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Percutaneous balloon angioplasty of inferior vena cava in Budd–Chiari syndrome-R1
International Journal of Cardiology 83 (2002) 175–178 www.elsevier.com / locate / ijcard
Percutaneous balloon angioplasty of inferior vena cava in Budd–Chiari syndrome-R1 a b, a a a a Tongguo Wu , Lexin Wang *, Qiang Xiao , Bosong Wang , Shanying Li , Xiurong Li , Jinying Zhang a a
Department of Cardiology, The Affiliated Hospital of Taishan Medical College, Taishan, China School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia
b
Received 17 January 2002; accepted 23 January 2002
Abstract This study was to evaluate the clinical effects of percutaneous balloon angioplasty of Budd–Chiari syndrome (BCS) caused by inferior vena cava (IVC) obstruction. Between 1993 and 1999, 28 men and 14 women with mean age of 44612 years underwent percutaneous balloon angioplasty for primary BCS. Color Doppler ultrasound and venography showed membranous and segmental obstruction of IVC in 29 and 13 patients, respectively. Fourteen patients also had left- and / or mid-hepatic vein obstruction. Angioplasty of IVC was successful in 41 patients (97.6%), resulting in a reduction of pressure gradient between IVC and the right atrium from 15.062.5 to 5.560.8 mmHg (P,0.01). A stent was placed in the site of obstruction in the patient with unsuccessful balloon angioplasty. Patients with successful angioplasty or stent placement had significant improvement in clinical symptoms indicated by a reduction in hepatomegaly and the degree of ascites. No specific attempt was made to treat the occluded left- and / or mid-hepatic vein due to the presence of potent right hepatic vein. Over the follow-up period of 32612 months, restenosis of IVC occurred in only one patient (2.4%), which was redilated successfully. Percutaneous balloon angioplasty is a safe and effective therapy for Budd–Chiari syndrome caused by IVC obstruction, therefore should be the first choice of treatment for this condition. 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Budd–Chiari syndrome; Percutaneous angioplasty
1. Introduction Budd–Chiari syndrome (BCS) is an uncommon condition in which obstruction occurs in the larger hepatic veins and / or the inferior vena cava (IVC), resulting in hepatic centrilobular congestion and necrosis [1–3]. The disease is traditionally managed by surgical procedures such as portal or mesenteric– systemic shunting [4–6] and / or liver transplantation [7–9]. The development of catheter-based treatments, such as transjugular intrahepatic portosystemic shunt*Corresponding author. Tel.: 161-2-6933-2905; fax: 161-2-69332587. E-mail address: [email protected] (L. Wang).
ing [10,11], percutaneous hepatic vein angioplasty and / or stent placement [12–15] has expanded the therapeutic options of this condition. Recently percutaneous balloon angioplasty and stent placement has been used to treat obstructed IVC at or above hepatic level in primary BCS [16–19]. We report the results of 42 BCS patients who underwent angioplasty for IVC obstruction. 2. Patients and methods
2.1. Patients Between September 1993 and September 1999, 42
0167-5273 / 02 / $ – see front matter 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 02 )00037-2
176
T. Wu et al. / International Journal of Cardiology 83 (2002) 175 – 178
BCS patients (male 28, mean age 44612 years, range 12–62 years) were treated with percutaneous balloon angioplasty for IVC obstruction. The most common symptoms of these patients were ascites, liver and spleen enlargement and pitting oedema of the lower limbs. BCS and IVC obstruction were initially diagnosed with colour Doppler ultrasound followed by venography, which shows membranous (the length of obstructed IVC ,1.0 cm) or segmental (the length of obstructed IVC .1.0 cm) obstruction of IVC at or above hepatic level. Two patients with segmental IVC obstruction experienced IVC thrombosis immediately before hospitalisation.
deflated 2–3 times. The end point of the dilation was disappearance of the waist in the obstruction segment following inferior venography, and appearance of forward venous flow towards the right atrium. The second end point was a reduction in the pressure gradient between the right atrium and IVC. With the two patients who had IVC thrombosis prior to hospitalization, balloon angioplasty was performed immediately after thrombolysis with urokinase (500,000 units, i.v.). Heparin (3000–5000 units) was administered intravenously during the procedure, and was continuously infused 5000–6000 units / day for 1 week following the procedure.
2.2. Procedures
2.3. Follow-up studies
Under local anaesthesia, a 6 French sheath was inserted into the right femoral and right subclavian vein, respectively. A pigtail catheter was advanced into IVC below the level of hepatic vein via the femoral vein to measure IVC pressure. A second pigtail catheter was inserted to the lower right atrium via the subclavian vein to measure the right atrial pressure. This catheter was also used to perform venography of suprahepatic IVC. Under anterior–posterior and lateral fluoroscope projection, a contrast medium was injected into IVC via the right femoral vein to locate the obstruction in IVC and hepatic vein. Complete IVC obstruction was diagnosed if there was no contrast showing in the right atrium after the injection of the contrast medium from femoral veins. Then the contrast medium was injected simultaneously into the subclavian and femoral vein to show the right atrium and IVC, which measures the length of IVC obstruction. A Brockenbrough transeptal needle (Bard Inc., MA, USA), guided by a 0.032-inch guidewire, was advanced to the IVC obstruction site via the femoral vein. The needle was then manipulated to go through the lesion 0.5–1.0 cm at a time until it reaches the right atrium. Ultrasound was used to help monitor the direction of the Brockenbrough needle. When the Brockenbrough needle had crossed the site of obstruction, a 15–22 mm Inoue balloon catheter was placed across the lesion via an exchange guidewire to dilate the obstruction. The balloon was inflated and
Follow-up studies were carried out at regular intervals by questionnaires in all patients and by repeated clinical, two-dimensional and colour Doppler ultrasound examinations.
2.4. Statistical analysis Data were expressed as mean value6S.D. An ANOVA test was used to examine the differences in IVC pressure gradients before and after balloon angioplasty.
3. Results Membranous and segmental occlusion was identified in 29 and 13 patients, respectively. Fourteen (33.3%) patients also had left and / or mid-hepatic vein obstruction, whereas the right hepatic veins remained patent in these patients. Before balloon angioplasty of IVC, the mean IVC pressure was 17.063.0 mmHg (range, 10.0–19.0). The average pressure gradient between the right atrium and IVC was 15.062.5 mmHg. Successful IVC balloon angioplasty was achieved in 41 (97.6%) patients. Following angioplasty, the pressure gradient between the right atrium and IVC was reduced to 5.560.8 mmHg (P,0.01). A stent (4 cm length, 1.2 cm in diameter, Jayu Medical Equipment, Sheng-yang, PR China) was placed in the area
T. Wu et al. / International Journal of Cardiology 83 (2002) 175 – 178
of obstruction in the patient with unsuccessful IVC angioplasty. Stenting was not performed in patients with successful angioplasty. Within 72 h of the procedure, patients with successful angioplasty or stent placement experienced significant improvement in clinical symptoms and signs, with an increase in urine volume, a decrease in hepatomegaly and a marked reduction in ascites or oedema of the lower limbs. The improvement in clinical symptoms was closely related to the reduction in the pressure gradient between the right atrium and IVC. Twenty-eight patients who had pressure gradient reduction of more than 10 mmHg experienced the most significant increase in urine volume and reduction in hepatomegaly or ascites. With respect to biochemical changes at diagnosis, there was only mild elevation of aspartate aminotransferase (AST, 98–245 IU / l) in nine of the 42 patients. A moderate elevation in alkaline phosphatase (246–653 IU / l) was observed in 12 (including nine with elevated AST) of the 42 patients. After successful angioplasty, the aspartate aminotransferase level returned to normal in six patients, in the other three patients there was no change during the first 4 weeks. After treatment, there was normalisation of alkaline phosphatase in nine out of the 12 patients during the first 4 weeks. In the three patients with no significant improvement in liver function, their pressure gradient reduction after angioplasty is less than 8 mmHg (4, 5 and 7 mmHg, respectively). In patients with mid- and / or left hepatic vein obstruction, angioplasty was not attempted to the occluded hepatic veins due to the presence of functional right hepatic vein. Patients were followed up for an average of 32612 months (range 6 to 72 months). All successfully treated patients had a relief of clinical symptoms. Physical examination and colour Doppler ultrasound showed no recurrence of IVC obstruction in all but one patient (2.4%), who had reocclusion of IVC 3 years after the first successful angioplasty. The restenosis of IVC in this patient was successfully redilated. Patients with normal liver function tests after the procedure, their plasma AST, alkaline phosphatase and bilirubin levels remain unchanged. Those with no improvement in AST or alkaline phosphatase after
177
treatment had no further deterioration in liver function tests during follow-up.
4. Discussion Membranous obstruction of the IVC is the most common cause of BCS; it accounts for up to 33% of the total number of cases reported worldwide [20,21]. Membranous or segmental obstruction of IVC was found in almost 2 / 3 of our patients. Among the patients who had hepatic venous obstruction, the right hepatic vein was spared, whereas the mid-hepatic vein was occluded in all. These pathological properties have made it possible for balloon angioplasty of IVC as the mainstay of treatment for this condition. In most of our patients, balloon angioplasty of IVC resulted in a significant improvement in clinical symptoms within 72 h of treatment. The clinical outcomes were closely related to the degree of pressure gradient reduction across the IVC obstruction site. In three patients, angioplasty of IVC failed to improve liver function tests. This is likely due to the mild to moderate reduction in pressure gradient after treatment, which may have limited the clinical effect of this technique in these patients. Transcatheter approach has also been used to treat hepatic obstructions in BCS. In patients with occlusion of all three major hepatic veins, transcatheter recanalization and stent placement in one of the three occluded hepatic veins can be achieved in more than 90% of patients [15]. This approach results in symptom relief and improvement of liver function after a 23-month follow up [15]. In our patients, the occluded mid-hepatic and / or left hepatic vein was left untreated because of the presence of potent right hepatic vein. After follow-up of an average of 32 months, a vast majority of patients remained in relief of clinical symptoms; there was no deterioration in liver function. These results indicate that right hepatic vein is sufficient to maintain adequate venous return to inferior vena cava through the collateral circulation established after the occlusion of the mid- and lefthepatic veins. One of the major concerns on percutaneous IVC angioplasty is restenosis, often occurring within 2
178
T. Wu et al. / International Journal of Cardiology 83 (2002) 175 – 178
years of the procedure. From this viewpoint, placement of a stent may be a better therapeutic option. However earlier evidence has shown that transluminal balloon angioplasty alone produces more than 50% of sustained IVC potency after 2 years [17,18]. Restenosis was detected in only one of our patients 3 years after the initial successful angioplasty. These results suggest that transluminal balloon angioplasty should remain the first choice of therapy for BCS caused by IVC obstruction. In conclusion, transluminal balloon angioplasty offers a safe and effective therapy for BCS caused by membranous or segmental IVC obstruction. The long-term therapeutic effects of this procedure, in particular its effect on liver function, need to be further investigated.
References [1] Parker RGF. Occlusion of the hepatic veins in man. Medicine 1959;38:369–402. [2] Mitchell MC, Boitnott JK, Kaufman S, Cameron JL, Maddrey WC. Budd–Chiari syndrome: etiology, diagnosis and management. Medicine 1982;61:199–218. [3] Ludwig J, Hashimoto E, McGill DB, van Heerden JA. Classification of hepatic venous outflow obstruction: ambiguous terminology of the Budd–Chiari syndrome. Mayo Clin Proc 1990;65:51–5. [4] Cameron JL, Herlong FH, Sanfey H et al. The Budd–Chiari syndrome: treatment by mesenteric–systemic venous shunts. Ann Surg 1983;198:335–46. [5] Orloff MJ, Daily PO, Orloff SL, Girard B, Orloff MS. A 27-year experience with surgical treatment of Budd–Chiari syndrome. Ann Surg 2001;232:340–50. [6] Slakey DP, Klein AS, Venbrux AC, Cameron JL. Budd–Chiari syndrome: current management. Ann Surg 2001;233:522–7. [7] Putnam CW, Porter KA, Weil R, Reid HAS, Starzl TE. Liver transplantation for Budd–Chiari syndrome. J Am Med Assoc 1976;236:1142–3.
[8] Halff G, Todo S, Tzakis AG, Gordon RD, Starzl TE. Liver transplantation for the Budd–Chiari syndrome. Ann Surg 1990;211:43–9. [9] Bismuth H, Sherlock DJ. Portosystemic shunting versus liver transplantation for the Budd–Chiari syndrome. Ann Surg 1991;214:581–9. [10] Ochs A, Sellinger M, Haag K et al. Transjugular intrahepatic portosystemic stent-shunt (TIPS) in the treatment of Budd–Chiari syndrome. J Hepatol 1993;18:217–25. [11] Blum U, Rossle M, Haag K et al. Budd–Chiari syndrome—technical, haemodynamic, and clinical results of treatment with transjugular intrahepatic portosystemic shunt. Radiology 1995;197:805–11. [12] Hosie KB, Bolia A, Watkin DFL. Treatment of Budd–Chiari syndrome by percutaneous transluminal angioplasty. Lancet 1988;2:158–9. [13] Lopez Jr. RR, Benner KG, Hall L, Rosch J, Pinson CW. Expandable venous stents for treatment of the Budd–Chiari syndrome. Gastroenterology 1991;100:1435–41. [14] Fisher NC, McCafferty I, Dolapci M et al. Managing Budd–Chiari syndrome: a retrospective review of percutaneous hepatic vein angioplasty and surgical shunting. Gut 1999;44:568–74. [15] Zhang CQ, Fu LN, Zhang GQ et al. Ultrasonically guided percutaneous transhepatic hepatic vein stent placement of Budd–Chiari syndrome. J Cardiovasc Interven Radiol 1999;10:933–40. [16] Gillams A, Dick R, Platts A, Irving D, Hobbs K. Dilatation of the inferior vena cava using an expandable metal stent in Budd–Chiari syndrome. J Hepatol 1991;13:149–51. [17] Xu K, He FX, Zhang HG et al. Budd–Chiari syndrome caused by obstruction of the hepatic inferior vena cava—immediate and 2-year treatment results of transluminal angioplasty and metallic stent placement. Cardiovasc Interven Radiol 1996;19:32–6. [18] Yang XL, Cheng TO, Chen CR. Successful treatment by percutaneous balloon angioplasty of Budd–Chiari syndrome caused by membranous obstruction of inferior vena cava: 8-year follow-up study. J Am Coll Cardiol 1996;28:1720–4. [19] Zhang CQ, Fu LN, Zhang GQ et al. Ultrasonically guided inferior vena cava stent placement: 83 cases. J Cardiovasc Interven Radiol 1999;10:85–91. [20] Hirooka M, Kimura C. Membranous obstruction of the hepatic portion of the inferior vena cava: surgical correction and etiological study. Arch Surg 1970;100:656–63. [21] Rector Jr. WG, Xu Y, Goldstein L, Peters RL, Reynolds TB. Membranous obstruction of the inferior vena cava in the United States. Medicine 1985;64:134–43.
Percutaneous balloon angioplasty of inferior vena cava in Budd–Chiari syndrome-R1 a b, a a a a Tongguo Wu , Lexin Wang *, Qiang Xiao , Bosong Wang , Shanying Li , Xiurong Li , Jinying Zhang a a
Department of Cardiology, The Affiliated Hospital of Taishan Medical College, Taishan, China School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia
b
Received 17 January 2002; accepted 23 January 2002
Abstract This study was to evaluate the clinical effects of percutaneous balloon angioplasty of Budd–Chiari syndrome (BCS) caused by inferior vena cava (IVC) obstruction. Between 1993 and 1999, 28 men and 14 women with mean age of 44612 years underwent percutaneous balloon angioplasty for primary BCS. Color Doppler ultrasound and venography showed membranous and segmental obstruction of IVC in 29 and 13 patients, respectively. Fourteen patients also had left- and / or mid-hepatic vein obstruction. Angioplasty of IVC was successful in 41 patients (97.6%), resulting in a reduction of pressure gradient between IVC and the right atrium from 15.062.5 to 5.560.8 mmHg (P,0.01). A stent was placed in the site of obstruction in the patient with unsuccessful balloon angioplasty. Patients with successful angioplasty or stent placement had significant improvement in clinical symptoms indicated by a reduction in hepatomegaly and the degree of ascites. No specific attempt was made to treat the occluded left- and / or mid-hepatic vein due to the presence of potent right hepatic vein. Over the follow-up period of 32612 months, restenosis of IVC occurred in only one patient (2.4%), which was redilated successfully. Percutaneous balloon angioplasty is a safe and effective therapy for Budd–Chiari syndrome caused by IVC obstruction, therefore should be the first choice of treatment for this condition. 2002 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Budd–Chiari syndrome; Percutaneous angioplasty
1. Introduction Budd–Chiari syndrome (BCS) is an uncommon condition in which obstruction occurs in the larger hepatic veins and / or the inferior vena cava (IVC), resulting in hepatic centrilobular congestion and necrosis [1–3]. The disease is traditionally managed by surgical procedures such as portal or mesenteric– systemic shunting [4–6] and / or liver transplantation [7–9]. The development of catheter-based treatments, such as transjugular intrahepatic portosystemic shunt*Corresponding author. Tel.: 161-2-6933-2905; fax: 161-2-69332587. E-mail address: [email protected] (L. Wang).
ing [10,11], percutaneous hepatic vein angioplasty and / or stent placement [12–15] has expanded the therapeutic options of this condition. Recently percutaneous balloon angioplasty and stent placement has been used to treat obstructed IVC at or above hepatic level in primary BCS [16–19]. We report the results of 42 BCS patients who underwent angioplasty for IVC obstruction. 2. Patients and methods
2.1. Patients Between September 1993 and September 1999, 42
0167-5273 / 02 / $ – see front matter 2002 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 02 )00037-2
176
T. Wu et al. / International Journal of Cardiology 83 (2002) 175 – 178
BCS patients (male 28, mean age 44612 years, range 12–62 years) were treated with percutaneous balloon angioplasty for IVC obstruction. The most common symptoms of these patients were ascites, liver and spleen enlargement and pitting oedema of the lower limbs. BCS and IVC obstruction were initially diagnosed with colour Doppler ultrasound followed by venography, which shows membranous (the length of obstructed IVC ,1.0 cm) or segmental (the length of obstructed IVC .1.0 cm) obstruction of IVC at or above hepatic level. Two patients with segmental IVC obstruction experienced IVC thrombosis immediately before hospitalisation.
deflated 2–3 times. The end point of the dilation was disappearance of the waist in the obstruction segment following inferior venography, and appearance of forward venous flow towards the right atrium. The second end point was a reduction in the pressure gradient between the right atrium and IVC. With the two patients who had IVC thrombosis prior to hospitalization, balloon angioplasty was performed immediately after thrombolysis with urokinase (500,000 units, i.v.). Heparin (3000–5000 units) was administered intravenously during the procedure, and was continuously infused 5000–6000 units / day for 1 week following the procedure.
2.2. Procedures
2.3. Follow-up studies
Under local anaesthesia, a 6 French sheath was inserted into the right femoral and right subclavian vein, respectively. A pigtail catheter was advanced into IVC below the level of hepatic vein via the femoral vein to measure IVC pressure. A second pigtail catheter was inserted to the lower right atrium via the subclavian vein to measure the right atrial pressure. This catheter was also used to perform venography of suprahepatic IVC. Under anterior–posterior and lateral fluoroscope projection, a contrast medium was injected into IVC via the right femoral vein to locate the obstruction in IVC and hepatic vein. Complete IVC obstruction was diagnosed if there was no contrast showing in the right atrium after the injection of the contrast medium from femoral veins. Then the contrast medium was injected simultaneously into the subclavian and femoral vein to show the right atrium and IVC, which measures the length of IVC obstruction. A Brockenbrough transeptal needle (Bard Inc., MA, USA), guided by a 0.032-inch guidewire, was advanced to the IVC obstruction site via the femoral vein. The needle was then manipulated to go through the lesion 0.5–1.0 cm at a time until it reaches the right atrium. Ultrasound was used to help monitor the direction of the Brockenbrough needle. When the Brockenbrough needle had crossed the site of obstruction, a 15–22 mm Inoue balloon catheter was placed across the lesion via an exchange guidewire to dilate the obstruction. The balloon was inflated and
Follow-up studies were carried out at regular intervals by questionnaires in all patients and by repeated clinical, two-dimensional and colour Doppler ultrasound examinations.
2.4. Statistical analysis Data were expressed as mean value6S.D. An ANOVA test was used to examine the differences in IVC pressure gradients before and after balloon angioplasty.
3. Results Membranous and segmental occlusion was identified in 29 and 13 patients, respectively. Fourteen (33.3%) patients also had left and / or mid-hepatic vein obstruction, whereas the right hepatic veins remained patent in these patients. Before balloon angioplasty of IVC, the mean IVC pressure was 17.063.0 mmHg (range, 10.0–19.0). The average pressure gradient between the right atrium and IVC was 15.062.5 mmHg. Successful IVC balloon angioplasty was achieved in 41 (97.6%) patients. Following angioplasty, the pressure gradient between the right atrium and IVC was reduced to 5.560.8 mmHg (P,0.01). A stent (4 cm length, 1.2 cm in diameter, Jayu Medical Equipment, Sheng-yang, PR China) was placed in the area
T. Wu et al. / International Journal of Cardiology 83 (2002) 175 – 178
of obstruction in the patient with unsuccessful IVC angioplasty. Stenting was not performed in patients with successful angioplasty. Within 72 h of the procedure, patients with successful angioplasty or stent placement experienced significant improvement in clinical symptoms and signs, with an increase in urine volume, a decrease in hepatomegaly and a marked reduction in ascites or oedema of the lower limbs. The improvement in clinical symptoms was closely related to the reduction in the pressure gradient between the right atrium and IVC. Twenty-eight patients who had pressure gradient reduction of more than 10 mmHg experienced the most significant increase in urine volume and reduction in hepatomegaly or ascites. With respect to biochemical changes at diagnosis, there was only mild elevation of aspartate aminotransferase (AST, 98–245 IU / l) in nine of the 42 patients. A moderate elevation in alkaline phosphatase (246–653 IU / l) was observed in 12 (including nine with elevated AST) of the 42 patients. After successful angioplasty, the aspartate aminotransferase level returned to normal in six patients, in the other three patients there was no change during the first 4 weeks. After treatment, there was normalisation of alkaline phosphatase in nine out of the 12 patients during the first 4 weeks. In the three patients with no significant improvement in liver function, their pressure gradient reduction after angioplasty is less than 8 mmHg (4, 5 and 7 mmHg, respectively). In patients with mid- and / or left hepatic vein obstruction, angioplasty was not attempted to the occluded hepatic veins due to the presence of functional right hepatic vein. Patients were followed up for an average of 32612 months (range 6 to 72 months). All successfully treated patients had a relief of clinical symptoms. Physical examination and colour Doppler ultrasound showed no recurrence of IVC obstruction in all but one patient (2.4%), who had reocclusion of IVC 3 years after the first successful angioplasty. The restenosis of IVC in this patient was successfully redilated. Patients with normal liver function tests after the procedure, their plasma AST, alkaline phosphatase and bilirubin levels remain unchanged. Those with no improvement in AST or alkaline phosphatase after
177
treatment had no further deterioration in liver function tests during follow-up.
4. Discussion Membranous obstruction of the IVC is the most common cause of BCS; it accounts for up to 33% of the total number of cases reported worldwide [20,21]. Membranous or segmental obstruction of IVC was found in almost 2 / 3 of our patients. Among the patients who had hepatic venous obstruction, the right hepatic vein was spared, whereas the mid-hepatic vein was occluded in all. These pathological properties have made it possible for balloon angioplasty of IVC as the mainstay of treatment for this condition. In most of our patients, balloon angioplasty of IVC resulted in a significant improvement in clinical symptoms within 72 h of treatment. The clinical outcomes were closely related to the degree of pressure gradient reduction across the IVC obstruction site. In three patients, angioplasty of IVC failed to improve liver function tests. This is likely due to the mild to moderate reduction in pressure gradient after treatment, which may have limited the clinical effect of this technique in these patients. Transcatheter approach has also been used to treat hepatic obstructions in BCS. In patients with occlusion of all three major hepatic veins, transcatheter recanalization and stent placement in one of the three occluded hepatic veins can be achieved in more than 90% of patients [15]. This approach results in symptom relief and improvement of liver function after a 23-month follow up [15]. In our patients, the occluded mid-hepatic and / or left hepatic vein was left untreated because of the presence of potent right hepatic vein. After follow-up of an average of 32 months, a vast majority of patients remained in relief of clinical symptoms; there was no deterioration in liver function. These results indicate that right hepatic vein is sufficient to maintain adequate venous return to inferior vena cava through the collateral circulation established after the occlusion of the mid- and lefthepatic veins. One of the major concerns on percutaneous IVC angioplasty is restenosis, often occurring within 2
178
T. Wu et al. / International Journal of Cardiology 83 (2002) 175 – 178
years of the procedure. From this viewpoint, placement of a stent may be a better therapeutic option. However earlier evidence has shown that transluminal balloon angioplasty alone produces more than 50% of sustained IVC potency after 2 years [17,18]. Restenosis was detected in only one of our patients 3 years after the initial successful angioplasty. These results suggest that transluminal balloon angioplasty should remain the first choice of therapy for BCS caused by IVC obstruction. In conclusion, transluminal balloon angioplasty offers a safe and effective therapy for BCS caused by membranous or segmental IVC obstruction. The long-term therapeutic effects of this procedure, in particular its effect on liver function, need to be further investigated.
References [1] Parker RGF. Occlusion of the hepatic veins in man. Medicine 1959;38:369–402. [2] Mitchell MC, Boitnott JK, Kaufman S, Cameron JL, Maddrey WC. Budd–Chiari syndrome: etiology, diagnosis and management. Medicine 1982;61:199–218. [3] Ludwig J, Hashimoto E, McGill DB, van Heerden JA. Classification of hepatic venous outflow obstruction: ambiguous terminology of the Budd–Chiari syndrome. Mayo Clin Proc 1990;65:51–5. [4] Cameron JL, Herlong FH, Sanfey H et al. The Budd–Chiari syndrome: treatment by mesenteric–systemic venous shunts. Ann Surg 1983;198:335–46. [5] Orloff MJ, Daily PO, Orloff SL, Girard B, Orloff MS. A 27-year experience with surgical treatment of Budd–Chiari syndrome. Ann Surg 2001;232:340–50. [6] Slakey DP, Klein AS, Venbrux AC, Cameron JL. Budd–Chiari syndrome: current management. Ann Surg 2001;233:522–7. [7] Putnam CW, Porter KA, Weil R, Reid HAS, Starzl TE. Liver transplantation for Budd–Chiari syndrome. J Am Med Assoc 1976;236:1142–3.
[8] Halff G, Todo S, Tzakis AG, Gordon RD, Starzl TE. Liver transplantation for the Budd–Chiari syndrome. Ann Surg 1990;211:43–9. [9] Bismuth H, Sherlock DJ. Portosystemic shunting versus liver transplantation for the Budd–Chiari syndrome. Ann Surg 1991;214:581–9. [10] Ochs A, Sellinger M, Haag K et al. Transjugular intrahepatic portosystemic stent-shunt (TIPS) in the treatment of Budd–Chiari syndrome. J Hepatol 1993;18:217–25. [11] Blum U, Rossle M, Haag K et al. Budd–Chiari syndrome—technical, haemodynamic, and clinical results of treatment with transjugular intrahepatic portosystemic shunt. Radiology 1995;197:805–11. [12] Hosie KB, Bolia A, Watkin DFL. Treatment of Budd–Chiari syndrome by percutaneous transluminal angioplasty. Lancet 1988;2:158–9. [13] Lopez Jr. RR, Benner KG, Hall L, Rosch J, Pinson CW. Expandable venous stents for treatment of the Budd–Chiari syndrome. Gastroenterology 1991;100:1435–41. [14] Fisher NC, McCafferty I, Dolapci M et al. Managing Budd–Chiari syndrome: a retrospective review of percutaneous hepatic vein angioplasty and surgical shunting. Gut 1999;44:568–74. [15] Zhang CQ, Fu LN, Zhang GQ et al. Ultrasonically guided percutaneous transhepatic hepatic vein stent placement of Budd–Chiari syndrome. J Cardiovasc Interven Radiol 1999;10:933–40. [16] Gillams A, Dick R, Platts A, Irving D, Hobbs K. Dilatation of the inferior vena cava using an expandable metal stent in Budd–Chiari syndrome. J Hepatol 1991;13:149–51. [17] Xu K, He FX, Zhang HG et al. Budd–Chiari syndrome caused by obstruction of the hepatic inferior vena cava—immediate and 2-year treatment results of transluminal angioplasty and metallic stent placement. Cardiovasc Interven Radiol 1996;19:32–6. [18] Yang XL, Cheng TO, Chen CR. Successful treatment by percutaneous balloon angioplasty of Budd–Chiari syndrome caused by membranous obstruction of inferior vena cava: 8-year follow-up study. J Am Coll Cardiol 1996;28:1720–4. [19] Zhang CQ, Fu LN, Zhang GQ et al. Ultrasonically guided inferior vena cava stent placement: 83 cases. J Cardiovasc Interven Radiol 1999;10:85–91. [20] Hirooka M, Kimura C. Membranous obstruction of the hepatic portion of the inferior vena cava: surgical correction and etiological study. Arch Surg 1970;100:656–63. [21] Rector Jr. WG, Xu Y, Goldstein L, Peters RL, Reynolds TB. Membranous obstruction of the inferior vena cava in the United States. Medicine 1985;64:134–43.