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Magnetic resonance imaging of vascular condults in coarctation of the aorta
February
482
Brief
Communications
Magnetic resonance imaging of vascutar conduits in coarctation of the aurta Anthony L. Pucillo, MD, Andrew G. Schechter, MD, Richard H. Kay, MD, and Michael V. Herman, MD. Valhalla,
N. Y.
From the Departments of Medicine and Radiology, New York Medical College. Reprint requests: Anthony L. Pucillo, MD, Division of Cardiology, New York Medical College and Westchester County Medical Center, Valhalla, NY 10595.
American
Heart
Magnetic resonanceimaging (MRI) is a useful method of assessing the thoracic aorta.’ This is particularly true with coarctation of the aorta in which the position and extent of the vascular abnormality is seen.2*3 Prosthetic vascular conduits are commonly used as part of the surgical correction of coarctation of the thoracic aorta.4The vascular conduits are susceptible to stenosis at either the proximal or distal anastomoticsite and to thrombosisand degenerative changeswith calcification leading to graft dysfunction. Cardiac catheterization and angiography are usually the proceduresselectedto assessvascular conduit patency. In this report we describe the use of MRI to determine the patency and structural integrity of prosthetic vascular conduits used in repair of coarctation of
1. A, Angiogram demonstrating stenosisat proximal end of vascular conduit (arrow). Ao, Ascending aorta. B, Sagittal MRI scan demonstrating stenosis at proximal end of vascular conduit (arrow) correspondingto angiogramin A. C, MRI scanshowspatent vascular conduit (white arrows) surrounded by exuberant fibrosis (black arrow) not seenon angiogram. Fig.
ISSS Journal
Volume Number
117 2
Brief
Fig.
2A. Sagittal MRI scanshowing patent vascular conduit (arrows).
the aorta. MRI was performed with a 1.5 Tesla superconducting magnet (GE-S&a, General Electric Medical Systems Group, Milwaukee, Wise.). Images were obtained with the use of the spin-echo acquisition technique and cardiac gating. The repetition time wasdetermined by the patient’s heart rate, and the echo time wasset at 20 or 25 msec. Images were obtained in the coronal and axial planes. In addition, sagittal-oblique imageswere obtained to visualize the entire course of the thoracic aorta in a single image. The field of view ranged from 32 to 40 cm and the acquisition matrix was set at 256 X 128 pixels to give an in-plane resolution of 1.25 X 2.50mm for the 32 cm field of view or 1.56 X 3.13 mm for the 40 cm field of view. Two excitations were performed for all images. Case No. 1. A 12-year-old boy with a long segment coarctation who had three previous corrective procedures was evaluated for recurrent hypertension and suspected graft dysfunction. Initial physical findings included a systolic blood pressurein the right arm of 175mm Hg with a 50 mm Hg pressuredifference betweenthe right arm and leg and markedly decreasedfemoral pulses.A loud harsh systolic ejection murmur at the right upper sternal border, a continuous murmur over the upper anterior chest bilaterally, and a holosystolic apical murmur were present. Angiography demonstratedstenosisof the proximal end of the conduit at the point at which it left the ascending aorta to bypassthe area of coarctation before entering the descendingaorta (Fig. 1, A). This area of stenosiswasseen
Communications
483
Ao, Ascending aorta.
by the MRI scan to closely correlate with the angiogram despite slight differences in imaging obliquity. In addition, exuberant fibrosis wasseento surround the vascular conduit which was patent and entered the descending thoracic aorta without obstruction (Fig. 1, B and C). Case No. 2. A 41-year-old man with a postductal coarctation, who had undergone repair at age 16 with excision and end-to-end anastomosisand had undergone reoperation at age 39 becauseof recurrent stenosiswith a left subclavian artery-to-descending aorta graft, wasevaluated becauseof malaise,atypical cheat pain, and dyspnea on exertion. Physical findings were remarkable for a normal blood pressurein the upper and lower extremities, a soft early-peaking grade 2/6 systolic ejection murmur at the base,a short diastolic grade 2/S decrescendomurmur at the left sternal border, and absent ventricular gallop. The MRI scan demonstrated graft patency (Fig. 2, A). However, an ascending thoracic aortic aneurysm and dissectionwere found (Fig. 2, B). Angiography confirmed the presenceof the aortic aneurysmand dissection(Fig. 2, C), which were repaired surgically with a prosthetic valve conduit. Coarctation of the aorta is found in 7% of patients with congenital heart disease.5Cardiac catheterization and angiography has been the traditional method of confirming the clinical diagnosis.Recently MRI hasbeenshownto be able to directly detect the coarctation in addition to the anatomic associations,2which include collateral vessels
484
Brief
Communications
American
February 1989 Heart Journal
Fig. 28 and C. B, Transverse MRI scan demonstrates ascendingaortic aneurysm (lo]w al “row) with intimal flap (short arrow) indicating aortic dissection. C, Angiogram confirming present:e of ascending aortic aneurysm (white arrow) and dissection (arrowhead).
and poststenotic aortic dilatation. After diagnosis,some clinically significant lesions are treated surgically with synthetic grafts that bypass the aortic coarctation.4 After ‘grafting, immediateand delayed complicationsmay occur, including graft dilatation, fiber breakdown with subsequent pseudoaneurysm, intraluminal deposit of fibrin, thrombosis of graft, or stenosisat the proximal or distal anastomoticsite.6-8 MRI may be of value in assessing these postoperative complications. We have presented two casesof patients with coarctation bypass grafts who experienced symptoms 23 and 2 years after grafting. In one patient, MRI demonstrated a stenosisat the proximal end of the vascular graft as the causeof the clinical syndrome. In the secondpatient, the
MRI demonstrated a normal graft, but an associated aortic aneurysm and dissectionwere found. At the present time there is no consensusregarding indications for invasive postoperative graft evaluation. There are some who recommend cardiac catheterization in all patients, though the timing may vary. Others perform an invasive evaluation only when a clinicalIy significant conduit lesion is suspected.Ultrasonographic assessmentis disappointing becauseof the lack of an adequate acoustic.windowas a result of the extracardiac position of the grafts? MRI can be used to noninvasively evaluate synthetic grafts usedin the repair of coarctation of the aorta with clinically suspectedconduit stenosisor aspart of the routine clinical evaluation without the need for invasive testing.
Volume Number
117 2
Brief Communications
REFERENCES
1. Glazer HS, Gutieney FR, Levitt RG, Lee JKT, Murphy WA. The thoracic aorta studied bv MR imasina. RadiolosvI- 1985: 157:149-55. 2. von Schulthess GK, Higasbino SM, Higgins SS, Didier D, Fisher MR. Higains CB. Coarctation of the aorta: MR imaging. Radiology 1986;158:469-74. of 3. Amparo EG, Higgins CB, Shafton EP. Demonstration coarctation of the aorta by magnetic resonance imaging. AJR 1984;143:1192-4. of the 4. deLeva1 M. Coarctation of the aorta and interruption aortic arch. In: Stark J, deLeval M, eds. Surgery for congenital heart disease. London: Grune & Stratton, 1983:218-29. 5. Friedman WF. Congenital heart disease. In: Petersdorf RG, Adams RD, Braunwald E, Isselbacher KJ, Martin JB, Wilson MD, eds. Harrison’s principles of internal medicine. 10th ed. New York: McGraw-Hill International Book Co, 1983:1392. 6. Perry MO. Early failure of Dacron prosthetic grafts. J Cardiovasc Surg (Torino) 1975;16:318-21. 7. Berger K, Sauvage LR. Late fiber deterioration in Dacron arterial grafts. Ann Surg 1981;193:477-91. 8. Watanabe T, Kusaba A, Kuma H, Kina M, Okadome K, Inokuchi K. Failure of dacron arterial prostheses caused by structural defects. J Cardiovasc Surg (Torino) 1983;24:95199. 9. Sahn DJ, Allen HD, McDonald F, Goldberg SJ. Real-time cross-sectional echocardiographic diagnosis of coarctation of the aorta. Circulation 1977;56:762-9. I
-
Aortocoronary saphenous vein graft spasm inducing ventricular fibrillation John G. Webb, MD, FRCP(C), Harold E. Aldridge, MB, FRCP(C), John Fulop, MD, FRCP(C), and Aminul Haq, MD, FRCP(C). Toronto, Ontario, Canada From the Division of Cardiology, Toronto General Hospital, University of Toronto. Reprint requests: John G. Webb, MD, Box 0124, University of California, San Francisco, San Francisco, CA 94143.
Spasm of saphenousvein aortocoronary grafts is a rare phenomenon,and the clinical significanceof such spasmis uncertain. This report describes spasm of a vein graft inducing ventricular fibrillation and leading to a myocardial infarction. Although autonomic influences appear to play a role in coronary spasm, innervation is not a prerequisite, as evidenced by documented arterial spasm in denervated and transplanted hearts.’ Recently spasmof internal mammary bypass grafts has been described.2 Inasmuch as saphenousveins are dynamic muscular vessels, it is perhaps not surprising that noninnervated aortocoronary grafts are capable of spasmas well. A 34-year-old woman was first seen with an inferior myocardial infarction. Postinfarction angina resulted in aortocoronary saphenousvein bypassof an isolated right coronary occlusion. Five years later the patient still had atypical chest pain. Resultsof selective coronary angiography showeda normal left system and proximal occlusion of the right coronary artery. Cannulation of the vein graft wasdifficult and required a number of catheter exchanges. However, subsequentinjection initially showeda widely patent graft (Fig. 1, A). Within minutes, however, chest pain and ST elevation were noted. Repeat graft injection showed diffuse subtotal occlusion (Fig. 1, B). Direct instillation of nitroglycerin, 400 pg, into the graft improved patency, but ventricular fibrillation rapidly ensued requiring electrical cardioversion. Repeat visualization showedthat the graft still narrowed severely, but this resolvedwith further injection of nitroglycerin, 300kg (Fig. 1, C). Pain subsided rapidly; however, inferior T wave changesevolved (Fig. 2) associatedwith recurrent bradycardia and an elevated creatine phosphokinaselevel of 559 U/L (normal = 110 U/L) and MB fraction of 11% (normal = 4%). Episodic typical chest pain remained unresponsiveto nitrates and calcium blockers. Results of ambulatory monitoring did not showevidenceof ischemia; neither did thallium imaging during pain. Treadmill exercise failed to reproduce symptoms or ECG changes. Although saphenous graft venospasm had been docu-
1. A, Saphenousvein graft to right coronary artery is widely patent. nitroglycerin.
Fig.
485
B,
Diffuse graft spasm.C, After
482
Brief
Communications
Magnetic resonance imaging of vascutar conduits in coarctation of the aurta Anthony L. Pucillo, MD, Andrew G. Schechter, MD, Richard H. Kay, MD, and Michael V. Herman, MD. Valhalla,
N. Y.
From the Departments of Medicine and Radiology, New York Medical College. Reprint requests: Anthony L. Pucillo, MD, Division of Cardiology, New York Medical College and Westchester County Medical Center, Valhalla, NY 10595.
American
Heart
Magnetic resonanceimaging (MRI) is a useful method of assessing the thoracic aorta.’ This is particularly true with coarctation of the aorta in which the position and extent of the vascular abnormality is seen.2*3 Prosthetic vascular conduits are commonly used as part of the surgical correction of coarctation of the thoracic aorta.4The vascular conduits are susceptible to stenosis at either the proximal or distal anastomoticsite and to thrombosisand degenerative changeswith calcification leading to graft dysfunction. Cardiac catheterization and angiography are usually the proceduresselectedto assessvascular conduit patency. In this report we describe the use of MRI to determine the patency and structural integrity of prosthetic vascular conduits used in repair of coarctation of
1. A, Angiogram demonstrating stenosisat proximal end of vascular conduit (arrow). Ao, Ascending aorta. B, Sagittal MRI scan demonstrating stenosis at proximal end of vascular conduit (arrow) correspondingto angiogramin A. C, MRI scanshowspatent vascular conduit (white arrows) surrounded by exuberant fibrosis (black arrow) not seenon angiogram. Fig.
ISSS Journal
Volume Number
117 2
Brief
Fig.
2A. Sagittal MRI scanshowing patent vascular conduit (arrows).
the aorta. MRI was performed with a 1.5 Tesla superconducting magnet (GE-S&a, General Electric Medical Systems Group, Milwaukee, Wise.). Images were obtained with the use of the spin-echo acquisition technique and cardiac gating. The repetition time wasdetermined by the patient’s heart rate, and the echo time wasset at 20 or 25 msec. Images were obtained in the coronal and axial planes. In addition, sagittal-oblique imageswere obtained to visualize the entire course of the thoracic aorta in a single image. The field of view ranged from 32 to 40 cm and the acquisition matrix was set at 256 X 128 pixels to give an in-plane resolution of 1.25 X 2.50mm for the 32 cm field of view or 1.56 X 3.13 mm for the 40 cm field of view. Two excitations were performed for all images. Case No. 1. A 12-year-old boy with a long segment coarctation who had three previous corrective procedures was evaluated for recurrent hypertension and suspected graft dysfunction. Initial physical findings included a systolic blood pressurein the right arm of 175mm Hg with a 50 mm Hg pressuredifference betweenthe right arm and leg and markedly decreasedfemoral pulses.A loud harsh systolic ejection murmur at the right upper sternal border, a continuous murmur over the upper anterior chest bilaterally, and a holosystolic apical murmur were present. Angiography demonstratedstenosisof the proximal end of the conduit at the point at which it left the ascending aorta to bypassthe area of coarctation before entering the descendingaorta (Fig. 1, A). This area of stenosiswasseen
Communications
483
Ao, Ascending aorta.
by the MRI scan to closely correlate with the angiogram despite slight differences in imaging obliquity. In addition, exuberant fibrosis wasseento surround the vascular conduit which was patent and entered the descending thoracic aorta without obstruction (Fig. 1, B and C). Case No. 2. A 41-year-old man with a postductal coarctation, who had undergone repair at age 16 with excision and end-to-end anastomosisand had undergone reoperation at age 39 becauseof recurrent stenosiswith a left subclavian artery-to-descending aorta graft, wasevaluated becauseof malaise,atypical cheat pain, and dyspnea on exertion. Physical findings were remarkable for a normal blood pressurein the upper and lower extremities, a soft early-peaking grade 2/6 systolic ejection murmur at the base,a short diastolic grade 2/S decrescendomurmur at the left sternal border, and absent ventricular gallop. The MRI scan demonstrated graft patency (Fig. 2, A). However, an ascending thoracic aortic aneurysm and dissectionwere found (Fig. 2, B). Angiography confirmed the presenceof the aortic aneurysmand dissection(Fig. 2, C), which were repaired surgically with a prosthetic valve conduit. Coarctation of the aorta is found in 7% of patients with congenital heart disease.5Cardiac catheterization and angiography has been the traditional method of confirming the clinical diagnosis.Recently MRI hasbeenshownto be able to directly detect the coarctation in addition to the anatomic associations,2which include collateral vessels
484
Brief
Communications
American
February 1989 Heart Journal
Fig. 28 and C. B, Transverse MRI scan demonstrates ascendingaortic aneurysm (lo]w al “row) with intimal flap (short arrow) indicating aortic dissection. C, Angiogram confirming present:e of ascending aortic aneurysm (white arrow) and dissection (arrowhead).
and poststenotic aortic dilatation. After diagnosis,some clinically significant lesions are treated surgically with synthetic grafts that bypass the aortic coarctation.4 After ‘grafting, immediateand delayed complicationsmay occur, including graft dilatation, fiber breakdown with subsequent pseudoaneurysm, intraluminal deposit of fibrin, thrombosis of graft, or stenosisat the proximal or distal anastomoticsite.6-8 MRI may be of value in assessing these postoperative complications. We have presented two casesof patients with coarctation bypass grafts who experienced symptoms 23 and 2 years after grafting. In one patient, MRI demonstrated a stenosisat the proximal end of the vascular graft as the causeof the clinical syndrome. In the secondpatient, the
MRI demonstrated a normal graft, but an associated aortic aneurysm and dissectionwere found. At the present time there is no consensusregarding indications for invasive postoperative graft evaluation. There are some who recommend cardiac catheterization in all patients, though the timing may vary. Others perform an invasive evaluation only when a clinicalIy significant conduit lesion is suspected.Ultrasonographic assessmentis disappointing becauseof the lack of an adequate acoustic.windowas a result of the extracardiac position of the grafts? MRI can be used to noninvasively evaluate synthetic grafts usedin the repair of coarctation of the aorta with clinically suspectedconduit stenosisor aspart of the routine clinical evaluation without the need for invasive testing.
Volume Number
117 2
Brief Communications
REFERENCES
1. Glazer HS, Gutieney FR, Levitt RG, Lee JKT, Murphy WA. The thoracic aorta studied bv MR imasina. RadiolosvI- 1985: 157:149-55. 2. von Schulthess GK, Higasbino SM, Higgins SS, Didier D, Fisher MR. Higains CB. Coarctation of the aorta: MR imaging. Radiology 1986;158:469-74. of 3. Amparo EG, Higgins CB, Shafton EP. Demonstration coarctation of the aorta by magnetic resonance imaging. AJR 1984;143:1192-4. of the 4. deLeva1 M. Coarctation of the aorta and interruption aortic arch. In: Stark J, deLeval M, eds. Surgery for congenital heart disease. London: Grune & Stratton, 1983:218-29. 5. Friedman WF. Congenital heart disease. In: Petersdorf RG, Adams RD, Braunwald E, Isselbacher KJ, Martin JB, Wilson MD, eds. Harrison’s principles of internal medicine. 10th ed. New York: McGraw-Hill International Book Co, 1983:1392. 6. Perry MO. Early failure of Dacron prosthetic grafts. J Cardiovasc Surg (Torino) 1975;16:318-21. 7. Berger K, Sauvage LR. Late fiber deterioration in Dacron arterial grafts. Ann Surg 1981;193:477-91. 8. Watanabe T, Kusaba A, Kuma H, Kina M, Okadome K, Inokuchi K. Failure of dacron arterial prostheses caused by structural defects. J Cardiovasc Surg (Torino) 1983;24:95199. 9. Sahn DJ, Allen HD, McDonald F, Goldberg SJ. Real-time cross-sectional echocardiographic diagnosis of coarctation of the aorta. Circulation 1977;56:762-9. I
-
Aortocoronary saphenous vein graft spasm inducing ventricular fibrillation John G. Webb, MD, FRCP(C), Harold E. Aldridge, MB, FRCP(C), John Fulop, MD, FRCP(C), and Aminul Haq, MD, FRCP(C). Toronto, Ontario, Canada From the Division of Cardiology, Toronto General Hospital, University of Toronto. Reprint requests: John G. Webb, MD, Box 0124, University of California, San Francisco, San Francisco, CA 94143.
Spasm of saphenousvein aortocoronary grafts is a rare phenomenon,and the clinical significanceof such spasmis uncertain. This report describes spasm of a vein graft inducing ventricular fibrillation and leading to a myocardial infarction. Although autonomic influences appear to play a role in coronary spasm, innervation is not a prerequisite, as evidenced by documented arterial spasm in denervated and transplanted hearts.’ Recently spasmof internal mammary bypass grafts has been described.2 Inasmuch as saphenousveins are dynamic muscular vessels, it is perhaps not surprising that noninnervated aortocoronary grafts are capable of spasmas well. A 34-year-old woman was first seen with an inferior myocardial infarction. Postinfarction angina resulted in aortocoronary saphenousvein bypassof an isolated right coronary occlusion. Five years later the patient still had atypical chest pain. Resultsof selective coronary angiography showeda normal left system and proximal occlusion of the right coronary artery. Cannulation of the vein graft wasdifficult and required a number of catheter exchanges. However, subsequentinjection initially showeda widely patent graft (Fig. 1, A). Within minutes, however, chest pain and ST elevation were noted. Repeat graft injection showed diffuse subtotal occlusion (Fig. 1, B). Direct instillation of nitroglycerin, 400 pg, into the graft improved patency, but ventricular fibrillation rapidly ensued requiring electrical cardioversion. Repeat visualization showedthat the graft still narrowed severely, but this resolvedwith further injection of nitroglycerin, 300kg (Fig. 1, C). Pain subsided rapidly; however, inferior T wave changesevolved (Fig. 2) associatedwith recurrent bradycardia and an elevated creatine phosphokinaselevel of 559 U/L (normal = 110 U/L) and MB fraction of 11% (normal = 4%). Episodic typical chest pain remained unresponsiveto nitrates and calcium blockers. Results of ambulatory monitoring did not showevidenceof ischemia; neither did thallium imaging during pain. Treadmill exercise failed to reproduce symptoms or ECG changes. Although saphenous graft venospasm had been docu-
1. A, Saphenousvein graft to right coronary artery is widely patent. nitroglycerin.
Fig.
485
B,
Diffuse graft spasm.C, After