CASE REPORTS
Acute Myocardial Infarction Due to Thrombolytic Reperfusion of Chronically Occluded Saphenous Vein Coronary Bypass Grafts John C. Gurley, MD, and Blair S. MacPhail. MD
L
ate occlusion of saphenous vein grafts is a major cause of recurrent angina in the years after successfulcoronary artery bypass surgery. Reestablishment of circulation to the involved artery is problematic, becausedirect angioplasty may be precluded by chronic occlusionof the native artery and extensive thrombus in the occluded vein graft. It has recently been demonstrated that chronically occluded aortocoronary saphenous vein grafts can be successfullyrecanalized by prolonged low-doseintragraft infusions of urokinase.‘-5 Hartmann et al2 achieved recanalization in 11 of 12 chronically occluded grafts using 16- to 72-hour urokinase infusions in total dosesranging from 870,000to 6,290,OOO U. Marx et al3 reported recanalization in 8 of 10 grafts with shorter urokinase infusions. Neither investigator reported significant cardiovascular complications as a result of the procedure.We report on 2 consecutivepatients who developed acute myocardial infarction as a direct result of successful thrombolytic reperfusion of chronically occludedsaphenousvein grafts.
grafts. The patient was treated medically, but returned 3 weeks later with a new syndrome of lifestyle-limiting exertional angina. Repeat cardiac catheterization showed no interval change in coronary anatomy, and well developed collaterals from the left coronary to the occluded right coronary artery were noted. It was determined that the occluded right coronary was responsible for this patient’s angina, and reperfusion with intragraft urokinase was recommended. A 6Fr AZ-multipurpose guiding catheter was placed in the ostiurn of the vein graft and an infusion wire (0.038-inch Cragg Convertible@, Medi-tech Corporation, Watertown, Massachusetts) was inserted into the region of the distal anastomosis over a 0.014-inch guidewire. Urokinase was administered at a rate of 100,000 U/hour (50,000 U/hour through theproxima1 catheter and 50,000 U/hour through the distal infusion catheter). Intravenous heparin was administered as a 10,000-U initial bolus followed by 1,000 U/hour continuous infusion. One hour afCASE 1: A 60-year-ald man was ter initiating the urokinase infuasymptomatic until he developed a sion, the patient began to experismall non-Q-wave myocardial in- ence recurrent episodes of severe farction 5 years after coronary by- substernal chest pressure associated with inferior ST-segment elepass surgery. Coronary arteriography revealed total occlusion of the vation. The chest discomfort persisted in a waxing and waningpatright coronary artery (as docutern for 8 hours before eventually mented 5 years earlier) and total occlusion of the saphenous vein resolving. Enzymes confirmed acute myocardial infarction, with graft to the right coronary artery. an increase in creatine kinase from All branches of the left coronary normal levels to 958 U/liter with artery were either patent or per4% MB fraction, and an increase in fused by normally functioning lactate dehydrogenase from norFrom the Division of Cardiology, Room MN 670, University qf Kentucky Medical Center, mal levels to 451 U/liter with re800 RoseStreet, Lexington, Kentucky 40536. versal of the 1:2 ratio. Follow-up 274
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
JULY 15, 1991
angiography after 60 hours of urokinase infusion demonstrated patency of the saphenous vein graft, good flow into the grafted portion of the native right coronary, and no evidence of embolized thrombus in the distal right coronary artery. Echocardiography demonstrated worsening of the inferior left ventricular wall motion abnormality with development of inferoposterior dyskinesia, a decline in shortening fraction from 28 to 22%, and enlargement of the left ventricle. There was no interval change in the left coronary anatomy. CASE 2: A 68-year-old man was hospitalized with medically refractory angina 7 years after coronary bypass surgery. Acute myocardial infarction was ruled out and coronary arteriography was performed. Grafts to the left coronary artery were patent, whereas both the native right coronary and its saphenous vein bypass graft were totally occluded. Reperfusion of the right coronary vein graft was performed using the same urokinase infusion protocol previously described (see case 1). The patient experienced no symptoms during the 48-hour course of urokinase infusion. However, serial cardiac enzymes demonstrated acute myocardial infarction on the first day of infusion, with an increase in creatine kinase from normal levels to 783 U/liter with 7% MB, and a peak lactate dehydrogenase level of 399 U/liter with reversal of the 1:2 ratio. Angiography after 24 hours of infusion demonstrated patency of the graft, but residual thrombus within the body of the graft. Migration of partially lysed thrombus into the native vessel with obstruction of a distal branch was observed (Figure 1). Angiography after 48 hours of infusion demonstrated patency of the graft without residual thrombus. Nonsustained ventricular tachycardia oc-
.
curred 48 hours after completion of the urokinase infusion.
We report 2 casesof acute myocardial infarction resulting directly from successfulthrombolytic reperfusion of chronically occluded aortocoronary saphenousvein grafts. In both cases, patients had exertional angina due to inadequate collateral perfusion of totally occluded coronary arteries. Existing collaterals were sufficient to prevent ischemiaat rest and recent infarction was excluded in both casesbefore attempting recanalization. Thus, acute infarction was conclusively linked to thrombolytic reperfusion of the grafts despite prior adequacyof collateral flow. Both patients had clinical sequelaeof infarction; ventricular enlargement in one and late ventricular arrhythmias in the other. Acute myocardial infarction during vein graft reperfusion is most likely explained by recurrent embolization of thrombus into the native vessel. With successfulreperfusion, flow into the distal right coronary artery may revert from a retrograde collateral pattern to a normal anterograde pattern. This would facilitate flow of thrombus into the small distal branchesof the reperfusedvessel,interrupting previously establishedcollateral flow patterns as well as normal anterograde flow patterns. The large mass of thrombus in occluded grafts may provide the basis for recurrent embolization, with involvement of many different distal branches. Subsequentlysis of small emboli leaves no evidence of the mechanismof infarction at follow-up angiography. The clinical course of patient 1 with waxing and waning ischemia and patent vesselsat follow-up angiography supports this hypothesis.
FtGURE 1. Arteriograms of saphe-nous vein graft of patient 2. Arrows indicate migration of Dartialtv bed thrombus from the graft body to native right coronary, with obstkction if ; branch vessel.
The incidenceof acute myocardial infarction due to graft reperfusion is unknown. Our report of clinically silent infarction and occurrencein 2 consecutive patients indicates that this complication may occur frequently. There has beenonly 1 other report of a patient with evidenceof acute myocardial infarction complicating urokinaseinfusion of a chronically occluded vein graft.6 This was recognizedby typical chest pain and ST-segment elevation. We conclude that acute myocardial infarction is a potential complication of late thrombolytic reperfusion of occluded aortocoronary saphenous vein grafts. Becausemyocardial infarction may be clinically silent, closeobservationand monitoring of the electrocardiogram and cardiac enzymesmust be performed wheneverthis procedureis undertaken. Acute myocardial infarction due to graft reperfusionmay result in deterioration of left ventricular function and late ventricular arrhythmias. Until a prospective study to
determine the incidence of this complication is completed,late thrombolytic reperfusion of chronically occluded saphenousvein bypassgrafts should be considered only when more conservative therapeutic options have failed.
1. Frumin H, Goldberg M, Rubenfire M, Levine F. Late thrombolysis of an occluded aortocoronary saphenous vein graft. Am Heart J 1983;106:401-403. 2. Hartmann .I, McKeever L, Teran J, Bufalino V, Marek .I, Brown A, Goodwin M, Amirparviz F, Motarjeme A. Prolonged infusion of urokinase for recanalization of chronically occluded aortocoronary bypass grafts. Am J Cardiol 1988;61:189-191. 3. Marx M, Armstrong W, Brent B, Wack J, Bernstein R, Gregoratos G. Transcatheter recanalization of a chronically occluded saphenous aortocoronary bypass graft. AJR 1987;148:375-377. 4. Grill H, Brinker J. Late thrombotic occlusion of saphenous vein grafts: Successful recanalization using thrombolytic therapy. Cathet Cardiouasc Diagn 1988;15:252-259. 5. McKeever L, Hartmann J, Bufalino V, Marek J, Brown A, Goodwin M, Stamato N, Cahill J, Colandrea M, Amirparviz F. Prolonged selective urokinase infusion in totally occluded coronary arteries and bypass grafts: two case reports. Carher Cardiouasc Diagn 1988;15:247-251. 6. Andersen RL, Kemp HG. A complication of prolonged urokinase infusion into a chronically occluded aortocoronary saphenous vein graft. Cathet Cardiouasc Diagn 1989;18:20-22.
CASE REPORTS
275
Acute Myocardial Infarction Due to Thrombolytic Reperfusion of Chronically Occluded Saphenous Vein Coronary Bypass Grafts John C. Gurley, MD, and Blair S. MacPhail. MD
L
ate occlusion of saphenous vein grafts is a major cause of recurrent angina in the years after successfulcoronary artery bypass surgery. Reestablishment of circulation to the involved artery is problematic, becausedirect angioplasty may be precluded by chronic occlusionof the native artery and extensive thrombus in the occluded vein graft. It has recently been demonstrated that chronically occluded aortocoronary saphenous vein grafts can be successfullyrecanalized by prolonged low-doseintragraft infusions of urokinase.‘-5 Hartmann et al2 achieved recanalization in 11 of 12 chronically occluded grafts using 16- to 72-hour urokinase infusions in total dosesranging from 870,000to 6,290,OOO U. Marx et al3 reported recanalization in 8 of 10 grafts with shorter urokinase infusions. Neither investigator reported significant cardiovascular complications as a result of the procedure.We report on 2 consecutivepatients who developed acute myocardial infarction as a direct result of successful thrombolytic reperfusion of chronically occludedsaphenousvein grafts.
grafts. The patient was treated medically, but returned 3 weeks later with a new syndrome of lifestyle-limiting exertional angina. Repeat cardiac catheterization showed no interval change in coronary anatomy, and well developed collaterals from the left coronary to the occluded right coronary artery were noted. It was determined that the occluded right coronary was responsible for this patient’s angina, and reperfusion with intragraft urokinase was recommended. A 6Fr AZ-multipurpose guiding catheter was placed in the ostiurn of the vein graft and an infusion wire (0.038-inch Cragg Convertible@, Medi-tech Corporation, Watertown, Massachusetts) was inserted into the region of the distal anastomosis over a 0.014-inch guidewire. Urokinase was administered at a rate of 100,000 U/hour (50,000 U/hour through theproxima1 catheter and 50,000 U/hour through the distal infusion catheter). Intravenous heparin was administered as a 10,000-U initial bolus followed by 1,000 U/hour continuous infusion. One hour afCASE 1: A 60-year-ald man was ter initiating the urokinase infuasymptomatic until he developed a sion, the patient began to experismall non-Q-wave myocardial in- ence recurrent episodes of severe farction 5 years after coronary by- substernal chest pressure associated with inferior ST-segment elepass surgery. Coronary arteriography revealed total occlusion of the vation. The chest discomfort persisted in a waxing and waningpatright coronary artery (as docutern for 8 hours before eventually mented 5 years earlier) and total occlusion of the saphenous vein resolving. Enzymes confirmed acute myocardial infarction, with graft to the right coronary artery. an increase in creatine kinase from All branches of the left coronary normal levels to 958 U/liter with artery were either patent or per4% MB fraction, and an increase in fused by normally functioning lactate dehydrogenase from norFrom the Division of Cardiology, Room MN 670, University qf Kentucky Medical Center, mal levels to 451 U/liter with re800 RoseStreet, Lexington, Kentucky 40536. versal of the 1:2 ratio. Follow-up 274
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 68
JULY 15, 1991
angiography after 60 hours of urokinase infusion demonstrated patency of the saphenous vein graft, good flow into the grafted portion of the native right coronary, and no evidence of embolized thrombus in the distal right coronary artery. Echocardiography demonstrated worsening of the inferior left ventricular wall motion abnormality with development of inferoposterior dyskinesia, a decline in shortening fraction from 28 to 22%, and enlargement of the left ventricle. There was no interval change in the left coronary anatomy. CASE 2: A 68-year-old man was hospitalized with medically refractory angina 7 years after coronary bypass surgery. Acute myocardial infarction was ruled out and coronary arteriography was performed. Grafts to the left coronary artery were patent, whereas both the native right coronary and its saphenous vein bypass graft were totally occluded. Reperfusion of the right coronary vein graft was performed using the same urokinase infusion protocol previously described (see case 1). The patient experienced no symptoms during the 48-hour course of urokinase infusion. However, serial cardiac enzymes demonstrated acute myocardial infarction on the first day of infusion, with an increase in creatine kinase from normal levels to 783 U/liter with 7% MB, and a peak lactate dehydrogenase level of 399 U/liter with reversal of the 1:2 ratio. Angiography after 24 hours of infusion demonstrated patency of the graft, but residual thrombus within the body of the graft. Migration of partially lysed thrombus into the native vessel with obstruction of a distal branch was observed (Figure 1). Angiography after 48 hours of infusion demonstrated patency of the graft without residual thrombus. Nonsustained ventricular tachycardia oc-
.
curred 48 hours after completion of the urokinase infusion.
We report 2 casesof acute myocardial infarction resulting directly from successfulthrombolytic reperfusion of chronically occluded aortocoronary saphenousvein grafts. In both cases, patients had exertional angina due to inadequate collateral perfusion of totally occluded coronary arteries. Existing collaterals were sufficient to prevent ischemiaat rest and recent infarction was excluded in both casesbefore attempting recanalization. Thus, acute infarction was conclusively linked to thrombolytic reperfusion of the grafts despite prior adequacyof collateral flow. Both patients had clinical sequelaeof infarction; ventricular enlargement in one and late ventricular arrhythmias in the other. Acute myocardial infarction during vein graft reperfusion is most likely explained by recurrent embolization of thrombus into the native vessel. With successfulreperfusion, flow into the distal right coronary artery may revert from a retrograde collateral pattern to a normal anterograde pattern. This would facilitate flow of thrombus into the small distal branchesof the reperfusedvessel,interrupting previously establishedcollateral flow patterns as well as normal anterograde flow patterns. The large mass of thrombus in occluded grafts may provide the basis for recurrent embolization, with involvement of many different distal branches. Subsequentlysis of small emboli leaves no evidence of the mechanismof infarction at follow-up angiography. The clinical course of patient 1 with waxing and waning ischemia and patent vesselsat follow-up angiography supports this hypothesis.
FtGURE 1. Arteriograms of saphe-nous vein graft of patient 2. Arrows indicate migration of Dartialtv bed thrombus from the graft body to native right coronary, with obstkction if ; branch vessel.
The incidenceof acute myocardial infarction due to graft reperfusion is unknown. Our report of clinically silent infarction and occurrencein 2 consecutive patients indicates that this complication may occur frequently. There has beenonly 1 other report of a patient with evidenceof acute myocardial infarction complicating urokinaseinfusion of a chronically occluded vein graft.6 This was recognizedby typical chest pain and ST-segment elevation. We conclude that acute myocardial infarction is a potential complication of late thrombolytic reperfusion of occluded aortocoronary saphenous vein grafts. Becausemyocardial infarction may be clinically silent, closeobservationand monitoring of the electrocardiogram and cardiac enzymesmust be performed wheneverthis procedureis undertaken. Acute myocardial infarction due to graft reperfusionmay result in deterioration of left ventricular function and late ventricular arrhythmias. Until a prospective study to
determine the incidence of this complication is completed,late thrombolytic reperfusion of chronically occluded saphenousvein bypassgrafts should be considered only when more conservative therapeutic options have failed.
1. Frumin H, Goldberg M, Rubenfire M, Levine F. Late thrombolysis of an occluded aortocoronary saphenous vein graft. Am Heart J 1983;106:401-403. 2. Hartmann .I, McKeever L, Teran J, Bufalino V, Marek .I, Brown A, Goodwin M, Amirparviz F, Motarjeme A. Prolonged infusion of urokinase for recanalization of chronically occluded aortocoronary bypass grafts. Am J Cardiol 1988;61:189-191. 3. Marx M, Armstrong W, Brent B, Wack J, Bernstein R, Gregoratos G. Transcatheter recanalization of a chronically occluded saphenous aortocoronary bypass graft. AJR 1987;148:375-377. 4. Grill H, Brinker J. Late thrombotic occlusion of saphenous vein grafts: Successful recanalization using thrombolytic therapy. Cathet Cardiouasc Diagn 1988;15:252-259. 5. McKeever L, Hartmann J, Bufalino V, Marek J, Brown A, Goodwin M, Stamato N, Cahill J, Colandrea M, Amirparviz F. Prolonged selective urokinase infusion in totally occluded coronary arteries and bypass grafts: two case reports. Carher Cardiouasc Diagn 1988;15:247-251. 6. Andersen RL, Kemp HG. A complication of prolonged urokinase infusion into a chronically occluded aortocoronary saphenous vein graft. Cathet Cardiouasc Diagn 1989;18:20-22.
CASE REPORTS
275
