176
lottrnal of VASCULAR SURGERY
Letters to the Editors
was similar to patients with occlusion at presentation. Finally two of the six patients who suffered a stroke at the time of occlusion had suffered a previous transient ischemic attack. Why did the patients not undergo surgery at this time? The prerequisite for natural history data is that information on a defined population is gathered prospectively and is complete. Clarification of the above questions would be most helpful in assessing the true significance of the authors' findings. Mary Paula Co,an, MD Dermot J. Moore, MD, FRCSI GregorD. Shanik, MD, MCh, FRCSI, FACS
Department of Surgery St. James's Hospital P.O. Box 580 Dublin 8, Ireland
REFERENCE 1. Roederer GO, Langlois YE, lager KA, et al. The natural history of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke 1984;15:605-13.
Reply
cussion. It relates to either the patients themselves or their referring physicians declining surgical therapy. To address the question raised bv Shanik et al. of progression to occlusion in specific populations, we analyzed data for two sequentially studied subpopulations. (1) Asymptomatic bruit, (2) Unoperated arteries in patients followed after contralateral endarterectomy. We believe these data must be analyzed and reported by the life-table method. The average annual incidence of occlusion over 5 years is 0.6% per annum in the asymptomatic bruit group, and 0.7% per annum in the follow-up thromboendarterectomy group. Incidentally, the crude incidence rate in the report bv Roederer et al, would be 3.2% (10 occlusions among 312 sides patent at entq,), and l~br the present asymptomatic bruit group, 16 of the 650, or 2.5%. We do not believe comparison of the crude rates allow meaningful comparisons, since thev do not make adjustment tbr time under observation. Stephen C. Nicholls, MD Robert Bergelin, MS D. Eugene Strandness, AID
Department of SurgeD, ZA- 16 Harborview Medical Center 325 Ninth Ave. Seattle, WA 98104
To the Editors:
We appreciate the opportunity to discuss the points raised by Shanik et al. in reference to our article, "Neurologic sequelae of unilateral carotid artery occlusion," (J VASC SURG 1989;10:542-8). The purpose of this report was to document the neurologic events relating to acute occlusion of the internal carotid artery. To this end we analyzed data drawn from our entire experience with 2700 patients undergoing carotid duplex scans. We evaluated all patients in whom carotid patency was documented on at least one occasion and subsequently was shown to have proceeded to occlusion. This sequence was noted in 31 patients. In 7, the artery had been previously endarterectomized, and these were excluded from further analysis. We therefore reported 24 patients. With regard to specific points raised (1) The analysis does not address the question of incidence of progression to occlusion in a selected population, nor does it differentiate patients returning for study on the basis of symptoms. (2) The question of contralateral symptoms is addressed in the "Results" section in paragraph 1. There was one contralateral transient ischemic attack. (3) The longterm outcome of patients progressing to occlusion versus those with established occlusion at presentation may be made by comparing the outcome of patients in this study with those in our previous report on the natural history of established occlusion (J VASC SURG 1986;4:479-85), bearing in mind that the patient numbers and follow-up intervals are different. (4) The question of patients with premonitory transient ischemic attack not undergoing prophylactic endarterectomy is addressed in the closing dis-
Histogenesis o f intimal hyperplasia and arterial dissection To the Editors:
In my previous letter I proposed that corticosteroids suppress intimal hyperplasia because of their antiangiogenic action? I would like to support this hypothesis by further evidence. Davies and AI-Tikriti2 have visualized large round clear cells surrounded by collagenous fibers in coronary allograft atherosclerosis. We interpret these cells as undifferentiated vascular endothelial cells involved in healing? As far as I know this is the first evidence that the same cells may fbrm capillary sprouts in the periarterial space, infiltrate the arterial wall, and participate in a formation of intimal hyperplasia. The observation of Davies and Al-Tik,riti 2 inspired mc to pay more attention to the vasa vasorum implicated recently again in a fbrmation of intimal thickening? The best book concerning this subject is undoubtly that written bv Winternitz et al. s who demonstrated a composition of atherosclerotic plaques with an extraordinary perspicuousness. They also visualize large round clear cells surrounded by collagenous fibers and containing red blood cells. The cells may undergo necrosis and leavy empty spaces filled by erythrocytes behind them, which may lead to arterial dissection. The fact that Winternitz et al.s do not realize a relationship between the undifferentiated and differentiated capillary endothelial cells considering the former to
Volume 13 Number 1 January 1991
be mononuclear phagocytes does not diminish their merits, because they draw a right conclusion from the observations: In the artery, "the response to injury is mediated through the capillary bed and is manifested by two more or less distinct and variably proportioned reactions: exudation and proliferation." It is well known that both processes may be controlled by corticosteroids. Having in mind that both arterial wall hemorrhage and dissection appear where undifferentiated endothelial cells undergo necrosis we may understand the pathogenesis of the dissecting aneurysm of the aorta and muscular arteries. Recently, Hartman and Eftychiadis6 described such dissections and try to explain them by a concept of the smooth muscle cells behaving as multipotential mesenchyma. A careful reader recognizes immediately that it is extremely difficult to attune this concept to the observations of Hartman and Eftychiadis? In return, their observation may be easily explained by a concept of the undifferentiated vascular endothelial cell. These cells form capillary sprouts into the cells of which red blood cells penetrate. A dissection is formed by a coalescence of individual cell cavities under the most probable influence of two factors: (a) proteolytic action of highly invasive undifferentiated endothelial cells,7 and (b) mechanical action o f blood pressure. One may even hypothesize that careful antiangiogenesis would be a suitable treatment for an evolving dissecting aneurysm. ~" Jiri T. Beranek, MD
Division of Cardiothoracic Surgery, Harper Hospital Department of Surgery Wayne State University School of Medicine Detroit, MI 48201
REFERENCES 1. Beranck JT. Efficacyof corticosteroids in suppression ofintimal hyperplasia: a possible antiangiogenic effect. J VASC SURG 1990; 11:609. 2. Davies H, AI-Tikriti S. Coronary arterial pathology in the transplanted human heart. Int J Cardiol 1989;25:99-118. 3. Beranek JT, Cavarocchi NC. Undifferentiated vascular endothelial cells in coronary allograft atherosclerosis. Int J Cardiol 1990;28:127-8. 4. Sarkisov DS, Kolocolchicova EG, Varava BN, Tjurmin AV, Peclo MM, Printseva OYu. Morphogenesis of intimal thickening in nonspecific aortoarteritis. Hum Pathol 1989;20: 1048-56. 5. Winternitz MC, Thomas RM, LeCompte PM. The biology of arteriosclerosis. Springfield: Charles C Thomas, 1938:1-142. 6. Hartman JD, Eftychiadis AS. Medical smooth-muscle cell lesions and dissection of the aorta and muscular arteries. Arch Pathol Lab Med 1990;114:50-61. 7. Rifkin DB, Tsuboi R, Mignatti P. The role of proteases in matrix break-down during cellular invasion. Am Rev Respir Dis 1989; 140:1112-3. 8. Beranek IT. Antiangiogenesis comes out of its shell. Cancer J 1988;2:87-8. 9. Beranek JT. Transformation of capillaries into interstitial tissue: further evidence in favour of the angiogenic hypothesis of repair and fibrosis. Br J Plast Surg 1989;42:725.
Letters to the Editors
177
Myocardial ischemia caused by postoperative malfunction o f a patent internal mammary coronary arterial graft To the Editors:
In a recent article article by Granke et al. (J VASC SURG 1990;11:659-64) carotid-subclavian bypass grafting was recommended as the procedure of choice for subclavian artery stenosis proximal to an internal mammary artery (IMA) graft when the stenosis resulted in myocardial ischemia (IMA steal). The authors also stated that percutaneous balloon angioplasty (VIA) o f the subclavian artery was unproven, citing an article by Kachel et al.~ A review of Kachel's article and reports of subclavian PTA by others, as well as our own experience with subclavian artery PTA, including IMA steal syndrome, leads us to different conclusions. In the article by Kachel et al. (1), all 21 subclavian artery stenoses were successfully dilated by VfA. Unfortunately, clinical follow-up is not given in this report. A review o f the literature on subclavian artery PTA (82 patients) validates Kachel's results. 2~s Technical success rates are high (95%). Major complications, for embolism and occlusion are infrequent (4%). Restenosis rates are low (10%) when patients have been followed as long as 5 years. We have performed subclavian artery PTA in 39 patients, including 3 patients with IMA steal syndrome. Technical success was achieved in 92%, including all three patients with IMA steal syndrome. Myocardial ischemia was relieved in these three patients, and subclavian artery, restenosis did not develop. We believe subclavian artery PTA is a safe and effective technique and the procedure o f choice for symptomatic subclavian artery stenosis and the IMA steal syndrome. Surgical bypass should be reserved for subclavian artery occlusions and PTA failures. Robert G. Levitt, M D Chester R. Jarmolowski, 214D Mark H. Whole, M D
Pittsburgh Vascular Institute Shadyside Hospital 5230 Centre Ave. Pittsburgh, PA 15232 REFERENCES 1. Kachel R, Endert G, Basche S, Grossmann K, Glaser FH. Percutaneous transluminal angioplasty (dilatation) of carotid, vertebral, and innominate artery stenoses. Cardiovasc Intervent Radiol 1987;10:142-6. 2. Ringelstein EB, Zeumer H. Delayed reversal of vertebral artery blood flow following percutaneous transluminal angioplasty for subclavian steal syndrome. Neuroradiology 1984;26:18990, 3. Motarjeme A, Keifer JW, Zuska AJ, Nabawi P, Percutaneous transluminal angioplasty for treatment of subclavian steal. Radiology 1985;155:611-3. 4. Vitek, JJ, Subclavian artery angioplasty and the origin of the vertebral artery. Radiology 1989;170:407-9. 5. Erbstein RA, Wholey MH, Smoot S. Subclavian artery steal syndrome: treatment by percutaneous transluminal angioplasty. AJR 1988;151:291-4.
lottrnal of VASCULAR SURGERY
Letters to the Editors
was similar to patients with occlusion at presentation. Finally two of the six patients who suffered a stroke at the time of occlusion had suffered a previous transient ischemic attack. Why did the patients not undergo surgery at this time? The prerequisite for natural history data is that information on a defined population is gathered prospectively and is complete. Clarification of the above questions would be most helpful in assessing the true significance of the authors' findings. Mary Paula Co,an, MD Dermot J. Moore, MD, FRCSI GregorD. Shanik, MD, MCh, FRCSI, FACS
Department of Surgery St. James's Hospital P.O. Box 580 Dublin 8, Ireland
REFERENCE 1. Roederer GO, Langlois YE, lager KA, et al. The natural history of carotid arterial disease in asymptomatic patients with cervical bruits. Stroke 1984;15:605-13.
Reply
cussion. It relates to either the patients themselves or their referring physicians declining surgical therapy. To address the question raised bv Shanik et al. of progression to occlusion in specific populations, we analyzed data for two sequentially studied subpopulations. (1) Asymptomatic bruit, (2) Unoperated arteries in patients followed after contralateral endarterectomy. We believe these data must be analyzed and reported by the life-table method. The average annual incidence of occlusion over 5 years is 0.6% per annum in the asymptomatic bruit group, and 0.7% per annum in the follow-up thromboendarterectomy group. Incidentally, the crude incidence rate in the report bv Roederer et al, would be 3.2% (10 occlusions among 312 sides patent at entq,), and l~br the present asymptomatic bruit group, 16 of the 650, or 2.5%. We do not believe comparison of the crude rates allow meaningful comparisons, since thev do not make adjustment tbr time under observation. Stephen C. Nicholls, MD Robert Bergelin, MS D. Eugene Strandness, AID
Department of SurgeD, ZA- 16 Harborview Medical Center 325 Ninth Ave. Seattle, WA 98104
To the Editors:
We appreciate the opportunity to discuss the points raised by Shanik et al. in reference to our article, "Neurologic sequelae of unilateral carotid artery occlusion," (J VASC SURG 1989;10:542-8). The purpose of this report was to document the neurologic events relating to acute occlusion of the internal carotid artery. To this end we analyzed data drawn from our entire experience with 2700 patients undergoing carotid duplex scans. We evaluated all patients in whom carotid patency was documented on at least one occasion and subsequently was shown to have proceeded to occlusion. This sequence was noted in 31 patients. In 7, the artery had been previously endarterectomized, and these were excluded from further analysis. We therefore reported 24 patients. With regard to specific points raised (1) The analysis does not address the question of incidence of progression to occlusion in a selected population, nor does it differentiate patients returning for study on the basis of symptoms. (2) The question of contralateral symptoms is addressed in the "Results" section in paragraph 1. There was one contralateral transient ischemic attack. (3) The longterm outcome of patients progressing to occlusion versus those with established occlusion at presentation may be made by comparing the outcome of patients in this study with those in our previous report on the natural history of established occlusion (J VASC SURG 1986;4:479-85), bearing in mind that the patient numbers and follow-up intervals are different. (4) The question of patients with premonitory transient ischemic attack not undergoing prophylactic endarterectomy is addressed in the closing dis-
Histogenesis o f intimal hyperplasia and arterial dissection To the Editors:
In my previous letter I proposed that corticosteroids suppress intimal hyperplasia because of their antiangiogenic action? I would like to support this hypothesis by further evidence. Davies and AI-Tikriti2 have visualized large round clear cells surrounded by collagenous fibers in coronary allograft atherosclerosis. We interpret these cells as undifferentiated vascular endothelial cells involved in healing? As far as I know this is the first evidence that the same cells may fbrm capillary sprouts in the periarterial space, infiltrate the arterial wall, and participate in a formation of intimal hyperplasia. The observation of Davies and Al-Tik,riti 2 inspired mc to pay more attention to the vasa vasorum implicated recently again in a fbrmation of intimal thickening? The best book concerning this subject is undoubtly that written bv Winternitz et al. s who demonstrated a composition of atherosclerotic plaques with an extraordinary perspicuousness. They also visualize large round clear cells surrounded by collagenous fibers and containing red blood cells. The cells may undergo necrosis and leavy empty spaces filled by erythrocytes behind them, which may lead to arterial dissection. The fact that Winternitz et al.s do not realize a relationship between the undifferentiated and differentiated capillary endothelial cells considering the former to
Volume 13 Number 1 January 1991
be mononuclear phagocytes does not diminish their merits, because they draw a right conclusion from the observations: In the artery, "the response to injury is mediated through the capillary bed and is manifested by two more or less distinct and variably proportioned reactions: exudation and proliferation." It is well known that both processes may be controlled by corticosteroids. Having in mind that both arterial wall hemorrhage and dissection appear where undifferentiated endothelial cells undergo necrosis we may understand the pathogenesis of the dissecting aneurysm of the aorta and muscular arteries. Recently, Hartman and Eftychiadis6 described such dissections and try to explain them by a concept of the smooth muscle cells behaving as multipotential mesenchyma. A careful reader recognizes immediately that it is extremely difficult to attune this concept to the observations of Hartman and Eftychiadis? In return, their observation may be easily explained by a concept of the undifferentiated vascular endothelial cell. These cells form capillary sprouts into the cells of which red blood cells penetrate. A dissection is formed by a coalescence of individual cell cavities under the most probable influence of two factors: (a) proteolytic action of highly invasive undifferentiated endothelial cells,7 and (b) mechanical action o f blood pressure. One may even hypothesize that careful antiangiogenesis would be a suitable treatment for an evolving dissecting aneurysm. ~" Jiri T. Beranek, MD
Division of Cardiothoracic Surgery, Harper Hospital Department of Surgery Wayne State University School of Medicine Detroit, MI 48201
REFERENCES 1. Beranck JT. Efficacyof corticosteroids in suppression ofintimal hyperplasia: a possible antiangiogenic effect. J VASC SURG 1990; 11:609. 2. Davies H, AI-Tikriti S. Coronary arterial pathology in the transplanted human heart. Int J Cardiol 1989;25:99-118. 3. Beranek JT, Cavarocchi NC. Undifferentiated vascular endothelial cells in coronary allograft atherosclerosis. Int J Cardiol 1990;28:127-8. 4. Sarkisov DS, Kolocolchicova EG, Varava BN, Tjurmin AV, Peclo MM, Printseva OYu. Morphogenesis of intimal thickening in nonspecific aortoarteritis. Hum Pathol 1989;20: 1048-56. 5. Winternitz MC, Thomas RM, LeCompte PM. The biology of arteriosclerosis. Springfield: Charles C Thomas, 1938:1-142. 6. Hartman JD, Eftychiadis AS. Medical smooth-muscle cell lesions and dissection of the aorta and muscular arteries. Arch Pathol Lab Med 1990;114:50-61. 7. Rifkin DB, Tsuboi R, Mignatti P. The role of proteases in matrix break-down during cellular invasion. Am Rev Respir Dis 1989; 140:1112-3. 8. Beranek IT. Antiangiogenesis comes out of its shell. Cancer J 1988;2:87-8. 9. Beranek JT. Transformation of capillaries into interstitial tissue: further evidence in favour of the angiogenic hypothesis of repair and fibrosis. Br J Plast Surg 1989;42:725.
Letters to the Editors
177
Myocardial ischemia caused by postoperative malfunction o f a patent internal mammary coronary arterial graft To the Editors:
In a recent article article by Granke et al. (J VASC SURG 1990;11:659-64) carotid-subclavian bypass grafting was recommended as the procedure of choice for subclavian artery stenosis proximal to an internal mammary artery (IMA) graft when the stenosis resulted in myocardial ischemia (IMA steal). The authors also stated that percutaneous balloon angioplasty (VIA) o f the subclavian artery was unproven, citing an article by Kachel et al.~ A review of Kachel's article and reports of subclavian PTA by others, as well as our own experience with subclavian artery PTA, including IMA steal syndrome, leads us to different conclusions. In the article by Kachel et al. (1), all 21 subclavian artery stenoses were successfully dilated by VfA. Unfortunately, clinical follow-up is not given in this report. A review o f the literature on subclavian artery PTA (82 patients) validates Kachel's results. 2~s Technical success rates are high (95%). Major complications, for embolism and occlusion are infrequent (4%). Restenosis rates are low (10%) when patients have been followed as long as 5 years. We have performed subclavian artery PTA in 39 patients, including 3 patients with IMA steal syndrome. Technical success was achieved in 92%, including all three patients with IMA steal syndrome. Myocardial ischemia was relieved in these three patients, and subclavian artery, restenosis did not develop. We believe subclavian artery PTA is a safe and effective technique and the procedure o f choice for symptomatic subclavian artery stenosis and the IMA steal syndrome. Surgical bypass should be reserved for subclavian artery occlusions and PTA failures. Robert G. Levitt, M D Chester R. Jarmolowski, 214D Mark H. Whole, M D
Pittsburgh Vascular Institute Shadyside Hospital 5230 Centre Ave. Pittsburgh, PA 15232 REFERENCES 1. Kachel R, Endert G, Basche S, Grossmann K, Glaser FH. Percutaneous transluminal angioplasty (dilatation) of carotid, vertebral, and innominate artery stenoses. Cardiovasc Intervent Radiol 1987;10:142-6. 2. Ringelstein EB, Zeumer H. Delayed reversal of vertebral artery blood flow following percutaneous transluminal angioplasty for subclavian steal syndrome. Neuroradiology 1984;26:18990, 3. Motarjeme A, Keifer JW, Zuska AJ, Nabawi P, Percutaneous transluminal angioplasty for treatment of subclavian steal. Radiology 1985;155:611-3. 4. Vitek, JJ, Subclavian artery angioplasty and the origin of the vertebral artery. Radiology 1989;170:407-9. 5. Erbstein RA, Wholey MH, Smoot S. Subclavian artery steal syndrome: treatment by percutaneous transluminal angioplasty. AJR 1988;151:291-4.
