- Email: [email protected]
Control of cerebral oedema by total hepatectomy and extracorporeal liver support in fulminant hepatic failure
References Nakano M, Worner TM, Leiber CS. Perivenular fibrosis in alcoholic injury: ultrastructure and histologic progression. Gastroenterology 1982; 83: 777-85.
2
Annoni G, Colombo M, Cantaluppi MC, Khlat B, Lampertico P, Rojkind M. Serum type III procollagen peptide and laminin (LAM-PI) detect alcoholic hepatitis in chronic alcohol abusers. Hepatology 1989; 9: 693-97.
3
Raedsch R, Stiehl A, Waldherr F, et al. Progollagen type III peptide serum concentrations in chronic persistent and chronic active hepatitis and in cirrhosis of the liver and their diagnostic value. Z Gastroenterol
4
Rohde H, Vargas L, Hahn EG, Kalbfleisch H, Brugera M, Timpl R. Radioimmunoassay for type III procollagen peptide and its application to human liver disease. Eur J Clin Invest 1979; 9: 451-59. Torres-Salinas M, Parés A, Caballeria J, et al. Serum procollagen type III peptide as a marker of hepatic fibrosis in alcoholic hepatitis. Gastroenterology 1986; 90: 1241-46. Weigand K, Zaugg P-Y, Frei A, Zimmerman A. Long-term follow-up of serum N-terminal propeptide of collagen III levels in patients with chronic liver disease. Hepatology 1984; 4: 835-38. Feely J, Barry M, Keeling PWN, Weir DG, Cooke T. Lipoprotein (a) in cirrhosis. BMJ 1992; 304: 545-46.
1982; 20: 738-43.
5
6
7
8
Marth E, Cazzalato G, Bittolo Bon G. Avogaro P, Kostner CM. Serum concentrations of Lp (a) and other lipoprotein parameters in heavy alcohol consumers. Ann Nutr Metab 1982; 26: 56-62.
9
Poynard T, Abella A, Pignon JP, Naveau S, Leluc R, Chaput JC. Apolipoprotein AI and alcoholic liver disease. Hepatology 1986; 6: 1391-95.
10
Camargo CA, Williams PT, Vranigan KM, et al. The effect of moderate alcohol intake on serum lipoproteins AI and AII: a controlled study. JAMA 1985; 253: 2854-57.
11 Cordova C, Musea A, Violi F, et al. Apolipoproteins AI, AII,and B in chronic active hepatitis and in liver cirrhotic patients. Clin Chim Acta
1984; 137: 61-66.
Nalpas B, Goldstein S, et al. Plasma lipoprotein and lipoprotein profile in alcoholic patients with and without liver disease:
12 Duhamel G,
Short
report
Control of cerebral oedema by total hepatectomy and extracorporeal liver support in fulminant hepatic failure
patient with fulminant hepatic failure (FHF) alive until a donor liver is available for transplantation can be a problem. We describe an 18-year-old woman with paracetamol-induced FHF, who was treated by total hepatectomy, hypothermia, plasma exchange, and extracorporeal liver support. The patient was anhepatic for 14 h. The liver-support system consisted of plasma separation and perfusion through a charcoal filter and a hollow-fibre module seeded with matrix-attached porcine hepatocytes.
Keeping
a
With artificial liver treatment there
reversal of severe neurological dysfunction, normalisation of intracranial pressure, and decreased serum ammonia. The patient underwent emergency transplantation with an ABOincompatible liver, followed by transplantation with a compatible organ eight days later. The patient has fully recovered and is neurologically intact.
Lancet 1993; 342: 898-99 898
the relative roles of alcohol and liver injury. Hepatology 1984; 4: 577-85. 13 Poynard T, Aubert A, Bedossa P, et al. A simple biological index for detection of alcoholic liver disease in drinkers. Gastroenterology 1991; 100: 1397-402. 14 Pugh RNH, Murray-Lyon IM, Dawson LJ, Pietroni MC, Williams R. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg 1973; 60: 640-49. on
1
was
15 Dickson ER, Grambsch PM, Fleming TR, Fisher LD, Langworthy A. Prognosis in primary biliary cirrhosis: model for decision making. Hepatology 1989; 10: 1-7. 16 Altman D, ed. Diagnostic tests. In: Practical statistics for medical research. London: Chapman & Hall, 1991: 408-19. 17 Sabesin SM. Lipoprotein abnormalities in primary biliary cirrhosis: information concerning control of plasma density lipoprotein levels. Gastroenterology 1985; 89: 1426-29. 18 Ragland JB, Bertram PD, Sabesin SM. The role of lecithin: cholesterol acyltransferase deficiency in the apoprotein metabolism of alcoholic hepatitis. Scand J Clin Lab Invest 1978; 38: 208-13. 19 Jahn CE, Schaefer EJ, Taam LA, et al. Lipoprotein abnormalities in primary biliary cirrhosis: association with hepatic lipase inhibition as well as altered cholesterol esterification. Gastroenterology 1985; 89: 1266-78. 20 Pierard D, Plomteux G, Amrani N, Robin M, Gielen J, Lapière OM. Type III collagen precursor sequences in sera of patients with hepatic diseases. In: Gerlach U PG, Rauterburg J, Voss B, eds. Connective tissue of the normal and fibrotic human liver. Stuttgart: Thieme, 1982: 217-18. 21 Schuppan D. Connective tissue polypeptides in serum as parameters to monitor antifibrotic treatment in hepatic fibrogenesis. J Hepatol 1991; 13 (suppl 3): S17-25. 22 Lotterer E, Gressner AM, Kropf J, Grobe E, von Krebel D, Bircher J. Higher levels of serum aminoterminal type III procollagen peptide and laminin in alcoholic and non-alcoholic cirrhsis of equal severity. J Hepatol 1992; 14: 71-77. 23 Clément B, Chesné C, Satie A-P, Guillouzo A. Effects of the prolyl 4-hydroxylase proinhibitor HOE 077 on human and rat hepatocytes in primary culture. J Hepatol 1991; 13 (suppl 3): 541-47.
Brain oedema is the leading cause of death in patients with fulminant hepatic failure (FHF).1 Orthotopic liver transplantation is the only effective method of treating FHF, however, many patients die before they can be transplanted and others die after transplantation because of irreversible brain damage. There is thus a need for a liver-support system that could be used to maintain patients alive, and neurologically intact, until an organ becomes available for transplantation. It has been reported that patients with liver necrosis improve after removal of their liver,2but this approach has been limited by lack of effective liver support. We have developed a bioartificial liver and report its first use in an anhepatic patient with FHF. An 18-year-old woman ingested about 60 g of paracetamol (acetaminophen) two days before admission. She was treated with n-acetylcysteine and supportive measures. She was jaundiced, lethargic, and her neurological examination was almost normal. The liver was not palpable and she had no stigmata of chronic liver disease. On admission, her serum aspartate aminotransferase and
alanine aminotransferase were 7150 IU/L and 8430 IU/L, with total bilirubin 80-4 umol/L, ammonia 265 pmol/L, lactate 35 mmol/L, blood pH 7-35, prothrombin time 56s, and paracetamol 10 ug/mL. Computed tomography scan of the brain revealed mild cerebral oedema. Within 12 h her condition deteriorated and she became unresponsive to pain and required endotracheal intubation. Intracranial pressure (ICP) was 28 mm Hg. The patient was treated with lactulose and mannitol and maintained in hyperventilated state to a pCO of 25 mm Hg; blood pH was maintained between 7 45 and 7-55. Despite optimal management, her ICP continued to increase and she assumed a decerebrate posture, with disconjugate gaze and dilated pupils with sluggish reactivity. A repeat brain computed tomography scan revealed cerebral oedema.
respectively,
The bioartificial liver, which consisted of a hepatocyte module and a charcoal column, was constructed as described previously.3 Briefly, 6 x 109 viable hepatocytes were harvested aseptically from the liver of miniature swine, attached to collagen-coated dextran microcarriers, and inoculated into the extracapillary space of a porous hollow-fibre module.3 A double-lumen dialysis catheter was placed in the patient’s saphenous vein. Blood was removed at 90 mL per min and separated continuously into plasma and cells.3 The charcoal column and hepatocyte module were placed in a second circuit where plasma was recirculated at 220 mL per min. After leaving the recirculation loop, plasma was reconstituted with cells and was returned to the patient.
The first artificial liver treatment lasted 7 h. 2 h after the start of treatment, there was substantial improvement in the patient’s neurologic status with abrogation of the decerebrate posturing and equilibration of the pupillary size and reflex. With the clinical improvement there was a concurrent decrease in ICP to 5 (SD 2) mm Hg. Serum ammonia decreased from 265 to 70 mol/L. This improvement was maintained throughout treatment and for 12 h thereafter. At that time, the patient’s neurological status deteriorated again (ICP 19 [2] mm Hg) and artificial liver treatment was repeated for another 7 h with similar improvement in condition and normalisation of ICP. However, on this occasion, the beneficial effect lasted for only 2 h after treatment. After this brief improvement, there was continuing deterioration of the patient’s neurological condition with an increase in ICP to 30 (2) mm Hg, which indicated that the effectiveness of artificial liver treatment had diminished. Because there was no liver available for transplantation, the patient underwent an end-to-side portocaval shunt and total hepatectomy under general anaesthesia with thiopental supplementation. During the 14 h anhepatic state, the patient was maintained at a low body temperature (34-5°C). After hepatectomy, the patient underwent totalplasma-volume exchange (2 h) with fresh frozen plasma, followed by artificial liver treatment for 7 h. ICP decreased to 15 (4) mm Hg after liver resection, but plasma exchange had no effect on ICP. Soon after the start of artificial liver treatment, ICP decreased to 6 (3) mm Hg and remained normal throughout the treatment and for 5 h thereafter. At that time, an ABO-incompatible liver became available and the patient was transplanted orthotopically. Eight days later, she was transplanted with an ABO-compatible liver. Postoperatively, the patient recovered completely and was discharged from hospital three weeks after transplantation. Total hepatectomy in FHF has not been done routinely because of the lack of liver-assist systems to support patients until a liver becomes available for transplantation. We have developed a bioartificial liver and tested it in experimental animals and a few patients with severe liver failure.3-5 Because of the beneficial effects noted in our animal studies, promising preliminary observations gathered from a small number of patients (n = 7), and
Table : Steps In the management of FHF when available for transplantation
a
liver Is not
patients with primary liver failure after transplantation showed improvement when rendered anhepatic,2,6 total hepatectomy and artificial liver support were carried out in our patient. Two other measures enhanced the efficacy of this approach: a single totalplasma-volume exchange was done after liver resection, to remove "toxic" plasma, and the patient was maintained at reports that
low temperature to decrease metabolic demands. This is the first report of successful reduction of ICP and neurological recovery in a patient with severe FHF, by a combination of total hepatectomy and extracorporeal liver support. Encouraged by the outcome in this patient, and based on our laboratory data and limited additional clinical experience with the bioartificial liver support, we plan to follow a deliberate step-wise plan in managing FHF patients (table). A clinical trial is in progress to determine the impact of this therapeutic approach on outcome in patients with FHF. Supported by NIH grant DK38763-08 and by institutional grants. References
O’Grady J, Gimson AES, O’Brien CP, Puckness A, Hughes R, Williams R. Control trials of charcoal hemoperfusion and prognostic factors in fulminant hepatic failure. Gastroenterology 1988; 94: 1186-92. 2 Ringe B, Lubbe N, Kuse E, Frei U, Pichlmayr R. Management of emergencies before and after liver transplantation by early total hepatectomy. Transplant Proc 1993; 25: 1090. 3 Rozga J, Holzman M, Ro MS, et al. Development of a hybrid bioartificial liver. Ann Surg 1993; 217: 502-11. 4 Rozga J, Neuzil D, Giorgio T, et al. Development of a bioartificial liver. Hepatology 1993; 17: 258-65. 5 Neuzil D, Rozga J, Ro MS, et al. Use of bioartificial liver to treat acute liver failure in a patient with alcoholic liver disease. Surgery 1993; 1
6
113: 340-43. So SKS, Barteau GA, Perdrizet GA, Marsh JW. Successful retransplantation after a 48-hour anhepatic state. Transplant Proc 1993; 25: 1962-63.
Liver Support Unit, Cedars-Sinal Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048-1865, USA (J Rozga MD, L Podesta MD, E LePage RN, A Hoffman MD, E Morsiani MD, L Sher MD, G M Woolf MD, L Makowka MD, A A Demetriou MD)
Correspondence to:
Dr Achilles A Demetriou
Measurement of coronary artery flow
by magnetic resonance velocity mapping in the aorta
reserve
Coronary artery flow occurs predominantly in diastole via retrograde flow in the ascending aorta, some of which supplies the coronary arteries while the remainder recirculates in the ascending aorta. We used magnetic resonance velocity mapping to measure global coronary artery diastolic flow in the ascending aorta. In eight normal subjects and in four patients with possible ischaemic heart disease but with normal perfusion scans, the mean coronary flow reserve (CFR) was 269 ml/min. CFR was zero in seven patients with coronary artery disease. We have shown that CFR can be measured non-invasively with this technique. Lancet
1993; 341: 899-900 899
2
Annoni G, Colombo M, Cantaluppi MC, Khlat B, Lampertico P, Rojkind M. Serum type III procollagen peptide and laminin (LAM-PI) detect alcoholic hepatitis in chronic alcohol abusers. Hepatology 1989; 9: 693-97.
3
Raedsch R, Stiehl A, Waldherr F, et al. Progollagen type III peptide serum concentrations in chronic persistent and chronic active hepatitis and in cirrhosis of the liver and their diagnostic value. Z Gastroenterol
4
Rohde H, Vargas L, Hahn EG, Kalbfleisch H, Brugera M, Timpl R. Radioimmunoassay for type III procollagen peptide and its application to human liver disease. Eur J Clin Invest 1979; 9: 451-59. Torres-Salinas M, Parés A, Caballeria J, et al. Serum procollagen type III peptide as a marker of hepatic fibrosis in alcoholic hepatitis. Gastroenterology 1986; 90: 1241-46. Weigand K, Zaugg P-Y, Frei A, Zimmerman A. Long-term follow-up of serum N-terminal propeptide of collagen III levels in patients with chronic liver disease. Hepatology 1984; 4: 835-38. Feely J, Barry M, Keeling PWN, Weir DG, Cooke T. Lipoprotein (a) in cirrhosis. BMJ 1992; 304: 545-46.
1982; 20: 738-43.
5
6
7
8
Marth E, Cazzalato G, Bittolo Bon G. Avogaro P, Kostner CM. Serum concentrations of Lp (a) and other lipoprotein parameters in heavy alcohol consumers. Ann Nutr Metab 1982; 26: 56-62.
9
Poynard T, Abella A, Pignon JP, Naveau S, Leluc R, Chaput JC. Apolipoprotein AI and alcoholic liver disease. Hepatology 1986; 6: 1391-95.
10
Camargo CA, Williams PT, Vranigan KM, et al. The effect of moderate alcohol intake on serum lipoproteins AI and AII: a controlled study. JAMA 1985; 253: 2854-57.
11 Cordova C, Musea A, Violi F, et al. Apolipoproteins AI, AII,and B in chronic active hepatitis and in liver cirrhotic patients. Clin Chim Acta
1984; 137: 61-66.
Nalpas B, Goldstein S, et al. Plasma lipoprotein and lipoprotein profile in alcoholic patients with and without liver disease:
12 Duhamel G,
Short
report
Control of cerebral oedema by total hepatectomy and extracorporeal liver support in fulminant hepatic failure
patient with fulminant hepatic failure (FHF) alive until a donor liver is available for transplantation can be a problem. We describe an 18-year-old woman with paracetamol-induced FHF, who was treated by total hepatectomy, hypothermia, plasma exchange, and extracorporeal liver support. The patient was anhepatic for 14 h. The liver-support system consisted of plasma separation and perfusion through a charcoal filter and a hollow-fibre module seeded with matrix-attached porcine hepatocytes.
Keeping
a
With artificial liver treatment there
reversal of severe neurological dysfunction, normalisation of intracranial pressure, and decreased serum ammonia. The patient underwent emergency transplantation with an ABOincompatible liver, followed by transplantation with a compatible organ eight days later. The patient has fully recovered and is neurologically intact.
Lancet 1993; 342: 898-99 898
the relative roles of alcohol and liver injury. Hepatology 1984; 4: 577-85. 13 Poynard T, Aubert A, Bedossa P, et al. A simple biological index for detection of alcoholic liver disease in drinkers. Gastroenterology 1991; 100: 1397-402. 14 Pugh RNH, Murray-Lyon IM, Dawson LJ, Pietroni MC, Williams R. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg 1973; 60: 640-49. on
1
was
15 Dickson ER, Grambsch PM, Fleming TR, Fisher LD, Langworthy A. Prognosis in primary biliary cirrhosis: model for decision making. Hepatology 1989; 10: 1-7. 16 Altman D, ed. Diagnostic tests. In: Practical statistics for medical research. London: Chapman & Hall, 1991: 408-19. 17 Sabesin SM. Lipoprotein abnormalities in primary biliary cirrhosis: information concerning control of plasma density lipoprotein levels. Gastroenterology 1985; 89: 1426-29. 18 Ragland JB, Bertram PD, Sabesin SM. The role of lecithin: cholesterol acyltransferase deficiency in the apoprotein metabolism of alcoholic hepatitis. Scand J Clin Lab Invest 1978; 38: 208-13. 19 Jahn CE, Schaefer EJ, Taam LA, et al. Lipoprotein abnormalities in primary biliary cirrhosis: association with hepatic lipase inhibition as well as altered cholesterol esterification. Gastroenterology 1985; 89: 1266-78. 20 Pierard D, Plomteux G, Amrani N, Robin M, Gielen J, Lapière OM. Type III collagen precursor sequences in sera of patients with hepatic diseases. In: Gerlach U PG, Rauterburg J, Voss B, eds. Connective tissue of the normal and fibrotic human liver. Stuttgart: Thieme, 1982: 217-18. 21 Schuppan D. Connective tissue polypeptides in serum as parameters to monitor antifibrotic treatment in hepatic fibrogenesis. J Hepatol 1991; 13 (suppl 3): S17-25. 22 Lotterer E, Gressner AM, Kropf J, Grobe E, von Krebel D, Bircher J. Higher levels of serum aminoterminal type III procollagen peptide and laminin in alcoholic and non-alcoholic cirrhsis of equal severity. J Hepatol 1992; 14: 71-77. 23 Clément B, Chesné C, Satie A-P, Guillouzo A. Effects of the prolyl 4-hydroxylase proinhibitor HOE 077 on human and rat hepatocytes in primary culture. J Hepatol 1991; 13 (suppl 3): 541-47.
Brain oedema is the leading cause of death in patients with fulminant hepatic failure (FHF).1 Orthotopic liver transplantation is the only effective method of treating FHF, however, many patients die before they can be transplanted and others die after transplantation because of irreversible brain damage. There is thus a need for a liver-support system that could be used to maintain patients alive, and neurologically intact, until an organ becomes available for transplantation. It has been reported that patients with liver necrosis improve after removal of their liver,2but this approach has been limited by lack of effective liver support. We have developed a bioartificial liver and report its first use in an anhepatic patient with FHF. An 18-year-old woman ingested about 60 g of paracetamol (acetaminophen) two days before admission. She was treated with n-acetylcysteine and supportive measures. She was jaundiced, lethargic, and her neurological examination was almost normal. The liver was not palpable and she had no stigmata of chronic liver disease. On admission, her serum aspartate aminotransferase and
alanine aminotransferase were 7150 IU/L and 8430 IU/L, with total bilirubin 80-4 umol/L, ammonia 265 pmol/L, lactate 35 mmol/L, blood pH 7-35, prothrombin time 56s, and paracetamol 10 ug/mL. Computed tomography scan of the brain revealed mild cerebral oedema. Within 12 h her condition deteriorated and she became unresponsive to pain and required endotracheal intubation. Intracranial pressure (ICP) was 28 mm Hg. The patient was treated with lactulose and mannitol and maintained in hyperventilated state to a pCO of 25 mm Hg; blood pH was maintained between 7 45 and 7-55. Despite optimal management, her ICP continued to increase and she assumed a decerebrate posture, with disconjugate gaze and dilated pupils with sluggish reactivity. A repeat brain computed tomography scan revealed cerebral oedema.
respectively,
The bioartificial liver, which consisted of a hepatocyte module and a charcoal column, was constructed as described previously.3 Briefly, 6 x 109 viable hepatocytes were harvested aseptically from the liver of miniature swine, attached to collagen-coated dextran microcarriers, and inoculated into the extracapillary space of a porous hollow-fibre module.3 A double-lumen dialysis catheter was placed in the patient’s saphenous vein. Blood was removed at 90 mL per min and separated continuously into plasma and cells.3 The charcoal column and hepatocyte module were placed in a second circuit where plasma was recirculated at 220 mL per min. After leaving the recirculation loop, plasma was reconstituted with cells and was returned to the patient.
The first artificial liver treatment lasted 7 h. 2 h after the start of treatment, there was substantial improvement in the patient’s neurologic status with abrogation of the decerebrate posturing and equilibration of the pupillary size and reflex. With the clinical improvement there was a concurrent decrease in ICP to 5 (SD 2) mm Hg. Serum ammonia decreased from 265 to 70 mol/L. This improvement was maintained throughout treatment and for 12 h thereafter. At that time, the patient’s neurological status deteriorated again (ICP 19 [2] mm Hg) and artificial liver treatment was repeated for another 7 h with similar improvement in condition and normalisation of ICP. However, on this occasion, the beneficial effect lasted for only 2 h after treatment. After this brief improvement, there was continuing deterioration of the patient’s neurological condition with an increase in ICP to 30 (2) mm Hg, which indicated that the effectiveness of artificial liver treatment had diminished. Because there was no liver available for transplantation, the patient underwent an end-to-side portocaval shunt and total hepatectomy under general anaesthesia with thiopental supplementation. During the 14 h anhepatic state, the patient was maintained at a low body temperature (34-5°C). After hepatectomy, the patient underwent totalplasma-volume exchange (2 h) with fresh frozen plasma, followed by artificial liver treatment for 7 h. ICP decreased to 15 (4) mm Hg after liver resection, but plasma exchange had no effect on ICP. Soon after the start of artificial liver treatment, ICP decreased to 6 (3) mm Hg and remained normal throughout the treatment and for 5 h thereafter. At that time, an ABO-incompatible liver became available and the patient was transplanted orthotopically. Eight days later, she was transplanted with an ABO-compatible liver. Postoperatively, the patient recovered completely and was discharged from hospital three weeks after transplantation. Total hepatectomy in FHF has not been done routinely because of the lack of liver-assist systems to support patients until a liver becomes available for transplantation. We have developed a bioartificial liver and tested it in experimental animals and a few patients with severe liver failure.3-5 Because of the beneficial effects noted in our animal studies, promising preliminary observations gathered from a small number of patients (n = 7), and
Table : Steps In the management of FHF when available for transplantation
a
liver Is not
patients with primary liver failure after transplantation showed improvement when rendered anhepatic,2,6 total hepatectomy and artificial liver support were carried out in our patient. Two other measures enhanced the efficacy of this approach: a single totalplasma-volume exchange was done after liver resection, to remove "toxic" plasma, and the patient was maintained at reports that
low temperature to decrease metabolic demands. This is the first report of successful reduction of ICP and neurological recovery in a patient with severe FHF, by a combination of total hepatectomy and extracorporeal liver support. Encouraged by the outcome in this patient, and based on our laboratory data and limited additional clinical experience with the bioartificial liver support, we plan to follow a deliberate step-wise plan in managing FHF patients (table). A clinical trial is in progress to determine the impact of this therapeutic approach on outcome in patients with FHF. Supported by NIH grant DK38763-08 and by institutional grants. References
O’Grady J, Gimson AES, O’Brien CP, Puckness A, Hughes R, Williams R. Control trials of charcoal hemoperfusion and prognostic factors in fulminant hepatic failure. Gastroenterology 1988; 94: 1186-92. 2 Ringe B, Lubbe N, Kuse E, Frei U, Pichlmayr R. Management of emergencies before and after liver transplantation by early total hepatectomy. Transplant Proc 1993; 25: 1090. 3 Rozga J, Holzman M, Ro MS, et al. Development of a hybrid bioartificial liver. Ann Surg 1993; 217: 502-11. 4 Rozga J, Neuzil D, Giorgio T, et al. Development of a bioartificial liver. Hepatology 1993; 17: 258-65. 5 Neuzil D, Rozga J, Ro MS, et al. Use of bioartificial liver to treat acute liver failure in a patient with alcoholic liver disease. Surgery 1993; 1
6
113: 340-43. So SKS, Barteau GA, Perdrizet GA, Marsh JW. Successful retransplantation after a 48-hour anhepatic state. Transplant Proc 1993; 25: 1962-63.
Liver Support Unit, Cedars-Sinal Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048-1865, USA (J Rozga MD, L Podesta MD, E LePage RN, A Hoffman MD, E Morsiani MD, L Sher MD, G M Woolf MD, L Makowka MD, A A Demetriou MD)
Correspondence to:
Dr Achilles A Demetriou
Measurement of coronary artery flow
by magnetic resonance velocity mapping in the aorta
reserve
Coronary artery flow occurs predominantly in diastole via retrograde flow in the ascending aorta, some of which supplies the coronary arteries while the remainder recirculates in the ascending aorta. We used magnetic resonance velocity mapping to measure global coronary artery diastolic flow in the ascending aorta. In eight normal subjects and in four patients with possible ischaemic heart disease but with normal perfusion scans, the mean coronary flow reserve (CFR) was 269 ml/min. CFR was zero in seven patients with coronary artery disease. We have shown that CFR can be measured non-invasively with this technique. Lancet
1993; 341: 899-900 899