in the work-up of hematuria to eliminate other more common vascular abnormalities fi-om the diagnosis (e.g., hemangiomas and arteriovenous malformations) . Direct imaging by retrograde phlebography is the gold standard test and permits pressure recordings, which are mandatory in current practice. Typically, LRV-IVC gradients have been recorded in the range of 5 to 7 mm Hg4y5 With understanding of the anatomic causes of NCS, treatment has centered on relieving venous outtlow obstruction. Previous surgical corrections have focused on venous manipulation.4~5 In this case the SMA was reimplanted inferior to the LRV by use of a retroperitoneal approach, thus removing the “clamp” from the renal vein. Several advantages are offered. By permanently eliminating “nutcracker’ anatomy, the cause is treated and recurrence may be
REFERENCES 1. de Schepper A. “Nutcracker” fenomeen van de vena renalis en veneuze pathologic van de linker nier. J Belge Radio1 1972; 55:507-11. 2. Barnes RW, Fleisher HI, III, Redman JF, Smith JW, Harshfield DL, Ferris EJ. Mesoaortic compression of the left renal vein (the so-called nutcracker syndrome): repair by a new stenting procedure. J VASC SURG 1988;8:415-21. 3. Coolsaet BL. Ureteric pathology in relation to right and left gonadal veins. Urology 1978;12:40-9. 4. Beinart C, Sniderman KW, Tamura S, Vaughan ED Jr, SOSTA. Left renal vein to inferior vena cava pressure relationship in humans. J Ural 1982;127:1070-1. 5. Stewart BH, Reiman G. Left renal venous hypertension “nutcracker” syndrome managed by direct renocaval reimplantation. Urology 1982;20:365-9. 24141139931
Aneurysms and experimental atherosckrosis To the Ed&m: I draw attention to the paper by Zarins et al.’ on “aneurysms” in cholesterol-fed cynomolgus monkeys. 1. The authors are unaware that an aneurysm is a
persistent localized dilation of a blood vesseland is distinct from diffuse dilation or ectasia. For example, left ventricular dilation is not aneurysmal dilation. The authors did not demonstrate aneurysmal dilation in any animal. They reported an increase in the cross-sectional area of the abdominal
aortic lumen at one specific site in the regression
group compared to animals in the other two groups on a high-cholesterol, high-fat diet in which the cross-sectional area of the lumen was reduced by the fat storage in the aortic intima and media. No indication of the extent of the dilation was provided. 2. The lumen of the regression monkeys would have heen reduced initially hecause of the high-cholesterol, high-fat diet and then would have increased after lipid depletion of the thickened intima in the regression phase. This group should have been compared with a true control
666
Letters to the Editors
group on a stock diet. The authors may have revealed some mild ectasia, but the failure to use an adequate control and their comparisons with aortic lumina reduced by cholesterol feeding give a false impression of the degree of ectasia produced by regression. Grossly overloading animals with cholesterol and fat cannot be assumed to be harmless to the vesselwall so at&ted becausemany of the smooth muscle cells will be laden with lipids and the interstitium will be heavily infiltrated with fat. The gross morphologic changes during induction must affect the function of the cellular components of the wall, and the calcification that ensues during regression2 indicates mural damage. 3. The weight of the monkeys varied from 3 to 5 kg, but no information was provided regarding the sizeand age distribution of the animals in each group. It is to be expected that the aortic diameters will also vary considerably as a consequence of such significant differences in animal size. The absence of this information when so few animals are in the groups invalidates the conclusions. 4. Contrary to the authors’ allegations, a highcholesterol, high-fat diet in experimental animals does not reproduce atherosclerosis as it occurs in man.3,4 Their previous paper on aneurysms in cholesterol-fed animals, which they cite as supportive evidence, cannot be regarded asscientific evidenceof aneurysm formation in monkeys on a high-cholesterol diet, as has been indicated.5 Some ectasia of the aortas of cholesterol-fed animals after cessation of the diet may be found, but Zarins et al. fail to provide satisfactory evidence for even that claim and certainly have not established any association between aortic aneurysm and cholesterol feeding. William
E. Stebbens, MD,
Dphil
Malaghan Institute of Medical Research Wellington School of Medicine PO Box 7060 Wellington South New Zealand REFERENCES 1. Zarins CK, Xu C, Glagov S. Aneurysmal enlargement of the aorta during regression of experimental atherosclerosis. J VASC SURG 1992;15:90-101. 2. St. Clair RW. Atherosclerosis regression in animal models: current concepts of cellular and biochemical mechanisms. Prog Cardiovasc Dis 1983;26: 109-32. 3. Stehbens WE. An appraisal of cholesterol-feeding in experimental atherogenesis. Prog Cardiovasc Dis 1986;29: 107-28. 4. Stehbens WE. Vascular complications in experimental atherosclerosis. Prog Cardiovasc Dis 1986;29:221-37. 5. Stehbens WE. Aneurysms in atherosclerosis. J VASC SURG 1991;13:766-7. 24/41/40225
Reply To the Editors:
Dr. Stehbens statesthat we are unaware that aneurysms are distinct from diffuse dilation and ectasia.Indeed we are
Journal of VASCULAR SURGERY
well aware of the distinction between ectasiaand aneurysm formation, and we carefully controlled for the possibility that diffuse ectasia may have occurred in our experiment. As stated in our article, we reported not only abdominal and thoracic aortic dimensions but also the relative size of the abdominal and thoracic aortas in each animal. We calculated the abdominal/thoracic (A/T) ratio for the lumen area as well as the A/r ratio for the internal elastic lamina (IEL) area. With difli.tse enlargement, or ectasia,the ratios would be unchanged. In the two diet induction groups (6 months and 12 months) the A/T lumen area ratios were 0.45 + 0.13 and 0.42 c 0.12, respectively, and this is the same ratio as is found in normal-diet control animals (unpublished observation). For the regression animals the lumen area ratio was increased to 0.64 -C 0.30 @ < 0.05), indicating aortic enlargement localized in the abdominal aorta. There was no enlargement of the thoracic aorta. Dr. Stehbens further alleges that we did not demonstrate aneurysmal dilation in any animal and that we did not indicate the extent of the dilation. On the contrary, we clearly demonstrated in the text and in Fig. 2 the extent of dilation for each animal in each of the three groups. In four of the six regression animals, the lumen area and IEL area were more than 1 SD greater than the mean of the same measuremenfi in the two dietary groups. In two regression animals, both lumen area and IEL area were more than 2 SD above the mean for both dietary groups and might be considered aneurysmal. We chose an even stricter definition of aneurysm. In one regression animal, both lumen area and IEL area were more than 4 SD greater than the mean for both dietary groups. This animal alsohad an m lumen area ratio more than 4 SD above the mean. This marked localized dilation of the abdominal aorta, more than twice the diameter of the normal aorta and more than 1.2 times larger than the thoracic aorta, can be appropriately classified as a true aneurysm by every criterion for the definition of aneurysms. Although it is true that intimal plaque deposition would tend to reduce lumen caliber, the true measure of aortic size is the area encompassed by the IEL, which would not be altered by intimal plaque deposition. We therefore used the IEL area to assessaortic size. We reported no difference in IEL area between 6-month and 12-month diet induction animals. Thoracic and abdominal aortic size in these diet-fed animals was no different from that in normal-diet control animals (unpublished observations). Although it is true that a 2% cholesterol/25% peanut oil diet affects the arterial wall, administration of this diet alone for a 12-month period did not result in aneurysmal dilation in our experiment. Yet, aswe indicated in our article, animals on a 6-month regression regimen after 6 months of atherogenic diet had a twofold enlargement of abdominal aortic IEL area during the same period (p c 0.05). We assessedthe relation of animal size and weight to aortic dimensions. There was no correlation between gross body weight and aortic size, although the numbers of animals studied were small. We also searchedfor relationships among body size, serum cholesterol, plaque forma-
