Volume 119
Number
Brief Communications
4
955
nary a n a t o m y m a y allow for r a p i d identification of the infarct vessel. Consideration of immediate P T C A should be made in an effort to relieve the obstruction and salvage myocardium where appropriate a n a t o m y permits. REFERENCES
Fig. 4. F i n a l angiogram p o s t - P T C A revealing a hazy appearance at the point of dilation (arrows). A residual b u t lesser stenosis still remains. incidence of systemic emoblization is low. Safian et al. 7 found no evidence of an embolic or cerebrovascular event in 170 patients undergoing PTAV. Cribier et al. s have suggested t h a t emboli rarely occur because the valve calcifications m a y be encased within the valve leaflets and are not easily freed during the procedure. We believe this to be the first instance of coronary artery embolization complicating P T A V successfully treated with P T C A to be reported. T h e r e have been two previous reports of periprocedural myocardial infarction associated with percutaneous transluminal valvuloplasty of both the aortic a n d mitral valves. 4, 5 In both cases, myocardial infarction occurred secondary to coronary artery embolization. Coronary artery embolization also seems to be the most likely cause of acute injury in our patient, though one can not be entirely certain. Thrombosis in situ, induced by a low-flow state during the procedure, may have been responsible for coronary artery occlusion. It has been shown t h a t brief periods of diminished coronary blood flow occur during PTAV. 9 However, the patient had been adequately anticoagulated during the procedure. In addition, the success of P T C A and the suggestion of distal migration of the embolus would appear to favor embolization of debris over thrombosis in situ. Intracoronary nitroglycerin was without benefit, suggesting t h a t spasm did not play a role here. Dash, 1~ in a recent editorial, anticipated an increase in the n u m b e r of reports of embolic events as the use of P T A V becomes more widespread. A bicuspid aortic valve has a l r e a d y been identified as a potential risk factor for embolization. "~ Extensive calcification of the aortic valve and a o r t a in our p a t i e n t m a y have increased the risk of embolization. As shown in this report, coronary artery embolization, unlike cerebral embolization, m a y afford the angiographer an o p p o r t u n i t y for acute intervention. Coronary artery embolization represents a complication of P T A V t h a t should be considered whenever signs and s y m p t o m s of acute myocardial infarction develop following the procedure. Furthermore, prior delineation of the coro-
1. Cribier A, Saoudi N, Berland J, Savin T, Rocha P, Letac B. Percutaneous transluminal valvuloplasty of acquired aortic stenosis in elderly patients: an alternative to valve replacement? Lancet 1986;1:63-7. 2. Palacios I, Block PC, Brandi S, et al. Percutaneous valvotomy for patients with severe mitral stenosis. Circulation 1987; 75:778-84. 3. Davidson CJ, Skelton TN, Kisslo KB. The risk for systemic embolization associated with percutaneous balloon valvuloplasty in adults. Ann Intern Med 1988;108:557-60. 4. Deligonul U, Kern MJ, Bell ST, et al. Acute myocardial infarction during percutaneous aortic balloon valvuloplasty. Cathet Cardiovasc Diagn 1988;15:164-8. 5. Wiegand V, Tebbe U, Helmchen U, Kreuzer H. Coronary arterial embolism due to valvular debris after percutaneous valvuloplasty of calcific mitral stenosis. Clin Cardiol 1988;11: 794-6. 6. Safian RD, Mandell VS, Thnrer RE, et al. Postmortem and intraoperative balloon valvnloplasty of calcific aortic stenosis in elderly patients: mechanisms of successful dilation. J Am Coll Cardiol 1987;9:655-60. 7. Safian RD, Berman AD, Mandell VS, et al. 13alloon aortic valvuloplasty in 170 consecutive patients. N Engl J Med 1988; 319:125-30. 8. Cribier A, Savin T, Berland J, et al. Percutaneous transluminal balloon valvuloplasty of adult aortic stenosis: report of 92 cases. J Am Coll Cardiol 1987;9:381-6. 9. Rousseau MF, Wyns W, Hammer F, Caucheteux D, Hue L, Pouleur H. Changes in coronary blood flow and myocardial metabolism during aortic balloon valvuloplasty. Am J Cardiol 1988;61:1080-4. 10. Dash H. Have balloon, will travel: expanded indications for nonoperative intravascular balloon dilatation. J Am Coll Cardiol 1987;9:387-8.
Thrombolytic therapy in coronary ectasia and acute myocardial infarction S. Tanveer Rab, MD, David W. Smith, MD, Benjamin N. Alimurung, MD, R a n a Rab, MD, and Spencer B. King III, MD. Atlanta, Ga.
A 65-year-old black m a n with a 20-year history of systemic arterial hypertension presented with suffocating chest pain. The initial electrocardiogram revealed atrial fibrillation with acute inferior ST segment elevation and reciprocal anterior S T segment changes (Fig. 1, A). The patient was given digoxin, 0.25 mg intravenously, hydrocortisone, 100 mg intravenously, and was started on an intravenous infusion of 1.2 million units of streptokinase 4 hours From the Division of Cardiology,Andreas Gruentzig Cardiovascular Center and Departments of Medicine and Radiology, Emory University. Reprint requests: Spencer B. King III, MD, Andreas Gruentzig Cardiovascular Center, Emory University Hospital, Suite F606,1364 Clifton Rd, N.E., Atlanta, GA 30322. 4/4/18635
April 1990
956
Brief Communications
American Heart Journal
Fig. 1. A, Electrocardiogram on admission. B, Electrocardiogram at 24 hours.
following onset of his symptoms. He was subsequently maintained with an intravenous heparin infusion. An electrocardiogram at 24 hours (Fig. 1, B) demonstrated sinus rhythm and resolution of the acute inferior epicardiai injury and reciprocal anterior ST segment changes. Creatinine phosphokinase (CPK) peaked at 24 hours at 1551 units/L, with a CK MB isoenzyme value of 150 ng/ml. Cardiac catheterization performed 48 hours after the infarction demonstrated excellent left ventricular function except for a small area of inferior hypokinesis. The coronary arteries were large and ectatic. There was a large thrombus in the right coronary artery (RCA) (Fig. 2, A) extending from the ostium to the beginning of the posterior descending branch, with flow of contrast around the thrombus in the distal segment. '!Hang-up" of dye around the distal portion of the thrombus was also noted. Intravenous heparin was continued and 325 mg per day of oral aspirin was started. Repeat coronary arteriography on day 7 demonstrated resolution of most of the RCA thrombus (Fig. 2, B). The patient was discharged home taking 80 mg of aspirin daily, warfarin sodium (maintaining prothrombin time at 1.5 times control), topical nitrates, and digoxin. Coronary arteriography performed on day 30 demonstrated complete resolution of the clot (Fig. 2, C). The patient has been maintained with aspirin and warfarin sodium and is asymptomatic at a 1 year follow-up. Coronary artery ectasia (aneurysm), defined as localized or diffuse dilatation of the coronary arteries, has a reported incidence between 1% and 4.9%, with a male predominance in autopsy and angiographic seriesJ ~ Common etiologies found at postmortem include atherosclerosis in
middle-aged adults with predominant involvement of the RCA.1, 5 Congenital ectasia was found in 17 % of patients in this autopsy study. 5 In children and young adults, inflammation, including Kawasaki disease, presents in the majority of casesJ The involvement of inflammatory mechanisms in atherosclerosis 6 raises the possibility that ectasia in atherosclerosis and inflammatory diseases may be related. Proposed mechanisms of thrombosis include stasis 3 and low shear stress 7 as well as spasm in the ectatic coronary vessels, s However, an alternative explanation invoking inflammatory mechanisms should be considered. Inflammatory mediators such as interleukin-1 and tumor necrosis factor can convert endothelial cells in vitro from antito procoagulant activity. 6 Thus inflammatory mediators could contribute to the extensive thrombosis in coronary ectasia. In one series of coronary ectasia, 28 of 30 patients had long-standing angina pectoris and 80% of the same group had a myocardial infarction. 2 The 5-year survival in the Coronary Artery Surgery Study (CASS) registry for the medically treated group of coronary artery ectasia patients was reduced to 74 % compared with a survival rate of 83 % in medically treated patients with nonectatic coronary artery disease. 4 Surgical revascularization has been an effective form of therapy in symptomatic patients with proximal coronary ectasia and suitable distal vessels. 9 The purpose of this case report is to demonstrate that intravenous thrombolytic therapy resulted in myocardial salvage and preservation of left ventricular function in a patient with thrombotic occlusion of an ectatic right coronary artery. Prolonged heparinization, treatment with as-
Volume 119
Number
Brief Communications
4
957
Fig. 2. Right coronary arteriography demonstrating coronary ectasia and (A) large clot at 48 hours (ar-
rows), (B) significant resolution of clot at day 7 (arrows), and (C) complete resolution on day 40.
pirin, and subsequent oral anticoagulation resulted in complete resolution of this thrombus. A similar case report has demonstrated reperfusion with intracoronary streptokinase. 1~ Aspirin therapy has been effective in preventing thrombosis in coronary aneurysms in children with Kawasaki disease 11 and may be useful in patients with asymptomatic coronary artery ectasia.
ectasia:incidence and results of coronary bypass surgery. AM HEARTJ 1978;96:309-15. 10. Theron HD, Kleynhans PH, Marx JD, Marks DS. Successful coronary reperfusion with intracoronary streptokinase in a patient with coronary ectasia. S Afr Med J 1987;72:502-3. 11. Kato H, Kolke S, Yokoyama T. Kawasaki disease:effect of treatment on coronary artery involvement. Pediatrics 1979; 63:175-9.
REFERENCES
HyperventUation-induced coronary vasospasm refractory to intracoronary nitroglycerin
1. Vermani R, Robinowitz M, Atkinson JB, Forman MB, Silver MD, McAllister HA. Acquired coronary arterial aneurysms. Hum Pathol 1986;17:575-83. 2. Markis JE, Joffe CD, Cohn PF, Feen DJ, Hermon MJ, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol 1976;37:217-22. 3. Hartnell GG, Parnell BM, Pride RB. Coronary artery ectasia. Its prevalence and significance in 4,993 patients. Br Heart J 1985;54:392-5. 4. Swaye PS, Fisher LD, Litwin P. Aneurysmal coronary artery disease. Circulation 1983;67:134-8. 5. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the coronary artery--report of ten cases and review of the literature. Am J Cardiol 1963;11:228-37. 6. Munro J, Cotran RS. The pathogenesis of atherosclerosis: atherogenesis and inflammation. Lab Invest 1988;58:249-61. 7. Badimon L, Badimon JJ, Galvez A, Chesebro JH, Fuster V. Influence of arterial damage and wall shear rate on platelet deposition. Arteriosclerosis 1986;6:312-20. 8. Bove AA, Vlietstra RD. Spasm in ectatic coronary arteries. Mayo Clin Proc 1985;60:822-6. 9. Aintablian A, Hamby RK, Hoffman I, Kramer RJ. Coronary
Stefano Ghio, MD, Luigi Angoli, MD, Ezio Bramucci, MD, Stefano de Servi, MD, and Giuseppe Specchia, MD. Pavia, Italy
In 1980 Buxton et al. 1 described five patients who had ergonovine-induced coronary vasospasm refractory to sublingual or intravenous nitrogliceryn; direct intracoronary administration of the d r u g was recommended by the From the Divisionedi Cardiologia,PoliclinicoS. Matteo. Reprintrequests: StefanoGhio,MD, Divisionedi Cardiologia,PoliclinicoS. Matteo, 27100-Pavia,Italy. 4/4/18634
Number
Brief Communications
4
955
nary a n a t o m y m a y allow for r a p i d identification of the infarct vessel. Consideration of immediate P T C A should be made in an effort to relieve the obstruction and salvage myocardium where appropriate a n a t o m y permits. REFERENCES
Fig. 4. F i n a l angiogram p o s t - P T C A revealing a hazy appearance at the point of dilation (arrows). A residual b u t lesser stenosis still remains. incidence of systemic emoblization is low. Safian et al. 7 found no evidence of an embolic or cerebrovascular event in 170 patients undergoing PTAV. Cribier et al. s have suggested t h a t emboli rarely occur because the valve calcifications m a y be encased within the valve leaflets and are not easily freed during the procedure. We believe this to be the first instance of coronary artery embolization complicating P T A V successfully treated with P T C A to be reported. T h e r e have been two previous reports of periprocedural myocardial infarction associated with percutaneous transluminal valvuloplasty of both the aortic a n d mitral valves. 4, 5 In both cases, myocardial infarction occurred secondary to coronary artery embolization. Coronary artery embolization also seems to be the most likely cause of acute injury in our patient, though one can not be entirely certain. Thrombosis in situ, induced by a low-flow state during the procedure, may have been responsible for coronary artery occlusion. It has been shown t h a t brief periods of diminished coronary blood flow occur during PTAV. 9 However, the patient had been adequately anticoagulated during the procedure. In addition, the success of P T C A and the suggestion of distal migration of the embolus would appear to favor embolization of debris over thrombosis in situ. Intracoronary nitroglycerin was without benefit, suggesting t h a t spasm did not play a role here. Dash, 1~ in a recent editorial, anticipated an increase in the n u m b e r of reports of embolic events as the use of P T A V becomes more widespread. A bicuspid aortic valve has a l r e a d y been identified as a potential risk factor for embolization. "~ Extensive calcification of the aortic valve and a o r t a in our p a t i e n t m a y have increased the risk of embolization. As shown in this report, coronary artery embolization, unlike cerebral embolization, m a y afford the angiographer an o p p o r t u n i t y for acute intervention. Coronary artery embolization represents a complication of P T A V t h a t should be considered whenever signs and s y m p t o m s of acute myocardial infarction develop following the procedure. Furthermore, prior delineation of the coro-
1. Cribier A, Saoudi N, Berland J, Savin T, Rocha P, Letac B. Percutaneous transluminal valvuloplasty of acquired aortic stenosis in elderly patients: an alternative to valve replacement? Lancet 1986;1:63-7. 2. Palacios I, Block PC, Brandi S, et al. Percutaneous valvotomy for patients with severe mitral stenosis. Circulation 1987; 75:778-84. 3. Davidson CJ, Skelton TN, Kisslo KB. The risk for systemic embolization associated with percutaneous balloon valvuloplasty in adults. Ann Intern Med 1988;108:557-60. 4. Deligonul U, Kern MJ, Bell ST, et al. Acute myocardial infarction during percutaneous aortic balloon valvuloplasty. Cathet Cardiovasc Diagn 1988;15:164-8. 5. Wiegand V, Tebbe U, Helmchen U, Kreuzer H. Coronary arterial embolism due to valvular debris after percutaneous valvuloplasty of calcific mitral stenosis. Clin Cardiol 1988;11: 794-6. 6. Safian RD, Mandell VS, Thnrer RE, et al. Postmortem and intraoperative balloon valvnloplasty of calcific aortic stenosis in elderly patients: mechanisms of successful dilation. J Am Coll Cardiol 1987;9:655-60. 7. Safian RD, Berman AD, Mandell VS, et al. 13alloon aortic valvuloplasty in 170 consecutive patients. N Engl J Med 1988; 319:125-30. 8. Cribier A, Savin T, Berland J, et al. Percutaneous transluminal balloon valvuloplasty of adult aortic stenosis: report of 92 cases. J Am Coll Cardiol 1987;9:381-6. 9. Rousseau MF, Wyns W, Hammer F, Caucheteux D, Hue L, Pouleur H. Changes in coronary blood flow and myocardial metabolism during aortic balloon valvuloplasty. Am J Cardiol 1988;61:1080-4. 10. Dash H. Have balloon, will travel: expanded indications for nonoperative intravascular balloon dilatation. J Am Coll Cardiol 1987;9:387-8.
Thrombolytic therapy in coronary ectasia and acute myocardial infarction S. Tanveer Rab, MD, David W. Smith, MD, Benjamin N. Alimurung, MD, R a n a Rab, MD, and Spencer B. King III, MD. Atlanta, Ga.
A 65-year-old black m a n with a 20-year history of systemic arterial hypertension presented with suffocating chest pain. The initial electrocardiogram revealed atrial fibrillation with acute inferior ST segment elevation and reciprocal anterior S T segment changes (Fig. 1, A). The patient was given digoxin, 0.25 mg intravenously, hydrocortisone, 100 mg intravenously, and was started on an intravenous infusion of 1.2 million units of streptokinase 4 hours From the Division of Cardiology,Andreas Gruentzig Cardiovascular Center and Departments of Medicine and Radiology, Emory University. Reprint requests: Spencer B. King III, MD, Andreas Gruentzig Cardiovascular Center, Emory University Hospital, Suite F606,1364 Clifton Rd, N.E., Atlanta, GA 30322. 4/4/18635
April 1990
956
Brief Communications
American Heart Journal
Fig. 1. A, Electrocardiogram on admission. B, Electrocardiogram at 24 hours.
following onset of his symptoms. He was subsequently maintained with an intravenous heparin infusion. An electrocardiogram at 24 hours (Fig. 1, B) demonstrated sinus rhythm and resolution of the acute inferior epicardiai injury and reciprocal anterior ST segment changes. Creatinine phosphokinase (CPK) peaked at 24 hours at 1551 units/L, with a CK MB isoenzyme value of 150 ng/ml. Cardiac catheterization performed 48 hours after the infarction demonstrated excellent left ventricular function except for a small area of inferior hypokinesis. The coronary arteries were large and ectatic. There was a large thrombus in the right coronary artery (RCA) (Fig. 2, A) extending from the ostium to the beginning of the posterior descending branch, with flow of contrast around the thrombus in the distal segment. '!Hang-up" of dye around the distal portion of the thrombus was also noted. Intravenous heparin was continued and 325 mg per day of oral aspirin was started. Repeat coronary arteriography on day 7 demonstrated resolution of most of the RCA thrombus (Fig. 2, B). The patient was discharged home taking 80 mg of aspirin daily, warfarin sodium (maintaining prothrombin time at 1.5 times control), topical nitrates, and digoxin. Coronary arteriography performed on day 30 demonstrated complete resolution of the clot (Fig. 2, C). The patient has been maintained with aspirin and warfarin sodium and is asymptomatic at a 1 year follow-up. Coronary artery ectasia (aneurysm), defined as localized or diffuse dilatation of the coronary arteries, has a reported incidence between 1% and 4.9%, with a male predominance in autopsy and angiographic seriesJ ~ Common etiologies found at postmortem include atherosclerosis in
middle-aged adults with predominant involvement of the RCA.1, 5 Congenital ectasia was found in 17 % of patients in this autopsy study. 5 In children and young adults, inflammation, including Kawasaki disease, presents in the majority of casesJ The involvement of inflammatory mechanisms in atherosclerosis 6 raises the possibility that ectasia in atherosclerosis and inflammatory diseases may be related. Proposed mechanisms of thrombosis include stasis 3 and low shear stress 7 as well as spasm in the ectatic coronary vessels, s However, an alternative explanation invoking inflammatory mechanisms should be considered. Inflammatory mediators such as interleukin-1 and tumor necrosis factor can convert endothelial cells in vitro from antito procoagulant activity. 6 Thus inflammatory mediators could contribute to the extensive thrombosis in coronary ectasia. In one series of coronary ectasia, 28 of 30 patients had long-standing angina pectoris and 80% of the same group had a myocardial infarction. 2 The 5-year survival in the Coronary Artery Surgery Study (CASS) registry for the medically treated group of coronary artery ectasia patients was reduced to 74 % compared with a survival rate of 83 % in medically treated patients with nonectatic coronary artery disease. 4 Surgical revascularization has been an effective form of therapy in symptomatic patients with proximal coronary ectasia and suitable distal vessels. 9 The purpose of this case report is to demonstrate that intravenous thrombolytic therapy resulted in myocardial salvage and preservation of left ventricular function in a patient with thrombotic occlusion of an ectatic right coronary artery. Prolonged heparinization, treatment with as-
Volume 119
Number
Brief Communications
4
957
Fig. 2. Right coronary arteriography demonstrating coronary ectasia and (A) large clot at 48 hours (ar-
rows), (B) significant resolution of clot at day 7 (arrows), and (C) complete resolution on day 40.
pirin, and subsequent oral anticoagulation resulted in complete resolution of this thrombus. A similar case report has demonstrated reperfusion with intracoronary streptokinase. 1~ Aspirin therapy has been effective in preventing thrombosis in coronary aneurysms in children with Kawasaki disease 11 and may be useful in patients with asymptomatic coronary artery ectasia.
ectasia:incidence and results of coronary bypass surgery. AM HEARTJ 1978;96:309-15. 10. Theron HD, Kleynhans PH, Marx JD, Marks DS. Successful coronary reperfusion with intracoronary streptokinase in a patient with coronary ectasia. S Afr Med J 1987;72:502-3. 11. Kato H, Kolke S, Yokoyama T. Kawasaki disease:effect of treatment on coronary artery involvement. Pediatrics 1979; 63:175-9.
REFERENCES
HyperventUation-induced coronary vasospasm refractory to intracoronary nitroglycerin
1. Vermani R, Robinowitz M, Atkinson JB, Forman MB, Silver MD, McAllister HA. Acquired coronary arterial aneurysms. Hum Pathol 1986;17:575-83. 2. Markis JE, Joffe CD, Cohn PF, Feen DJ, Hermon MJ, Gorlin R. Clinical significance of coronary arterial ectasia. Am J Cardiol 1976;37:217-22. 3. Hartnell GG, Parnell BM, Pride RB. Coronary artery ectasia. Its prevalence and significance in 4,993 patients. Br Heart J 1985;54:392-5. 4. Swaye PS, Fisher LD, Litwin P. Aneurysmal coronary artery disease. Circulation 1983;67:134-8. 5. Daoud AS, Pankin D, Tulgan H, Florentin RA. Aneurysms of the coronary artery--report of ten cases and review of the literature. Am J Cardiol 1963;11:228-37. 6. Munro J, Cotran RS. The pathogenesis of atherosclerosis: atherogenesis and inflammation. Lab Invest 1988;58:249-61. 7. Badimon L, Badimon JJ, Galvez A, Chesebro JH, Fuster V. Influence of arterial damage and wall shear rate on platelet deposition. Arteriosclerosis 1986;6:312-20. 8. Bove AA, Vlietstra RD. Spasm in ectatic coronary arteries. Mayo Clin Proc 1985;60:822-6. 9. Aintablian A, Hamby RK, Hoffman I, Kramer RJ. Coronary
Stefano Ghio, MD, Luigi Angoli, MD, Ezio Bramucci, MD, Stefano de Servi, MD, and Giuseppe Specchia, MD. Pavia, Italy
In 1980 Buxton et al. 1 described five patients who had ergonovine-induced coronary vasospasm refractory to sublingual or intravenous nitrogliceryn; direct intracoronary administration of the d r u g was recommended by the From the Divisionedi Cardiologia,PoliclinicoS. Matteo. Reprintrequests: StefanoGhio,MD, Divisionedi Cardiologia,PoliclinicoS. Matteo, 27100-Pavia,Italy. 4/4/18634
