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Acute life-threatening hypertension following balloon angioplasty of native coarctation of the aorta
Volume 125, Number 3 American Heart Jo~rk4
Tani et al.
Acute life-threatening hypertension following balloon angioplasty of native coarctation of the aorta Lloyd Y. Tani, MD, Garth S. Orsmond, MD, Mark M. Boucek, MD, and Robert E. Shaddy, Salt Lahe city, Ufah
MD
The first reports of percutaneous balloon angioplasty of aortic coarctation first appeared in the early 198Os.*x ’ Since then, its use has spread and it is now considered by some to be the treatment of choice for aortic recoarctation. Its role in the treatment of native coarctation remains less clear because of reports of the development of aneurysms at the site of coarctation following angioplasty.3,4 One of the stated advantages of balloon angioplasty has been the lack of postdilation paradoxical hypertension.’ Postoperative systemic hypertension is a well-recognized, frequent problem after surgery for coarctation,” but is rare after balloon angioplasty of native aortic coarctation. This report describes a case of severe, acute life-threatening hypertension following balloon dilation of native coarctation. An asymptomatic 7-year-old boy was admitted for cardiac catheterization of coarctation of the aorta. On examination, right arm blood pressure was 140/100 mm Hg and left leg pressure was 80 mm Hg systolic by Doppler echocardiography. Heart rate and respirations were normal. A grade 3/6 systolic ejection murmur was heard best at the upper left sternal border and in back on the left. Right and left arm pulses were easily palpable and equal, while lower extremity pulses were absent. A chest x-ray film showed dilation of the descending aorta, but heart size and pulmonary vascularity were normal. No rib notching was seen. The electrocardiogram was normal. An echocardiogram showed coarctation of the aorta with left ventricular hypertrophy. At catheterization, right heart pressures and saturations were normal. On left heart catheterization, there was no gradient across the aortic valve. Ascending aortic pressure was 144/80 (mean 100) mm Hg and descending aortic pressure was 85/75 (mean 78) mm Hg. An aortogram showed moderately severe coarctation distal to the origin of the left subclavian artery, with a dilated descending aorta and multiple collaterals. Using calibration blocks, the aortic isthmus measured 13 mm and the coarctation site measured 6.5 mm in diameter. Two milligrams ofpropranolol was given intravenously before dilation. A 12 mm balloon angioplasty catheter (Meditech, Watertown, Mass.) was advanced over an exchange wire to the site of coarctation. The balloon was inflated with dilute contrast to 4 atm pressure. Because there was a minimal reduction in gradient, the balloon dilation was repeated using a 15 From mary Reprint dren’s
the Division Children’s
of Pediatric Cardiology, Department of Pediatrics. Medical Center and the University of Utah.
requests: Lloyd Y. Tani, Medical Center, 100 North
Au k&AH?‘
MD, Pediatric Medical Drive,
,I 1993:125:907-908.
Copyright 1993 0002.87O:CX?&1.00
by Mosby-Year Book, + .lO 4/4/43463
Inc.
Cardiology, Salt Lake
Pri-
Primary ChilCity, UT84113.
907
mm balloon angioplasty catheter (Meditech Devices, Inc.). Following this dilation, pressures were 135186 and 120186 mm Hg in the ascending aorta and descending aorta, respectively. Following catheter removal and hemostasis, left leg pulses were normal while right leg pulses were palpable but slightly decreased. The patient was conscious and alert when admitted to the ward. Propranolol (1 mg/ kg) was given orally shortly after admission. Right arm blood pressure was 140/104 mm Hg and the heart rate was 60 beats/min. Vital signs were monitored every 30 minutes. Three hours after the procedure, the blood pressure was noted to be 195/130 mm Hg. The pulse rate slowed to 30 beats/min, with a wide complex QRS noted on a bedside monitor. Peripheral perfusion was poor. The patient lost consciousness. Atropine and hydralazine were given, resulting in sinus rhythm at 75 beats/min and a blood pressure of 120/70 mm Hg. A nitroprusside infusion was started but was discontinued 1 hour later with no further elevations in blood pressure. The patient’s mental status and neurologic examination quickly returned to normal. He was discharged 2 days later receiving oral propranolol. Right arm blood pressure was 110/70 mm Hg at a follow-up visit. Postoperative hypertension after surgical repair of coarctation is well documented, occurring in the majority of patients.6 The sympathetic nervous system and the reninangiotensin system are believed to be important in the pathogenesis of this hypertension.” Prophylactic propranolo1 started 2 weeks before surgery and given during the first postoperative week has been shown to blunt the hypertension following surgical repair of coarctation? Complications reported after balloon angioplasty of native coarctation include aneurysms, femoral artery thrombosis, prolonged bleeding, and even death.’ Paradoxical hypertension has been reported to occur after balloon dilation of recoarctation and rarely after balloon dilation of native coarctation.gm’l However, in this setting, the hypertension has been reportedly mild. Choy et al.,” in comparing surgery and balloon angioplasty, showed increases in catecholamines and renin activity following surgery but not after balloon angioplasty. This correlated with the lack of paradoxical hypertension seen after balloon angioplasty in these patients. In a recent report of the Valvuloplasty and Angioplasty of Congenital Anomalies registry (VACA),‘, le hypertension occurred in 2 r r of patients following balloon angioplasty of recoarctation of the aorta,” but was not reported in patients following balloon angioplasty of native coarctati0n.s The mechanism of the paradoxical hypertension occurring in the patient in this report is unknown. One might speculate that increased sympathetic activity (with inadequate p-blockade), unopposed e-mediated vasoconstriction, or increased plasma renin activity were important in the pathogenesis of the severe hypertension, but plasma catecholamines and renin activity were not measured. What is certain is that the hypertension was severe and required immediate treatment. Interestingly, the hypertension developed despite the previous administration of propranolol. We conclude that, although uncommon, hypertension may occur after balloon angioplasty of native coarctation and may be severe, even life-threatening. Be-
American
cause of this and other reported complications, close observation and monitoring (including blood pressure) oi’ patients after balloon angioplasty of native coarctation are advisable. REFERENCES 1. Lock
JE, Bass .JL, Amplatz K, Fuhrman BP, CastanedaZuniga W. Balloon dilation angioplasty of aortic coarctations in infants and children. Circulation 1983;68:109-16. 2. Kan ,JS, White RI, Mitchell SE, Farmlett Eel, Donahoo .JS.
Gardner TJ. Treatment of restenosis of coarctation by percutaneous transluminal angioplasty. Circulation 1983;68:108794. :i. Hrandt
B III,
Marvin
Wcl Jr, Rose EF, Majoney
LT.
Surgical
treatment of coarctation of the aorta after balloon angioplasty. .I Thorac Cardiovas Surg 1987:94:715-g. 4. Marvin WJ, Mahoney LT, Rose EF. Pathologic sequelae ot <5
balloon dilation angioplasty for unoperated coarctation of the aorta in children [Abstract]. J Am Co11 Cardiol 1986;7:117A. Choy M, Rorchini AP, Beekman RH, Rosenthal A, Dick M, Crowley D, Behrendt D, Snider AR. Paradoxical hypertension after repair of coarctation of the aorta in children: balloon angioplasty versus surgical repair. Circulation 1987;75:1186-91.
6. Rocchini AP, Rosenthal A, Barger AC, Castaneda AR, Nadas AS. Pathogenesis of paradoxical hypertension after coarctation
resection.
Circulation
1976;54:382-7.
R, Szpunar CA, Moore7. Gidding SS, Rocchini AP, Beekman head C, Behrendt D, Rosenthal A. Therapeutic effect of propranolol on paradoxical tion of’ the aorta. N
hypertension
after
repair
of coarcta-
Engl J Med 1985:312:1224-8. 8. Tvnan M, Finley JR. Fontes V, Hess J. Kan J. Balloon ang-ioplasty for the treatment of native coarctation: results of Valvuloplasty and Angioplasty of Congenital Am J Cardiol 1990;65:790-2.
9. Rae PS. Transcatheter
Anomalies
registry.
treatment of pulmonary stenosis and
coarctation of the aorta: experience with percutaneous balloon dilation. Br Heart .I 1986;56:250-8. del,ezo J, Sancho M, Pan M, Romero M, Olivera C. 10. Suarez Luque M. Angiographic follow-up after balloon angioplasty for coarctation ofthe aorta. .J Am Co11 Cardiol 1989;13:689-95. 11. Lababidi Z, Madigan N, Wu J, Murphy TJ. Balloon coarctation angioplasty in an adult. Am .J Cardiol 1984;53:350-1. 12. Hellenhrand WE, Allen HD? Golinke R,J, Hagler DJ, Lutin W. Kan .I. Balloon angioplasty for aortic recoarctation: results nl Valvuloplastv and Angioplasty of Congenital Anomalies regist rv. Am J Cardioi 1990:65:793-7.
lmmunohistochemical analysis of a human coronary artery exposed to excimer laser angioplasty in vivo: Evidence for release of fibroblast growth factor at the site of injury Jan Nilsson, MD,a Istvan Herzfeld, MD,b Lars Grip, MD,’ Bengt Aberg, MD,d and Lars Ryden, MD, FACC’ Stockholm. Sweden From the Departments “Thoracic Surgery, holm. Sweden.
ofaMedicine, “Thoracic Radiology, Karolinska Sjukhuset. Karolinska
Supported Swedish
by grants from the Swedish MedIcal Research Council.
Reprint SJukhuwt
requests: Jan Nilsson, MD, Department of Medicine, Bm 60500, S-104 01 Stockholm, Sweden.
An1 HRAII’I‘
Heart
.I 1993:1‘L5:908~912.
Copyright 1993 by Mrmby-Year Book, 0l)o2-8i(l:i/H:1/61.oO + .l(l -t/4/43381
Inc.
and Lung
‘Cardiology. Institute%. Foundation
and Stockand the
Karolinska
March 1993 tieart Journal
Laser technology provides new means to t.reat coronary ant peripheral artery disease. In contrast to initial expectntions, recent clinical trials indicate that the rate of rest enosis is similar to that reported after balloon angioplasty.‘, ’ The mechanisms responsible for the development of restenosis after angioplasty remain poorly understood. Histologic studies indicate that the major f’actor involved in restenosis is a rapid intimal proliferation of smooth muscle cells? ’ The present report describes the histology of a coronary artery removed at surgery 2 hours after excimer laser angioplasty. Lsing antibodies against platelet-derived growth factor. basic and acidic fibroblast growth factor, and cell-specific antibodies. we have tried to analyze the biologic processes involved in the acut.e reaction of a human artery to excimer laser injury. The patient, a 68.year-old man with a history of four previous myocardial infarcts (as assessed by conventional enzymatic criteria) had experienced effort-related angina pectoris for several years. It increased in intensity after the last infarct, which occurred 3 months before the procedure. A preprocedure coronary’ arteriogram (Fig. 1, ‘4; :! months before angioplasty) revealed double-vessel disease with a 9.5’, stenosis in the mid portion of the right coronary artery. Left ventricular function was normal. The immediate preprocedure angiogram showed that the artery had become t.otally occluded with incomp1et.e collateral filling to the distal parts from the left coronary artery (Fig. 1. 6rl. Heparin was given during the procedure. The dosage was guided by the activated coagulation time, which was kept above 400 seconds. The occlusion was passed with a 0.018 inch guide wire. The tip, which was clearly visible in the distal part of the right coronary artery, was positioned in the posterior descending branch (Fig. 1, CJ. The laser source was a 308 nm. xenon chloride excimer device (Advanced Interventional Systems, Inc., Irvine, Calif.) calibrated to emit energy pulses of 40 mJ/mm”. In all, 1280 pulses were delivered through a :! mm laser catheter at t.he proximal site of’ the occlusion. This was, however, impossible to pass with use of a moderate pressure. A control angiogram demonstrated extravasation of x-ray contrast medium (Fig. 1. DJ. The patient was immediately brought to the operating room because of this perforation. He remained hemodynamically stable until and during surgery, during which a saphenous vein graft was anastomosed to the peripheral part of the right artery. Because of bleeding at the site of the perforation a section of’ the vessel which was approximately 30 mm long. was removed. The postoperative course was uneventful without any signs of’ myocardial infarction. Air-dried, 4 to e5pm thick cryostat sections of the artery were fixed in acetone. Endogenous peroxidase was blocked by incubating the sections in 3 ‘( aqueous hydrogen peroxide for 5 minutes. The specimens were then rinsed in phosphate-buffered saline, exposed to 10’; normal goat serum for 30 minutes, and incubated with antibodies against platelet-derived growth factor. acidic fibroblast growth factor, basic fibroblast growth fact.or (Boehringer Mannheim GMHH, Mannheim. Germany). human monocytes (CDllc), 7’ helper lymphocytes (CD1). ‘l? suppressor lym.phocytes (CDS. Becton Dickinson. Mountain View, Calif.), and smooth muscle cells in a humidifving chamber for 2-I
Tani et al.
Acute life-threatening hypertension following balloon angioplasty of native coarctation of the aorta Lloyd Y. Tani, MD, Garth S. Orsmond, MD, Mark M. Boucek, MD, and Robert E. Shaddy, Salt Lahe city, Ufah
MD
The first reports of percutaneous balloon angioplasty of aortic coarctation first appeared in the early 198Os.*x ’ Since then, its use has spread and it is now considered by some to be the treatment of choice for aortic recoarctation. Its role in the treatment of native coarctation remains less clear because of reports of the development of aneurysms at the site of coarctation following angioplasty.3,4 One of the stated advantages of balloon angioplasty has been the lack of postdilation paradoxical hypertension.’ Postoperative systemic hypertension is a well-recognized, frequent problem after surgery for coarctation,” but is rare after balloon angioplasty of native aortic coarctation. This report describes a case of severe, acute life-threatening hypertension following balloon dilation of native coarctation. An asymptomatic 7-year-old boy was admitted for cardiac catheterization of coarctation of the aorta. On examination, right arm blood pressure was 140/100 mm Hg and left leg pressure was 80 mm Hg systolic by Doppler echocardiography. Heart rate and respirations were normal. A grade 3/6 systolic ejection murmur was heard best at the upper left sternal border and in back on the left. Right and left arm pulses were easily palpable and equal, while lower extremity pulses were absent. A chest x-ray film showed dilation of the descending aorta, but heart size and pulmonary vascularity were normal. No rib notching was seen. The electrocardiogram was normal. An echocardiogram showed coarctation of the aorta with left ventricular hypertrophy. At catheterization, right heart pressures and saturations were normal. On left heart catheterization, there was no gradient across the aortic valve. Ascending aortic pressure was 144/80 (mean 100) mm Hg and descending aortic pressure was 85/75 (mean 78) mm Hg. An aortogram showed moderately severe coarctation distal to the origin of the left subclavian artery, with a dilated descending aorta and multiple collaterals. Using calibration blocks, the aortic isthmus measured 13 mm and the coarctation site measured 6.5 mm in diameter. Two milligrams ofpropranolol was given intravenously before dilation. A 12 mm balloon angioplasty catheter (Meditech, Watertown, Mass.) was advanced over an exchange wire to the site of coarctation. The balloon was inflated with dilute contrast to 4 atm pressure. Because there was a minimal reduction in gradient, the balloon dilation was repeated using a 15 From mary Reprint dren’s
the Division Children’s
of Pediatric Cardiology, Department of Pediatrics. Medical Center and the University of Utah.
requests: Lloyd Y. Tani, Medical Center, 100 North
Au k&AH?‘
MD, Pediatric Medical Drive,
,I 1993:125:907-908.
Copyright 1993 0002.87O:CX?&1.00
by Mosby-Year Book, + .lO 4/4/43463
Inc.
Cardiology, Salt Lake
Pri-
Primary ChilCity, UT84113.
907
mm balloon angioplasty catheter (Meditech Devices, Inc.). Following this dilation, pressures were 135186 and 120186 mm Hg in the ascending aorta and descending aorta, respectively. Following catheter removal and hemostasis, left leg pulses were normal while right leg pulses were palpable but slightly decreased. The patient was conscious and alert when admitted to the ward. Propranolol (1 mg/ kg) was given orally shortly after admission. Right arm blood pressure was 140/104 mm Hg and the heart rate was 60 beats/min. Vital signs were monitored every 30 minutes. Three hours after the procedure, the blood pressure was noted to be 195/130 mm Hg. The pulse rate slowed to 30 beats/min, with a wide complex QRS noted on a bedside monitor. Peripheral perfusion was poor. The patient lost consciousness. Atropine and hydralazine were given, resulting in sinus rhythm at 75 beats/min and a blood pressure of 120/70 mm Hg. A nitroprusside infusion was started but was discontinued 1 hour later with no further elevations in blood pressure. The patient’s mental status and neurologic examination quickly returned to normal. He was discharged 2 days later receiving oral propranolol. Right arm blood pressure was 110/70 mm Hg at a follow-up visit. Postoperative hypertension after surgical repair of coarctation is well documented, occurring in the majority of patients.6 The sympathetic nervous system and the reninangiotensin system are believed to be important in the pathogenesis of this hypertension.” Prophylactic propranolo1 started 2 weeks before surgery and given during the first postoperative week has been shown to blunt the hypertension following surgical repair of coarctation? Complications reported after balloon angioplasty of native coarctation include aneurysms, femoral artery thrombosis, prolonged bleeding, and even death.’ Paradoxical hypertension has been reported to occur after balloon dilation of recoarctation and rarely after balloon dilation of native coarctation.gm’l However, in this setting, the hypertension has been reportedly mild. Choy et al.,” in comparing surgery and balloon angioplasty, showed increases in catecholamines and renin activity following surgery but not after balloon angioplasty. This correlated with the lack of paradoxical hypertension seen after balloon angioplasty in these patients. In a recent report of the Valvuloplasty and Angioplasty of Congenital Anomalies registry (VACA),‘, le hypertension occurred in 2 r r of patients following balloon angioplasty of recoarctation of the aorta,” but was not reported in patients following balloon angioplasty of native coarctati0n.s The mechanism of the paradoxical hypertension occurring in the patient in this report is unknown. One might speculate that increased sympathetic activity (with inadequate p-blockade), unopposed e-mediated vasoconstriction, or increased plasma renin activity were important in the pathogenesis of the severe hypertension, but plasma catecholamines and renin activity were not measured. What is certain is that the hypertension was severe and required immediate treatment. Interestingly, the hypertension developed despite the previous administration of propranolol. We conclude that, although uncommon, hypertension may occur after balloon angioplasty of native coarctation and may be severe, even life-threatening. Be-
American
cause of this and other reported complications, close observation and monitoring (including blood pressure) oi’ patients after balloon angioplasty of native coarctation are advisable. REFERENCES 1. Lock
JE, Bass .JL, Amplatz K, Fuhrman BP, CastanedaZuniga W. Balloon dilation angioplasty of aortic coarctations in infants and children. Circulation 1983;68:109-16. 2. Kan ,JS, White RI, Mitchell SE, Farmlett Eel, Donahoo .JS.
Gardner TJ. Treatment of restenosis of coarctation by percutaneous transluminal angioplasty. Circulation 1983;68:108794. :i. Hrandt
B III,
Marvin
Wcl Jr, Rose EF, Majoney
LT.
Surgical
treatment of coarctation of the aorta after balloon angioplasty. .I Thorac Cardiovas Surg 1987:94:715-g. 4. Marvin WJ, Mahoney LT, Rose EF. Pathologic sequelae ot <5
balloon dilation angioplasty for unoperated coarctation of the aorta in children [Abstract]. J Am Co11 Cardiol 1986;7:117A. Choy M, Rorchini AP, Beekman RH, Rosenthal A, Dick M, Crowley D, Behrendt D, Snider AR. Paradoxical hypertension after repair of coarctation of the aorta in children: balloon angioplasty versus surgical repair. Circulation 1987;75:1186-91.
6. Rocchini AP, Rosenthal A, Barger AC, Castaneda AR, Nadas AS. Pathogenesis of paradoxical hypertension after coarctation
resection.
Circulation
1976;54:382-7.
R, Szpunar CA, Moore7. Gidding SS, Rocchini AP, Beekman head C, Behrendt D, Rosenthal A. Therapeutic effect of propranolol on paradoxical tion of’ the aorta. N
hypertension
after
repair
of coarcta-
Engl J Med 1985:312:1224-8. 8. Tvnan M, Finley JR. Fontes V, Hess J. Kan J. Balloon ang-ioplasty for the treatment of native coarctation: results of Valvuloplasty and Angioplasty of Congenital Am J Cardiol 1990;65:790-2.
9. Rae PS. Transcatheter
Anomalies
registry.
treatment of pulmonary stenosis and
coarctation of the aorta: experience with percutaneous balloon dilation. Br Heart .I 1986;56:250-8. del,ezo J, Sancho M, Pan M, Romero M, Olivera C. 10. Suarez Luque M. Angiographic follow-up after balloon angioplasty for coarctation ofthe aorta. .J Am Co11 Cardiol 1989;13:689-95. 11. Lababidi Z, Madigan N, Wu J, Murphy TJ. Balloon coarctation angioplasty in an adult. Am .J Cardiol 1984;53:350-1. 12. Hellenhrand WE, Allen HD? Golinke R,J, Hagler DJ, Lutin W. Kan .I. Balloon angioplasty for aortic recoarctation: results nl Valvuloplastv and Angioplasty of Congenital Anomalies regist rv. Am J Cardioi 1990:65:793-7.
lmmunohistochemical analysis of a human coronary artery exposed to excimer laser angioplasty in vivo: Evidence for release of fibroblast growth factor at the site of injury Jan Nilsson, MD,a Istvan Herzfeld, MD,b Lars Grip, MD,’ Bengt Aberg, MD,d and Lars Ryden, MD, FACC’ Stockholm. Sweden From the Departments “Thoracic Surgery, holm. Sweden.
ofaMedicine, “Thoracic Radiology, Karolinska Sjukhuset. Karolinska
Supported Swedish
by grants from the Swedish MedIcal Research Council.
Reprint SJukhuwt
requests: Jan Nilsson, MD, Department of Medicine, Bm 60500, S-104 01 Stockholm, Sweden.
An1 HRAII’I‘
Heart
.I 1993:1‘L5:908~912.
Copyright 1993 by Mrmby-Year Book, 0l)o2-8i(l:i/H:1/61.oO + .l(l -t/4/43381
Inc.
and Lung
‘Cardiology. Institute%. Foundation
and Stockand the
Karolinska
March 1993 tieart Journal
Laser technology provides new means to t.reat coronary ant peripheral artery disease. In contrast to initial expectntions, recent clinical trials indicate that the rate of rest enosis is similar to that reported after balloon angioplasty.‘, ’ The mechanisms responsible for the development of restenosis after angioplasty remain poorly understood. Histologic studies indicate that the major f’actor involved in restenosis is a rapid intimal proliferation of smooth muscle cells? ’ The present report describes the histology of a coronary artery removed at surgery 2 hours after excimer laser angioplasty. Lsing antibodies against platelet-derived growth factor. basic and acidic fibroblast growth factor, and cell-specific antibodies. we have tried to analyze the biologic processes involved in the acut.e reaction of a human artery to excimer laser injury. The patient, a 68.year-old man with a history of four previous myocardial infarcts (as assessed by conventional enzymatic criteria) had experienced effort-related angina pectoris for several years. It increased in intensity after the last infarct, which occurred 3 months before the procedure. A preprocedure coronary’ arteriogram (Fig. 1, ‘4; :! months before angioplasty) revealed double-vessel disease with a 9.5’, stenosis in the mid portion of the right coronary artery. Left ventricular function was normal. The immediate preprocedure angiogram showed that the artery had become t.otally occluded with incomp1et.e collateral filling to the distal parts from the left coronary artery (Fig. 1. 6rl. Heparin was given during the procedure. The dosage was guided by the activated coagulation time, which was kept above 400 seconds. The occlusion was passed with a 0.018 inch guide wire. The tip, which was clearly visible in the distal part of the right coronary artery, was positioned in the posterior descending branch (Fig. 1, CJ. The laser source was a 308 nm. xenon chloride excimer device (Advanced Interventional Systems, Inc., Irvine, Calif.) calibrated to emit energy pulses of 40 mJ/mm”. In all, 1280 pulses were delivered through a :! mm laser catheter at t.he proximal site of’ the occlusion. This was, however, impossible to pass with use of a moderate pressure. A control angiogram demonstrated extravasation of x-ray contrast medium (Fig. 1. DJ. The patient was immediately brought to the operating room because of this perforation. He remained hemodynamically stable until and during surgery, during which a saphenous vein graft was anastomosed to the peripheral part of the right artery. Because of bleeding at the site of the perforation a section of’ the vessel which was approximately 30 mm long. was removed. The postoperative course was uneventful without any signs of’ myocardial infarction. Air-dried, 4 to e5pm thick cryostat sections of the artery were fixed in acetone. Endogenous peroxidase was blocked by incubating the sections in 3 ‘( aqueous hydrogen peroxide for 5 minutes. The specimens were then rinsed in phosphate-buffered saline, exposed to 10’; normal goat serum for 30 minutes, and incubated with antibodies against platelet-derived growth factor. acidic fibroblast growth factor, basic fibroblast growth fact.or (Boehringer Mannheim GMHH, Mannheim. Germany). human monocytes (CDllc), 7’ helper lymphocytes (CD1). ‘l? suppressor lym.phocytes (CDS. Becton Dickinson. Mountain View, Calif.), and smooth muscle cells in a humidifving chamber for 2-I