- Email: [email protected]
The combined presence of myocardial bridging and fixed coronary artery stenosis
1170
Parashara
et al.
cular hyperplasia: extension of the therapeutic outcome. Reof the University Hospital Zurich Cooperation Study on fibromuscular hyperplasia. Nephron 1986;44(suppl. 1):109-14. James TA, Froggatt P, Marshall TK. Sudden death in young athletes. Ann Intern Med 1967;67:1013-21. dames TA, Marshall TK. De subitaneis mortibus XVII. Multifocal stenoses due to fibromuscular dysplasia of the sinus node artery. Circulation 1976;53:736-42. Rossi L, Thiene G. Recent advances in clinicohistopathologic correlates of sudden cardiac death. AM HEART J 1981;102:47884. 7. Nichols GR II, Davis GJ, Lefkowitz JB. Sudden death due to fibromuscuiar dysplasia of the sinoatrial nodal artery. KMA J 1989;87:504-5. 8. Lie JT, Berg KK. Isolated fibromuscular dysplasia of the coronary arteries with spontaneous dissection and myocardial infarction. Hum Path01 1987;18:654-6. sults
The combined presence of myocardial bridging and fixed coronary artery stenosis Deepak K. Parashara, MD, Gary S. Ledley, MD, Morris N. Kotler, MD, and Shahriar Yazdanfar, MD Philadelphia, Pa.
Myocardial bridging of the coronary arteries can be diagnosed in vivo by angiography only. Myocardial bridging is defined as embedment of a segment of the coronary artery into the myocardium so that during ventricular systole the segment of artery is compressed. Several studies have reported that atherosclerotic lesions are not found at the level of myocardial bridging.ie4 It has been postulated that the intramyocardial course of the coronary artery has a “protective” effect from the development of atherosclerosis at the site of the myocardial bridge. In this report we present an unusual case of coronary stenosis at the site of myocardial bridging. A 65year-old man with a history of heavy cigarette smoking had new onset of chest pain of 2 months’ duration. An exercise thallium test was performed. The patient achieved 71 % of the predicted maximal heart rate for his age with a 9.5 MET work load, and the ECG was positive for ischemia in the anterolateral leads. The thallium scan showed extensive myocardial perfusion abnormalities involving the anterior, apical, inferior, and septal walls with incomplete redistribution. The patient underwent cardiac catheterization. Left ventriculography revealed mild anterolateral wall hypokinesis and normal overall left ventric-
From the Department of Medicine, Division of Cardiovascular Diseases, and Women’s League for Medical Research Laboratory, Albert Einstein Medical Center, Temple University School of Medicine. Reprint requests: Shahriar Yazdanfar, MD, Division of Cardiology, Albert Einstein Medical Center, York and Tabor Rd., Philadelphia, PA 19141. AM HEART J 1993;125:1170-1172. Copyright ‘c 1993 by Mosby-Year Book, Inc. 0002.8703/93/$1 .OO + .10 4/4/44075
American
April 1993 Heart Journal
ular function with an ejection fraction of 71’ ,, Coronary cineangiography demonstrated that the mid left anterior descending coronary artery had an intramyocardial course with severe systolic constriction and a 95’; fixed atherosclerotic stenosis (Fig. 1). There was another 60 (; discrete stenosis in the mid left anterior descending coronary artery proximal to the intramyocardial segment. The left anterior descending coronary artery distal to the systolic constriction was free of disease. The left circumflex coronary artery was diffusely diseased. The first obtuse marginal coronary artery had an 80’ ; ostial and a 60’,. proximal stenosis. The third obtuse marginal coronary artery had a 60 r( proximal stenosis. The codominant right coronary artery had a 40”, proximal and another 60c; midluminal stenosis. The acute marginal coronary artery had an 80r; proximal stenosis. The patient underwent coronary artery bypass graft surgery, and the diseased intramyocardial course of the left. anterior descending coronary artery was confirmed. A left internal mammary artery was anastomosed to the left ant,erior descending coronary artery, and saphenous vein grafts were placed to the first obtuse marginal, the second obtuse marginal, and the distal right coronary arteries. The postoperative course was uneventful except for the development of paroxysmal atria1 fibrillation. It has long been known that the coronary arteries and their main branches are normally positioned subepicardially. At times a segment of the coronary artery, usually the left anterior descending coronary artery, may tunnel under a “bridge” of superficial myocardial fibers for a short distance. In 1960 Portsmann and Iwig’ were the first to describe myocardial bridging angiographically. In vivo myocardial bridges are primarily recognized by the “systolic milking effect” as seen on coronary cineangiograms. No systematic anatomically controlled study has been undertaken to correlate angiographically documented “systolic constriction” with pathologic findings. Most angiographers believe that systolic narrowing of a coronary artery segment is caused by myocardial bridging. The prevalence of myocardial bridges among consecutive patients undergoing coronary angiography varies between 0.5“p,e and 16’, ’ with most studies reporting an incidence of less than 2”, . Autopsy series report a prevalence of muscle bridges ranging from 5.4“; *t to 85.7’; ,’ which seems to depend on the precision of the dissection.” The marked disparity between the high prevalence of myocardial bridging reported in anat,omic studies and the lower prevalence in angiographic studies has been attributed to the fact that a pressure in excess of what is generated under normal physiologic conditions is needed to compress the artery.s The potentiation of the degree of systolic constriction after nitroglycerin confirms this hypothesis. Moreover, Angelini et al.” noted that the angiographic evidence of myocardial bridging may depend on the thickness and length of the bridge, the reciprocal orientation of the coronary artery and the myocardial fibers, and the nature of the tissue interposed between the coronary artery and the myocardial bridge. The presence of a proximal fixed coronary obstruction and the intrinsic coronary arterial wall
Volume American
125, Number Heart
4
Parusharu
Journal
et al.
1171
1. A, Right anterior oblique projection of left coronary cineangiogramduring diastole. Arrowhead showsfixed atherosclerotic stenosisof left anterior descendingcoronary artery. B, Right anterior oblique projection of left coronary cineangiogram during systole. Open. arrow shows systolic constriction of intramyocardial segmentof left anterior descendingcoronary artery. C, Lateral projection of left coronary cineangiogramduring diastole. Arrowhead showsfixed atherosclerotic stenosisof left anterior descending coronary artery. D, Lateral projection of left coronary cineangiogramduring systole. Open arrow shows systolic constriction of intramyocardial segmentof left anterior descendingcoronary artery. Fig.
tone may also play a role in the development and the degreeof systolic constriction. A review of the literature, with the exception of onecasereportlo and oneautopsy study,ll showsthat myocardial bridging hasa protective effect on the intramyocardial portion of the coronary artery with regard to the development of atherosclerosis.Findings in a recent histopathologic study12 and a recent large angiographic study8 of 1102 consecutive patients have further substantiated this observation. The exact mechanismby which the protective effect is exerted is not known. The important role of hemodynamic stressin the development of atherosclerosishasrecently beenreemphasized.13* I4The intramyocardial courseof the coronary artery is protected from the pulsatile nature of the blood flow and thus also from the vibration-induced mechanicalstress.We propose this asa possiblemechanismfor protection of the coronary artery from atherosclerosis.The presentreport is unique in that we have angiographically demonstrated a severeatherosclerotic coronary stenosisin the myocardial bridged segmentof the left anterior descendingcoronary artery. We thus conclude that the intramyocardial portions of the
coronary arteries may not be totally protected from the development of atherosclerotic disease. REFERENCES
1. Geiringer E. The mural coronary artery. AM HEART J 1951; 41:359-68. 2. Polacek P, Zechmeister A. The occurrence and significance of myocardial bridges and loops on coronary arteries. Opuscola Cardioloeica. Acta Facultatis Medicae Univesitatis Brunensis. Brno, 1968. 3. Stolte M, Weis I’, Prestele H. Muscle bridges over the left anterior descending coronary artery: their influence on arterial disease. Virchows Arch Path01 Anat 197737523-36. 4. Lee SS, WU TL. The role of mural coronary artery in prevention of coronary atherosclerosis. Arch Path01 1972;93:32-5. 5. Portsmann W, Iwig J. Die intramurale Koronaroeterie im Angiogramm. Fortschr Roentenstr 1960;92:129-33. 6. Noble J, Bourassa MG, Petitclerc R, et al. Myocardial bridging and milking effect of the left anterior descending coronary artery: normal variant or obstruction. Am J Cardiol 1976; 37:993-g. 7. Hashimoto A: Takekoshi N, Murakami E. Clinical significance of myocardial bridging of the coronary artery. Jpn Heart J 1984;25:913-22.
1172
Bell et al.
Amencan
8. Charmer K, Bukis E, Hartnell G, et al. Myocardial bridging of the coronary arteries. Clin Radio1 1989;40:355-9. 9. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75-88. 10. Laif’er LI. Weiner BH. Percutaneous transluminal coronarv angioplasry of a coronary stenosis at the site of myocardial bridging. Cardiology 1991;79:245-8. 11. Edwards JC, Burnsides CH, Swarm RL, et al. Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-42. 12. Ishii T, Asuwa N, Masuda S, et al. Atherosclerosis suppression in the anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. Mod Path01 1991;4:424-31. 13. Stehbens WE. The lipid hypothesis and the role of hemodynamics in atherogenesis. Prog Cardiovasc Dis 1990;2:119-36. 14. Stehben WE. Hemodynamics and the blood vessel wall. Springfield, IL: Charles C Thomas, 1979.
Coronary atherectomy complicated by coronary embolus in a cardiac transplant recipient Calvin Bell, MD, Morton J. Kern, MD, Frank Aguirre, MD, Leslie Miller, MD, Richard Bach, MD, Thomas Donohue, MD, and Frederick Dressler, MD St. Louis, MO.
Coronary atherectomy is now commonly performed for focal, noncalcified atherosclerotic coronary artery narrowings.id4 To date, there has been only one reported study of this procedure being employed for obstructive coronary arteriopathy in cardiac transplant recipients.s We present a unique case of directional atherectomy complicated by coronary embolus in a patient with an orthotopic heart transplant. This patient example indicates the potential complications and benefits of direcbional endoluminal tis sue excision as a means to treat and advance our understanding of transplant-related coronary artery disease. A 63-year-old man underwent orthotopic cardiac transplant in 1987. A recent routine yearly surveillance angiography demonstrated a high-grade left anterior descending lesion (80% diameter narrowing by visual estimate). Because of advanced coronary arteriopathy, he was subsequently admitted for atherectomy of the proximal left anterior descending coronary artery lesion. During the Z-week interim between the diagnostic and interventional procedures, the patient remained asymptomatic despite developing new electrocardiogram changes that showed sinus tachycardia, bifascicular block (right bundle branch block From
the Cardiology
Division,
St. Louis
University
Hospital.
Reprint requests: Morton J. Kern, MD, Director, J. G. Mudd Cardiac Catheterization Laboratory, St. Louis University Hospital, 3635 Vista Ave. at Grand Blvd., St. Louis, MO 63110-0250. A.% Hwm’r
J 1993;125:1172-1175.
Copyright ” 1993 0002-870:~/93/$1.00
by Mosby-Year Book, + .I0 4/4/44070
Inc.
April 1993 Heart Journal
and left anterior fascicular block). and anteroseptal myocardial infarction. These findings were not present on the electrocardiogram obtained after the diagnostic study. Before the procedure, the blood pressure was IlO/ mm IIg, pulse was 98/min, respiratory rate was 16/min, and temperature was 97.2” F. Cardiac examination was normal except for a summation gallop. The examination of the lungs, abdomen, and extremities was unremarkable. The laboratory profile was normal except for a creatinine of 1.9 mg/ dl. A chest roentgenogram was also normal with t,he exception of the sternal wires from the previous surgery. Coronary angiograph y immediately before atherectomy revealed minimal irregularities of the right coronary artery and moderate (61 ‘C narrowing) disease involving the second obtuse marginal branch, with an otherwise normal circumflex artery. There was total occlusion of the left anterior descending artery, which was a new finding compared with a study performed 2 weeks earlier (Fig. I). Left ventriculography revealed anterolateral akinesis and severe apical hypokinesis, with an ejection fraction of 31’,:. (Two-dimensional echocardiographic left ventricular wall motion at the previous admission indicated only mild anterior hypokinesis. Contrast ventriculography had been deferred.) After consultation with the attending transplantation service physicians and because of the recent total occlusion of the left anterior descending artery, angioplasty and atherectomy were elected. A 10,000 unit bolus and continuous intravenous infusion of heparin were administered. A 2.0 Magnum balloon system Schneider (USA), Inc., Plymouth, Minn. was initially used, leaving a patent vessel with a residual lesion of 62”, . A 7F atherocatheter device (Atherocath, Devices for Vascular Intervention, Redwood City, Calif.) was then introduced over an 0.014 inch guide wire into the proximal left anterior descending artery. Eight directional cuts were performed with an inflation pressure of 10 to 1:j psi. A total of 12.0 gm of tissue was obtained and was transferred to specially prepared media for histologic and immunopathologic staining. The final diameter narrowing was 15”,, (Fig. 2). However, shortly after withdrawal of the atherocatheter, total occlusion of the proximal circumflex branch was observed, presumably caused by embolization of thrombotic or atherosclerotic material (Fig. 3). There were no symptoms, electrocardiographic, or hemodynamic changes associated with the new obtuse marginal branch occlusion. The obtuse marginal and circumflex arteries were immediately dilated with a 3.0 mm balloon catheter (Shadow, Scimed, Inc., Minneapolis, Minn.) without difficulty, leaving a residual circumHex narrowing of 3’, The second obtuse marginal branch had a residual lesion of 18’~’ (Fig. 4). The patient remained asymptomatic during and after the procedure. Following the procedure, a continuous intravenous heparin infusion (1000 units/hr) was maintained for an additional 48 hours. The remainder of the hospital course and a s-month follow-up were uneventful, and the patient’s arteries remained angiographically patent. The typical features of classic at.heroscierosis usually demonstrate fibrosis, lipid, and atherosclerotic inclusion material. Trans-
Parashara
et al.
cular hyperplasia: extension of the therapeutic outcome. Reof the University Hospital Zurich Cooperation Study on fibromuscular hyperplasia. Nephron 1986;44(suppl. 1):109-14. James TA, Froggatt P, Marshall TK. Sudden death in young athletes. Ann Intern Med 1967;67:1013-21. dames TA, Marshall TK. De subitaneis mortibus XVII. Multifocal stenoses due to fibromuscular dysplasia of the sinus node artery. Circulation 1976;53:736-42. Rossi L, Thiene G. Recent advances in clinicohistopathologic correlates of sudden cardiac death. AM HEART J 1981;102:47884. 7. Nichols GR II, Davis GJ, Lefkowitz JB. Sudden death due to fibromuscuiar dysplasia of the sinoatrial nodal artery. KMA J 1989;87:504-5. 8. Lie JT, Berg KK. Isolated fibromuscular dysplasia of the coronary arteries with spontaneous dissection and myocardial infarction. Hum Path01 1987;18:654-6. sults
The combined presence of myocardial bridging and fixed coronary artery stenosis Deepak K. Parashara, MD, Gary S. Ledley, MD, Morris N. Kotler, MD, and Shahriar Yazdanfar, MD Philadelphia, Pa.
Myocardial bridging of the coronary arteries can be diagnosed in vivo by angiography only. Myocardial bridging is defined as embedment of a segment of the coronary artery into the myocardium so that during ventricular systole the segment of artery is compressed. Several studies have reported that atherosclerotic lesions are not found at the level of myocardial bridging.ie4 It has been postulated that the intramyocardial course of the coronary artery has a “protective” effect from the development of atherosclerosis at the site of the myocardial bridge. In this report we present an unusual case of coronary stenosis at the site of myocardial bridging. A 65year-old man with a history of heavy cigarette smoking had new onset of chest pain of 2 months’ duration. An exercise thallium test was performed. The patient achieved 71 % of the predicted maximal heart rate for his age with a 9.5 MET work load, and the ECG was positive for ischemia in the anterolateral leads. The thallium scan showed extensive myocardial perfusion abnormalities involving the anterior, apical, inferior, and septal walls with incomplete redistribution. The patient underwent cardiac catheterization. Left ventriculography revealed mild anterolateral wall hypokinesis and normal overall left ventric-
From the Department of Medicine, Division of Cardiovascular Diseases, and Women’s League for Medical Research Laboratory, Albert Einstein Medical Center, Temple University School of Medicine. Reprint requests: Shahriar Yazdanfar, MD, Division of Cardiology, Albert Einstein Medical Center, York and Tabor Rd., Philadelphia, PA 19141. AM HEART J 1993;125:1170-1172. Copyright ‘c 1993 by Mosby-Year Book, Inc. 0002.8703/93/$1 .OO + .10 4/4/44075
American
April 1993 Heart Journal
ular function with an ejection fraction of 71’ ,, Coronary cineangiography demonstrated that the mid left anterior descending coronary artery had an intramyocardial course with severe systolic constriction and a 95’; fixed atherosclerotic stenosis (Fig. 1). There was another 60 (; discrete stenosis in the mid left anterior descending coronary artery proximal to the intramyocardial segment. The left anterior descending coronary artery distal to the systolic constriction was free of disease. The left circumflex coronary artery was diffusely diseased. The first obtuse marginal coronary artery had an 80’ ; ostial and a 60’,. proximal stenosis. The third obtuse marginal coronary artery had a 60 r( proximal stenosis. The codominant right coronary artery had a 40”, proximal and another 60c; midluminal stenosis. The acute marginal coronary artery had an 80r; proximal stenosis. The patient underwent coronary artery bypass graft surgery, and the diseased intramyocardial course of the left. anterior descending coronary artery was confirmed. A left internal mammary artery was anastomosed to the left ant,erior descending coronary artery, and saphenous vein grafts were placed to the first obtuse marginal, the second obtuse marginal, and the distal right coronary arteries. The postoperative course was uneventful except for the development of paroxysmal atria1 fibrillation. It has long been known that the coronary arteries and their main branches are normally positioned subepicardially. At times a segment of the coronary artery, usually the left anterior descending coronary artery, may tunnel under a “bridge” of superficial myocardial fibers for a short distance. In 1960 Portsmann and Iwig’ were the first to describe myocardial bridging angiographically. In vivo myocardial bridges are primarily recognized by the “systolic milking effect” as seen on coronary cineangiograms. No systematic anatomically controlled study has been undertaken to correlate angiographically documented “systolic constriction” with pathologic findings. Most angiographers believe that systolic narrowing of a coronary artery segment is caused by myocardial bridging. The prevalence of myocardial bridges among consecutive patients undergoing coronary angiography varies between 0.5“p,e and 16’, ’ with most studies reporting an incidence of less than 2”, . Autopsy series report a prevalence of muscle bridges ranging from 5.4“; *t to 85.7’; ,’ which seems to depend on the precision of the dissection.” The marked disparity between the high prevalence of myocardial bridging reported in anat,omic studies and the lower prevalence in angiographic studies has been attributed to the fact that a pressure in excess of what is generated under normal physiologic conditions is needed to compress the artery.s The potentiation of the degree of systolic constriction after nitroglycerin confirms this hypothesis. Moreover, Angelini et al.” noted that the angiographic evidence of myocardial bridging may depend on the thickness and length of the bridge, the reciprocal orientation of the coronary artery and the myocardial fibers, and the nature of the tissue interposed between the coronary artery and the myocardial bridge. The presence of a proximal fixed coronary obstruction and the intrinsic coronary arterial wall
Volume American
125, Number Heart
4
Parusharu
Journal
et al.
1171
1. A, Right anterior oblique projection of left coronary cineangiogramduring diastole. Arrowhead showsfixed atherosclerotic stenosisof left anterior descendingcoronary artery. B, Right anterior oblique projection of left coronary cineangiogram during systole. Open. arrow shows systolic constriction of intramyocardial segmentof left anterior descendingcoronary artery. C, Lateral projection of left coronary cineangiogramduring diastole. Arrowhead showsfixed atherosclerotic stenosisof left anterior descending coronary artery. D, Lateral projection of left coronary cineangiogramduring systole. Open arrow shows systolic constriction of intramyocardial segmentof left anterior descendingcoronary artery. Fig.
tone may also play a role in the development and the degreeof systolic constriction. A review of the literature, with the exception of onecasereportlo and oneautopsy study,ll showsthat myocardial bridging hasa protective effect on the intramyocardial portion of the coronary artery with regard to the development of atherosclerosis.Findings in a recent histopathologic study12 and a recent large angiographic study8 of 1102 consecutive patients have further substantiated this observation. The exact mechanismby which the protective effect is exerted is not known. The important role of hemodynamic stressin the development of atherosclerosishasrecently beenreemphasized.13* I4The intramyocardial courseof the coronary artery is protected from the pulsatile nature of the blood flow and thus also from the vibration-induced mechanicalstress.We propose this asa possiblemechanismfor protection of the coronary artery from atherosclerosis.The presentreport is unique in that we have angiographically demonstrated a severeatherosclerotic coronary stenosisin the myocardial bridged segmentof the left anterior descendingcoronary artery. We thus conclude that the intramyocardial portions of the
coronary arteries may not be totally protected from the development of atherosclerotic disease. REFERENCES
1. Geiringer E. The mural coronary artery. AM HEART J 1951; 41:359-68. 2. Polacek P, Zechmeister A. The occurrence and significance of myocardial bridges and loops on coronary arteries. Opuscola Cardioloeica. Acta Facultatis Medicae Univesitatis Brunensis. Brno, 1968. 3. Stolte M, Weis I’, Prestele H. Muscle bridges over the left anterior descending coronary artery: their influence on arterial disease. Virchows Arch Path01 Anat 197737523-36. 4. Lee SS, WU TL. The role of mural coronary artery in prevention of coronary atherosclerosis. Arch Path01 1972;93:32-5. 5. Portsmann W, Iwig J. Die intramurale Koronaroeterie im Angiogramm. Fortschr Roentenstr 1960;92:129-33. 6. Noble J, Bourassa MG, Petitclerc R, et al. Myocardial bridging and milking effect of the left anterior descending coronary artery: normal variant or obstruction. Am J Cardiol 1976; 37:993-g. 7. Hashimoto A: Takekoshi N, Murakami E. Clinical significance of myocardial bridging of the coronary artery. Jpn Heart J 1984;25:913-22.
1172
Bell et al.
Amencan
8. Charmer K, Bukis E, Hartnell G, et al. Myocardial bridging of the coronary arteries. Clin Radio1 1989;40:355-9. 9. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75-88. 10. Laif’er LI. Weiner BH. Percutaneous transluminal coronarv angioplasry of a coronary stenosis at the site of myocardial bridging. Cardiology 1991;79:245-8. 11. Edwards JC, Burnsides CH, Swarm RL, et al. Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-42. 12. Ishii T, Asuwa N, Masuda S, et al. Atherosclerosis suppression in the anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. Mod Path01 1991;4:424-31. 13. Stehbens WE. The lipid hypothesis and the role of hemodynamics in atherogenesis. Prog Cardiovasc Dis 1990;2:119-36. 14. Stehben WE. Hemodynamics and the blood vessel wall. Springfield, IL: Charles C Thomas, 1979.
Coronary atherectomy complicated by coronary embolus in a cardiac transplant recipient Calvin Bell, MD, Morton J. Kern, MD, Frank Aguirre, MD, Leslie Miller, MD, Richard Bach, MD, Thomas Donohue, MD, and Frederick Dressler, MD St. Louis, MO.
Coronary atherectomy is now commonly performed for focal, noncalcified atherosclerotic coronary artery narrowings.id4 To date, there has been only one reported study of this procedure being employed for obstructive coronary arteriopathy in cardiac transplant recipients.s We present a unique case of directional atherectomy complicated by coronary embolus in a patient with an orthotopic heart transplant. This patient example indicates the potential complications and benefits of direcbional endoluminal tis sue excision as a means to treat and advance our understanding of transplant-related coronary artery disease. A 63-year-old man underwent orthotopic cardiac transplant in 1987. A recent routine yearly surveillance angiography demonstrated a high-grade left anterior descending lesion (80% diameter narrowing by visual estimate). Because of advanced coronary arteriopathy, he was subsequently admitted for atherectomy of the proximal left anterior descending coronary artery lesion. During the Z-week interim between the diagnostic and interventional procedures, the patient remained asymptomatic despite developing new electrocardiogram changes that showed sinus tachycardia, bifascicular block (right bundle branch block From
the Cardiology
Division,
St. Louis
University
Hospital.
Reprint requests: Morton J. Kern, MD, Director, J. G. Mudd Cardiac Catheterization Laboratory, St. Louis University Hospital, 3635 Vista Ave. at Grand Blvd., St. Louis, MO 63110-0250. A.% Hwm’r
J 1993;125:1172-1175.
Copyright ” 1993 0002-870:~/93/$1.00
by Mosby-Year Book, + .I0 4/4/44070
Inc.
April 1993 Heart Journal
and left anterior fascicular block). and anteroseptal myocardial infarction. These findings were not present on the electrocardiogram obtained after the diagnostic study. Before the procedure, the blood pressure was IlO/ mm IIg, pulse was 98/min, respiratory rate was 16/min, and temperature was 97.2” F. Cardiac examination was normal except for a summation gallop. The examination of the lungs, abdomen, and extremities was unremarkable. The laboratory profile was normal except for a creatinine of 1.9 mg/ dl. A chest roentgenogram was also normal with t,he exception of the sternal wires from the previous surgery. Coronary angiograph y immediately before atherectomy revealed minimal irregularities of the right coronary artery and moderate (61 ‘C narrowing) disease involving the second obtuse marginal branch, with an otherwise normal circumflex artery. There was total occlusion of the left anterior descending artery, which was a new finding compared with a study performed 2 weeks earlier (Fig. I). Left ventriculography revealed anterolateral akinesis and severe apical hypokinesis, with an ejection fraction of 31’,:. (Two-dimensional echocardiographic left ventricular wall motion at the previous admission indicated only mild anterior hypokinesis. Contrast ventriculography had been deferred.) After consultation with the attending transplantation service physicians and because of the recent total occlusion of the left anterior descending artery, angioplasty and atherectomy were elected. A 10,000 unit bolus and continuous intravenous infusion of heparin were administered. A 2.0 Magnum balloon system Schneider (USA), Inc., Plymouth, Minn. was initially used, leaving a patent vessel with a residual lesion of 62”, . A 7F atherocatheter device (Atherocath, Devices for Vascular Intervention, Redwood City, Calif.) was then introduced over an 0.014 inch guide wire into the proximal left anterior descending artery. Eight directional cuts were performed with an inflation pressure of 10 to 1:j psi. A total of 12.0 gm of tissue was obtained and was transferred to specially prepared media for histologic and immunopathologic staining. The final diameter narrowing was 15”,, (Fig. 2). However, shortly after withdrawal of the atherocatheter, total occlusion of the proximal circumflex branch was observed, presumably caused by embolization of thrombotic or atherosclerotic material (Fig. 3). There were no symptoms, electrocardiographic, or hemodynamic changes associated with the new obtuse marginal branch occlusion. The obtuse marginal and circumflex arteries were immediately dilated with a 3.0 mm balloon catheter (Shadow, Scimed, Inc., Minneapolis, Minn.) without difficulty, leaving a residual circumHex narrowing of 3’, The second obtuse marginal branch had a residual lesion of 18’~’ (Fig. 4). The patient remained asymptomatic during and after the procedure. Following the procedure, a continuous intravenous heparin infusion (1000 units/hr) was maintained for an additional 48 hours. The remainder of the hospital course and a s-month follow-up were uneventful, and the patient’s arteries remained angiographically patent. The typical features of classic at.heroscierosis usually demonstrate fibrosis, lipid, and atherosclerotic inclusion material. Trans-