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Late quadriplegia after adult coarctation repair
268
CASE REPORT PETERS ET AL LATE QUADRIPLEGIA AFTER COARCTATION REPAIR
5. Borst HG, Laas J, Heinemann M. Type A aortic dissection: diagnosis and management of malperfusion phenomena. Semin Thorac Cardiovasc Surg 1991;3:238 –41. 6. Tanaka H, Kazui T, Sato H, Inoue N, Yamada O, Komatsu S. Experimental study on the optimum flow rate and pressure for selective cerebral perfusion. Ann Thorac Surg 1995;59: 651–7. 7. Shiiya N, Kunihara T, Imamura M, Murashita T, Matsui Y, Yasuda K. Surgical management of atherosclerotic aortic arch aneurysms using selective cerebral perfusion: 7-year experience in 52 patients. Eur J Cardio Thorac Surg 2000;17:266 –71. 8. Imanaka K, Kyo S, Tanabe H, Asano H, Yokote Y. Fatal intraoperative dissection of the innominate artery due to perfusion through the right axillary artery. J Thorac Cardiovasc Surg 2000;120:405–6. CASE REPORTS
Late Quadriplegia After Adult Coarctation Repair Paul Peters, FRCS(CTh), Jeffrey W. Brennan, MBBS, Clifford F. Hughes, FRACS, Martin McGee-Collett, FRACS, and Geoffrey Parker, FRACR Departments of Cardiothoracic Surgery, Neurosurgery, and Radiology, Royal Prince Alfred Hospital, Camperdown, Sydney, Australia
Quadriplegia developed suddenly 1 month after coarctation repair in a 53-year-old human. Cervical cord ischemia caused by thrombosis in an enlarged anterior spinal artery collateral was diagnosed on magnetic resonance scan and spinal angiography. After urgent cord decompression and anticoagulation there was neurologic improvement over a period of several months. Urgent investigation of neurologic abnormalities occurring late after coarctation repair may enable intervention to avert permanent neurologic sequelae. (Ann Thorac Surg 2003;75:268 –70) © 2003 by The Society of Thoracic Surgeons
N
eurologic complications associated with aortic coarctation may occur in one of three forms; central nervous system manifestations of proximal hypertension (ruptured berry aneurysm or stroke), spinal syndromes associated with aneurysmal spinal artery collaterals causing myelopathy by compression or hemorrhage, or perioperative spinal ischemia [1,2]. We report an example of a fourth, late type of neurologic complication of coarctation in an adult; a late thrombosed anterior spinal artery collateral. This required urgent neurosurgical intervention to prevent permanent quadriplegia. A 53-year-old human with longstanding hypertension presented with sudden onset of left-sided hemiparesis
Accepted for publication May 1, 2002. Address reprint requests to Dr Hughes, Department of Cardiothoracic Surgery, Royal Prince Alfred Hospital, Missenden Rd, Camperdown, Sydney, NSW 2050 Australia; e-mail: [email protected]. gov.au.
© 2003 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2003;75:268 –70
and left hemifacial parasthesia. Clinical examination and investigations confirmed ischemic stroke (involving the right medial temporal lobe and posterior thalamus) and findings that are typical of adult coarctation including central hypertension. The carotid and intracranial circulations appeared normal. Four months later, after recovering from his stroke, the patient underwent coarctation repair. At the left posterolateral fourth space thoracotomy, extensive chest wall collateralization was encountered. The coarcted segment was identified and mobilized. Immediately two distal 5-mm spinal collaterals were controlled and preserved. Because of extensive collateralization no specific spinal protection measures were used. Under heparinization the coarcted segment was resected, and a 20-mm Dacron graft interposed. Clamp time was 45 minutes. The initial postoperative course was uneventful apart from persisting hypertension managed medically, and there were no abnormal neurologic findings on discharge. One month later he represented with rapidly progressing weakness of all four limbs. He had virtual paralysis of his hands, markedly weak elbow extension, weak elbow flexion and preserved shoulder power. There was flaccid, hyporeflexic weakness in the lower limbs with sensory deficit to pinprick below level T2. Dorsal column function was intact. Blood pressure on admission was 100/70 mm Hg. Spinal magnetic resonance imaging suggested an extensive intrathecal arterial abnormality with cord compression anteriorly from C5 to T1. Urgent surgical decompression of the cord was achieved by posterior cervical laminectomy from C4 to C7 at which multiple large paraspinal muscular collaterals were noted. Postoperatively his condition stabilized. Forty-eight hours later a sudden loss of proximal limb power was noted. Repeat magnetic resonance imaging suggested cord edema and possibly infarction. The anterior thecal vessels were larger and hypointense suggesting thrombosis (Fig 1). Spinal angiography demonstrated segmental occlusion of the lower cervical anterior spinal artery (Fig 2). A large radiculo-medullary vessel from the left vertebral artery at C4 –5 (artery of Lazorthe) [3] supplying an enlarged anterior spinal artery was visualized. The anterior spinal artery was patent above C4 but thrombosed below the junction with the artery of Lazorthe to the level C7. The patient was anticoagulated with intravenous heparin. Dexamethasone was commenced, blood pressure support with intravenous fluids and inotropic agents were continued, and hyperbaric oxygen was administered. He remained stable on warfarin and was discharged to a rehabilitation unit for 3 months, and his condition improved. One month later he was walking unaided and independently handling activities of daily living, although he had residual weakness of elbow extension and wasting intrinsic hand musculature. Follow-up magnetic resonance imaging demonstrated completed partial anterior spinal artery territory infarction from C4 to T2. 0003-4975/03/$30.00 PII S0003-4975(02)04126-7
CASE REPORT PETERS ET AL LATE QUADRIPLEGIA AFTER COARCTATION REPAIR
269
CASE REPORTS
Ann Thorac Surg 2003;75:268 –70
Fig 2. Spinal angiography (late arterial phase, oblique) showing artery of Lazorthe (l) arising from left vertebral artery (v) at C4 –5. The anterior spinal artery (s) is thrombosed from the junction with the artery of Lazorthe inferiorly (arrowheads).
Fig 1. Sagittal T2-weighted magnetic resonance imaging demonstrating spinal cord edema in the anterior half of the cord between C4 and T2 and an enlarged anterior spinal artery (s).
Comment Aortic coarctation occurs in approximately 30 of 100,000 live births [4]. Improvements in imaging techniques increasingly allow early diagnosis and treatment, so the rare entity of adult coarctation may become even less common. Nevertheless, neurologic conditions associated with coarctation and its treatment can be devastating. Reviews of coarctation operations suggest that perioperative spinal cord damage leading to paraplegia occurs in 0.3 to 0.6% of patients [2, 5]. The relative rarity of perioperative spinal cord damage leading to paraplegia occurring compared with that associated with aortic operations for other conditions, despite the fact that spinal protection is not commonly used, is thought to be caused by the extensive collateralization of blood flow around the coarcted segment leading to maintenance of spinal and lower body blood flow during clamping of the descending thoracic aorta. Reported late complications of coarctation repair mostly describe re-coarctation or false aneurysm formation at the operated site [6]. We postulate that this late
neurologic complication occurred after repair of this severe coarctation, because the pressure differential along enlarged and tortuous spinal artery collaterals was markedly reduced. The consequent fall in collateral blood flow precipitated stasis and thrombosis. Because we recognize that pressure differentials along collaterals are probably independent of systemic blood pressure after coarctation repair, we doubt that aggressive management of this patient’s hypertension contributed to this complication. This case demonstrates that close postoperative follow-up of such patients is essential. Early investigation of neurologic symptoms is mandatory. Unless the diagnosis is made at an early stage it would be possible to miss the small window of opportunity for successful intervention by way of surgical decompression or anticoagulation. The consequences of missing such an opportunity could be catastrophic.
References 1. Aaron BL, Loew AG, Mullen JT. Coarctation of the aorta with spontaneous quadriparesis. J Thorac Cardiovasc Surg 1974; 68:76 –9. 2. Brewer LA 3d, Fosberg RG, Mulder GA, Verskaa JJ. Spinal cord complications following surgery for coarctation of the aorta. J Thorac Cardiovasc Surg 1972;64:368 –81. 3. Lasjaunias P, Berenstein A. Functional vascular anatomy of brain, spinal cord & spine. In: Surgical Neuroangiography. Heidelburg: Springer Verlag, 1990, Vol 3, 55– 8. 4. Grech V. Diagnostic and surgical trends, and epidemiology of
270
CASE REPORT KATO ET AL INTERNAL MAMMARY ARTERY STEAL
coarctation in a population based study. Int J Cardiol 1999; 68(2):197–202. 5. Keen G. Spinal cord damage and operations for coarctation of the aorta: etiology, practice and prospects. Thorax 1987;42(1): 11–8. 6. Bobby JJ, Emami JM, Farmer RD, Newman CG. Operative survival and 40 year follow up of surgical repair of aortic coarctation. Br Heart J 1991;65(5):271–6.
CASE REPORTS
Internal Mammary Artery Steal in a Dialysis Patient Hiroshi Kato, MD, Seiichiro Ikawa, MD, Akio Hayashi, MD, and Kenji Yokoyama, MD Divisions of Cardiovascular Surgery and Nephrology, Toyonaka Municipal Hospital, Osaka, Japan
A 67-year-old man with chronic renal failure who was being treated with dialysis through an arteriovenous fistula in the left arm was scheduled to undergo off-pump coronary artery bypass grafting. Angiography detected the steal phenomenon in the left internal mammary artery during the diastolic phase. Postoperative study with Doppler guidewire showed that the steal of the left internal mammary artery was due to an ipsilateral arteriovenous fistula. Preoperative angiography of the internal mammary artery is therefore recommended for patients on dialysis. (Ann Thorac Surg 2003;75:270 –1) © 2003 by The Society of Thoracic Surgeons
T
he internal mamma/ry artery (IMA) is reported to be an excellent graft for dialysis patients [1]. There have been no reports that an arteriovenous fistual could cause ipsilateral IMA steal. We present the case of a 67-year-old patient with IMA steal on the same side as the arteriovenous fistual. A 67-year-old man was admitted to our hospital with unstable angina on 10 August 2000. He had chronic renal failure and was being treated with dialysis. A side-to-end arteriovenous fistula was constructed in the left wrist on 20 July 1993. Another arteriovenous fistula, the side of the cephalic vein to the side of the brachial artery anastomosis, was constructed in the left antecubital fossa on 12 June 1998 because of dysfunctioning of the former fistula. The coronary angiography demonstrated three-vessel disease and the culprit lesion was thought to be the left anterior descending coronary artery with severe proximal stenosis. On 11 September 2000 angiography of the Accepted for publication Aug 2, 2002. Address reprint requests to Dr Kato, Division of Cardiovascular Surgery, Toyonaka Municipal Hospital, 14-1, 4-chome, Shibahara-cho, Toyonaka, Osaka 560-8565, Japan.
© 2003 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2003;75:270 –1
left IMA demonstrated that the steal occurred during diastole. That is, the antegrade flow of the left IMA was observed during systole and the retrograde flow during diastole without stenosis in the left subclavian artery (Fig 1). On 18 September 2000 the right IMA was grafted to the left anterior descending coronary artery without cardiopulmonary bypass and the postoperative course was uneventful. The subsequent study was performed on 18 October 2000 after the patient had given informed consent. The phasic flow velocity in the proximal left IMA was recorded with a 0.014 inch 15 MHz Doppler guidewire (FloWire; Cardiometrics, Mountain View, CA) and a velocimeter (FloMap; Cardiometrics). When the fistula in the left antecubital fossa was open the antegrade flow was observed during systole and the retrograde flow during diastole (Fig 2A). However when the fistula was occluded with a pneumatic cuff the antegrade flow was observed during both systole and diastole (Fig 2B). Cardiac output was measured by means of thermodilution before and after occlusion of the arteriovenous fistula in the left antecubital fossa. Cardiac output was 7.22 L/min before occlusion and 6.15 L/min after occlusion. The patient remained asymptomatic 1 year postoperatively without any intervention to treat the remaining coronary artery lesions.
Comment IMA patency was found to be superior to the saphenous vein graft after coronary artery bypass grafting in patients with chronic renal failure [1]. There have been no reports of IMA steal occurring on the same side as the arteriovenous fistula before and after coronary artery bypass grafting nor of steal in the IMA graft occurring in patients with coronary artery bypass grafting shortly after the arteriovenous fistula has been constructed on the same side as the IMA. In the unused IMA the forward flow is observed during both systole and diastole, although mainly during systole. But when this IMA is connected to the left anterior descending artery the diastolic component becomes much larger [2]. Therefore a contralateral IMA or a free IMA graft should be used when the retrograde flow or steal is observed during diastole on preoperative angiography of the IMA on the same side as the arteriovenous fistula. Judging from the postoperative study with the Doppler guidewire it was obvious that IMA steal was due to the arteriovenous fistula in our case. It is very difficult to measure the flow in an arteriovenous fistula. Frank and colleagues [3] reported that if the blood flow in an arteriovenous fistula is moderate, the increase in cardiac output secondary to the arteriovenous fistula has the same value as the blood flow value. Because in our case the flow volume through the fistula was approximately 1L/min and for optimal management the flow volume through the fistula should be at least within the range of 400 to 600 mL/min [4], the fistula flow in our case may have been slightly high. Our postoperative study did not 0003-4975/03/$30.00 PII S0003-4975(02)04306-0
CASE REPORT PETERS ET AL LATE QUADRIPLEGIA AFTER COARCTATION REPAIR
5. Borst HG, Laas J, Heinemann M. Type A aortic dissection: diagnosis and management of malperfusion phenomena. Semin Thorac Cardiovasc Surg 1991;3:238 –41. 6. Tanaka H, Kazui T, Sato H, Inoue N, Yamada O, Komatsu S. Experimental study on the optimum flow rate and pressure for selective cerebral perfusion. Ann Thorac Surg 1995;59: 651–7. 7. Shiiya N, Kunihara T, Imamura M, Murashita T, Matsui Y, Yasuda K. Surgical management of atherosclerotic aortic arch aneurysms using selective cerebral perfusion: 7-year experience in 52 patients. Eur J Cardio Thorac Surg 2000;17:266 –71. 8. Imanaka K, Kyo S, Tanabe H, Asano H, Yokote Y. Fatal intraoperative dissection of the innominate artery due to perfusion through the right axillary artery. J Thorac Cardiovasc Surg 2000;120:405–6. CASE REPORTS
Late Quadriplegia After Adult Coarctation Repair Paul Peters, FRCS(CTh), Jeffrey W. Brennan, MBBS, Clifford F. Hughes, FRACS, Martin McGee-Collett, FRACS, and Geoffrey Parker, FRACR Departments of Cardiothoracic Surgery, Neurosurgery, and Radiology, Royal Prince Alfred Hospital, Camperdown, Sydney, Australia
Quadriplegia developed suddenly 1 month after coarctation repair in a 53-year-old human. Cervical cord ischemia caused by thrombosis in an enlarged anterior spinal artery collateral was diagnosed on magnetic resonance scan and spinal angiography. After urgent cord decompression and anticoagulation there was neurologic improvement over a period of several months. Urgent investigation of neurologic abnormalities occurring late after coarctation repair may enable intervention to avert permanent neurologic sequelae. (Ann Thorac Surg 2003;75:268 –70) © 2003 by The Society of Thoracic Surgeons
N
eurologic complications associated with aortic coarctation may occur in one of three forms; central nervous system manifestations of proximal hypertension (ruptured berry aneurysm or stroke), spinal syndromes associated with aneurysmal spinal artery collaterals causing myelopathy by compression or hemorrhage, or perioperative spinal ischemia [1,2]. We report an example of a fourth, late type of neurologic complication of coarctation in an adult; a late thrombosed anterior spinal artery collateral. This required urgent neurosurgical intervention to prevent permanent quadriplegia. A 53-year-old human with longstanding hypertension presented with sudden onset of left-sided hemiparesis
Accepted for publication May 1, 2002. Address reprint requests to Dr Hughes, Department of Cardiothoracic Surgery, Royal Prince Alfred Hospital, Missenden Rd, Camperdown, Sydney, NSW 2050 Australia; e-mail: [email protected]. gov.au.
© 2003 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2003;75:268 –70
and left hemifacial parasthesia. Clinical examination and investigations confirmed ischemic stroke (involving the right medial temporal lobe and posterior thalamus) and findings that are typical of adult coarctation including central hypertension. The carotid and intracranial circulations appeared normal. Four months later, after recovering from his stroke, the patient underwent coarctation repair. At the left posterolateral fourth space thoracotomy, extensive chest wall collateralization was encountered. The coarcted segment was identified and mobilized. Immediately two distal 5-mm spinal collaterals were controlled and preserved. Because of extensive collateralization no specific spinal protection measures were used. Under heparinization the coarcted segment was resected, and a 20-mm Dacron graft interposed. Clamp time was 45 minutes. The initial postoperative course was uneventful apart from persisting hypertension managed medically, and there were no abnormal neurologic findings on discharge. One month later he represented with rapidly progressing weakness of all four limbs. He had virtual paralysis of his hands, markedly weak elbow extension, weak elbow flexion and preserved shoulder power. There was flaccid, hyporeflexic weakness in the lower limbs with sensory deficit to pinprick below level T2. Dorsal column function was intact. Blood pressure on admission was 100/70 mm Hg. Spinal magnetic resonance imaging suggested an extensive intrathecal arterial abnormality with cord compression anteriorly from C5 to T1. Urgent surgical decompression of the cord was achieved by posterior cervical laminectomy from C4 to C7 at which multiple large paraspinal muscular collaterals were noted. Postoperatively his condition stabilized. Forty-eight hours later a sudden loss of proximal limb power was noted. Repeat magnetic resonance imaging suggested cord edema and possibly infarction. The anterior thecal vessels were larger and hypointense suggesting thrombosis (Fig 1). Spinal angiography demonstrated segmental occlusion of the lower cervical anterior spinal artery (Fig 2). A large radiculo-medullary vessel from the left vertebral artery at C4 –5 (artery of Lazorthe) [3] supplying an enlarged anterior spinal artery was visualized. The anterior spinal artery was patent above C4 but thrombosed below the junction with the artery of Lazorthe to the level C7. The patient was anticoagulated with intravenous heparin. Dexamethasone was commenced, blood pressure support with intravenous fluids and inotropic agents were continued, and hyperbaric oxygen was administered. He remained stable on warfarin and was discharged to a rehabilitation unit for 3 months, and his condition improved. One month later he was walking unaided and independently handling activities of daily living, although he had residual weakness of elbow extension and wasting intrinsic hand musculature. Follow-up magnetic resonance imaging demonstrated completed partial anterior spinal artery territory infarction from C4 to T2. 0003-4975/03/$30.00 PII S0003-4975(02)04126-7
CASE REPORT PETERS ET AL LATE QUADRIPLEGIA AFTER COARCTATION REPAIR
269
CASE REPORTS
Ann Thorac Surg 2003;75:268 –70
Fig 2. Spinal angiography (late arterial phase, oblique) showing artery of Lazorthe (l) arising from left vertebral artery (v) at C4 –5. The anterior spinal artery (s) is thrombosed from the junction with the artery of Lazorthe inferiorly (arrowheads).
Fig 1. Sagittal T2-weighted magnetic resonance imaging demonstrating spinal cord edema in the anterior half of the cord between C4 and T2 and an enlarged anterior spinal artery (s).
Comment Aortic coarctation occurs in approximately 30 of 100,000 live births [4]. Improvements in imaging techniques increasingly allow early diagnosis and treatment, so the rare entity of adult coarctation may become even less common. Nevertheless, neurologic conditions associated with coarctation and its treatment can be devastating. Reviews of coarctation operations suggest that perioperative spinal cord damage leading to paraplegia occurs in 0.3 to 0.6% of patients [2, 5]. The relative rarity of perioperative spinal cord damage leading to paraplegia occurring compared with that associated with aortic operations for other conditions, despite the fact that spinal protection is not commonly used, is thought to be caused by the extensive collateralization of blood flow around the coarcted segment leading to maintenance of spinal and lower body blood flow during clamping of the descending thoracic aorta. Reported late complications of coarctation repair mostly describe re-coarctation or false aneurysm formation at the operated site [6]. We postulate that this late
neurologic complication occurred after repair of this severe coarctation, because the pressure differential along enlarged and tortuous spinal artery collaterals was markedly reduced. The consequent fall in collateral blood flow precipitated stasis and thrombosis. Because we recognize that pressure differentials along collaterals are probably independent of systemic blood pressure after coarctation repair, we doubt that aggressive management of this patient’s hypertension contributed to this complication. This case demonstrates that close postoperative follow-up of such patients is essential. Early investigation of neurologic symptoms is mandatory. Unless the diagnosis is made at an early stage it would be possible to miss the small window of opportunity for successful intervention by way of surgical decompression or anticoagulation. The consequences of missing such an opportunity could be catastrophic.
References 1. Aaron BL, Loew AG, Mullen JT. Coarctation of the aorta with spontaneous quadriparesis. J Thorac Cardiovasc Surg 1974; 68:76 –9. 2. Brewer LA 3d, Fosberg RG, Mulder GA, Verskaa JJ. Spinal cord complications following surgery for coarctation of the aorta. J Thorac Cardiovasc Surg 1972;64:368 –81. 3. Lasjaunias P, Berenstein A. Functional vascular anatomy of brain, spinal cord & spine. In: Surgical Neuroangiography. Heidelburg: Springer Verlag, 1990, Vol 3, 55– 8. 4. Grech V. Diagnostic and surgical trends, and epidemiology of
270
CASE REPORT KATO ET AL INTERNAL MAMMARY ARTERY STEAL
coarctation in a population based study. Int J Cardiol 1999; 68(2):197–202. 5. Keen G. Spinal cord damage and operations for coarctation of the aorta: etiology, practice and prospects. Thorax 1987;42(1): 11–8. 6. Bobby JJ, Emami JM, Farmer RD, Newman CG. Operative survival and 40 year follow up of surgical repair of aortic coarctation. Br Heart J 1991;65(5):271–6.
CASE REPORTS
Internal Mammary Artery Steal in a Dialysis Patient Hiroshi Kato, MD, Seiichiro Ikawa, MD, Akio Hayashi, MD, and Kenji Yokoyama, MD Divisions of Cardiovascular Surgery and Nephrology, Toyonaka Municipal Hospital, Osaka, Japan
A 67-year-old man with chronic renal failure who was being treated with dialysis through an arteriovenous fistula in the left arm was scheduled to undergo off-pump coronary artery bypass grafting. Angiography detected the steal phenomenon in the left internal mammary artery during the diastolic phase. Postoperative study with Doppler guidewire showed that the steal of the left internal mammary artery was due to an ipsilateral arteriovenous fistula. Preoperative angiography of the internal mammary artery is therefore recommended for patients on dialysis. (Ann Thorac Surg 2003;75:270 –1) © 2003 by The Society of Thoracic Surgeons
T
he internal mamma/ry artery (IMA) is reported to be an excellent graft for dialysis patients [1]. There have been no reports that an arteriovenous fistual could cause ipsilateral IMA steal. We present the case of a 67-year-old patient with IMA steal on the same side as the arteriovenous fistual. A 67-year-old man was admitted to our hospital with unstable angina on 10 August 2000. He had chronic renal failure and was being treated with dialysis. A side-to-end arteriovenous fistula was constructed in the left wrist on 20 July 1993. Another arteriovenous fistula, the side of the cephalic vein to the side of the brachial artery anastomosis, was constructed in the left antecubital fossa on 12 June 1998 because of dysfunctioning of the former fistula. The coronary angiography demonstrated three-vessel disease and the culprit lesion was thought to be the left anterior descending coronary artery with severe proximal stenosis. On 11 September 2000 angiography of the Accepted for publication Aug 2, 2002. Address reprint requests to Dr Kato, Division of Cardiovascular Surgery, Toyonaka Municipal Hospital, 14-1, 4-chome, Shibahara-cho, Toyonaka, Osaka 560-8565, Japan.
© 2003 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Ann Thorac Surg 2003;75:270 –1
left IMA demonstrated that the steal occurred during diastole. That is, the antegrade flow of the left IMA was observed during systole and the retrograde flow during diastole without stenosis in the left subclavian artery (Fig 1). On 18 September 2000 the right IMA was grafted to the left anterior descending coronary artery without cardiopulmonary bypass and the postoperative course was uneventful. The subsequent study was performed on 18 October 2000 after the patient had given informed consent. The phasic flow velocity in the proximal left IMA was recorded with a 0.014 inch 15 MHz Doppler guidewire (FloWire; Cardiometrics, Mountain View, CA) and a velocimeter (FloMap; Cardiometrics). When the fistula in the left antecubital fossa was open the antegrade flow was observed during systole and the retrograde flow during diastole (Fig 2A). However when the fistula was occluded with a pneumatic cuff the antegrade flow was observed during both systole and diastole (Fig 2B). Cardiac output was measured by means of thermodilution before and after occlusion of the arteriovenous fistula in the left antecubital fossa. Cardiac output was 7.22 L/min before occlusion and 6.15 L/min after occlusion. The patient remained asymptomatic 1 year postoperatively without any intervention to treat the remaining coronary artery lesions.
Comment IMA patency was found to be superior to the saphenous vein graft after coronary artery bypass grafting in patients with chronic renal failure [1]. There have been no reports of IMA steal occurring on the same side as the arteriovenous fistula before and after coronary artery bypass grafting nor of steal in the IMA graft occurring in patients with coronary artery bypass grafting shortly after the arteriovenous fistula has been constructed on the same side as the IMA. In the unused IMA the forward flow is observed during both systole and diastole, although mainly during systole. But when this IMA is connected to the left anterior descending artery the diastolic component becomes much larger [2]. Therefore a contralateral IMA or a free IMA graft should be used when the retrograde flow or steal is observed during diastole on preoperative angiography of the IMA on the same side as the arteriovenous fistula. Judging from the postoperative study with the Doppler guidewire it was obvious that IMA steal was due to the arteriovenous fistula in our case. It is very difficult to measure the flow in an arteriovenous fistula. Frank and colleagues [3] reported that if the blood flow in an arteriovenous fistula is moderate, the increase in cardiac output secondary to the arteriovenous fistula has the same value as the blood flow value. Because in our case the flow volume through the fistula was approximately 1L/min and for optimal management the flow volume through the fistula should be at least within the range of 400 to 600 mL/min [4], the fistula flow in our case may have been slightly high. Our postoperative study did not 0003-4975/03/$30.00 PII S0003-4975(02)04306-0