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Angiographic presence of myocardial bridge after successful percutaneous transluminal coronary angioplasty
January 1996
196 Colleran et al. mitral valve area was 0.8 cm2, and the left atrial dimension was enlarged at 56 mm. No thrombi were seen in any of the cardiac chambers. Color-Doppler echocardiography revealed severe mitral regurgitation and moderate aortic regurgitation. Transesophageal echocardiography disclosed spontaneous echocardiographic contrast through the entire left atrium. A second cardiac catheterization was performed 3 weeks after the patient's admission. Left ventriculography showed global reduction in wall motion with akinesis of the anterolateral wall. Coronary arteriography revealed complete recanalization of the three lesions (Fig. 2). Coronary thromboemboli complicating valvular heart disease rarely have been documented by emergent coronary arteriography. In particular, simultaneous and multiple emboli in the coronary arteries have not been reported. The mechanism for the multiple coronary thromboemboli in the absence of systemic embolization may be explained as follows. A relatively large thrombus may have been disrupted during passage through the left main trunk, resulting in the occlusion of the different branches of the left coronary artery. This occurrence is more probable than the likelihood of consecutive coronary thromboemboli occurring in the different coronary branches during a short time. Although thrombolytic therapy is considered to be efficacious treatment for a coronary thromboembolism, intracoronary thrombolysis has been reported to be unsuccessful for recanalization of embolic lesions. 4"6A potential reason for the unsuccessful thrombolysis may be related to the age of the thrombus. In this case intracoronary thrombolysis was ineffective. However, crossing a guide wire over the occluded D2 resulted in recanalization of the artery. Disruption of the thrombus by the guide wire thus facilitated recanalization of the D2. Balloon angioplasty of the left circumflex coronary artery has been ineffective probably because of its small diameter. To our knowledge this report is the first to demonstrate multiple coronary thromboemboli for which coronary intervention therapy was performed. Our results suggest that for coronary thromboemboli the disruption of the thrombus by a guide wire should be attempted after unsuccessful thrombolysis. Further studies are required to establish the optimal reperfusion strategies for patients with coronary thromboemboli. REFERENCES
1. Coulshed N, Epstein EJ, McKendrick CS, Walker E. Systemic embolism in mitral valve disease. Br Heart J 1970;32:26-34. 2. Abernathy WS, Willis PW. Thromboembolic complication ofrheumatic heart disease. Cardiovasc Clin 1973;5:131-75. 3. Hwang J, Kuan P, Lin S, Chen W, Lei M, Ko Y, Cheng J, Lin J, Chen J, Lien W. Reappraisal by transesophageal echocardiography of the significance of left atrial thrombi in the prediction of systemic arterial embolization in rheumatic mitral valve disease. Am J Cardiol 1992; 70:769-73. 4. Nakao T, Kanaya H, Namura M, Ohsato K, Araki T, Ohka T, Seki M. A case of mitral stenosis associated with myocardial infarction, demonstrating coronary emboli and giant left atrial thrombus in acute phase [in Japanese]. Heart 1990;22:1303-08. 5. Funayama N, Terai H, Yazaki K. A case of mitral stenosis associated
American Heart Journal
with acute myocardial infarction induced by lei~ atrial thrombus [in Japanese]. Coronary 1991;8:56-60. 6. Kamishirado H, Yamanaka T, Morooka S, Takayanagi K, Sasaki T, Koshikawa K, Matsunaga R, Maekawa Y, Takabatake Y. A case of coronary artery embolism associated with combined valvular heart disease [in Japanese]. Kokyu To Junkan 1993;41:81-4.
Angiographic presence of myocardial bridge after successful percutaneous transluminal coronary angioplasty John A. Colleran, DO, John P. Tierney, RN, Richard Prokopchak, MD, Daniel J. Diver, MD, and Jeffrey A. Breall, MD, PhD Washington, D.C. It has previously been reported that portions of epicardial coronary arteries within segments of myocardial bridging are free of significant atherosclerosisfl 2 Although the mechanism of coronary protection in these segments is not known, it has been postulated that the coronary arteries coursing through the myocardium are not exposed to the pulsatile blood flow; thus the mechanical stress placed on the vessel is limited. 3 We report an unusual case of left anterior descending coronary artery stenosis at the site of a myocardial bridge, which was not evident until successful percutaneous transluminal coronary angioplasty was performed. A 44-year-old black man with a history of hypertension and cigarette smoking came to a local emergency department with acute onset of substernal chest pressure. The electrocardiogram (ECG) revealed 2 mm ST segment eleVation in the precordial leads consistent with an acute anterior myocardial infarction, and he was therefore treated with thrombolytic therapy, intravenous heparin, and nitroglycerin. Subsequently his symptoms subsided, and the ECG abnormalities resolved. No evidence of myocardial necrosis by serial cardiac enzymes (creatine kinase, creatine kinase-MB) was found. Several days later an exercise scintigraphy with technetium sestamibi was performed according to the Bruce protocol. The patient achieved a work level of 10 METs with a maximal heart rate of 144 (82% peak maximal heart rate) and a peak blood pressure of 156/104 mm Hg. Exercise was limited by fatigue; otherwise the patient had no symptoms. No evidence ofischemia was seen on ECG. The scintigram revealed a mild inferior reversible defect that was believed to be attenuation rather than ischemia. The anterior wall appeared normal. The patient was discharged on a medical regimen including From the Institute for Cardiovascular Sciences, Division of Cardiology, Department of Medicine, Georgetown University Medical Center. Reprint requests: Jeffrey A. Breall, MD, PhD, Division of Cardiology, 4 North M4217, Georgetown University Medical Center, 3800 Reservoir Rd. N.W., Washington, D.C. 20007. AM HEARTJ 1996;131:196-8. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4/4168066
Volume 131, Number 1 American Heart Journal
Colleran et al.
197
Fig. 1. A, Coronary angiogram in left anterior oblique view showing discrete 70% stenosis (arrow) with hazy appearance in mid-left anterior descending coronary artery during diastole. B, No significant change is noted in mid-left anterior descending coronary artery stenosis (arrow) during systole.
Fig. 2. A, After angioplasty of mid-left anterior descending coronary artery is performed, minimal residual stenosis (arrow) is noted during diastole. B, Same view during systole demonstrates compression of vessel (between arrows) consistent with myocardial bridge. aspirin and a calcium channel antagonist; however, I week later he had episodes of progressive exertional angina. He was therefore readmitted to our hospital for diagnostic cardiac catheterization. Right-sided and left-sided hemodynamic parameters were normal. Left ventriculography demonstrated normal left ventricular systolic function with a calculated ejection fraction of 66%. Coronary angiography revealed a discrete 70% stenosis in the mid-left anterior descending coronary artery that was very hazy in appearance and persisted after intracoronary nitroglycerin was administered. Because of this patient's history and recurring angina it was elected to perform percutaneous transluminal coronary angioplasty. After serial nominal inflations of a 3.0 × 20 mm perfusion balloon (Stack
perfusion balloon, Advanced Cardiovascular Systems Inc., Temecula, Calif.) were performed, a 10% to 20% residual stenosis with brisk antegrade flow and no evidence of dissection was noted during diastole (Fig. 1). However, significant compression consistent with a myocardial bridge was then obvious during systole (Fig. 2); this compression had not been apparent before the angioplasty was performed. The myocardial bridge is a relatively common congenital anomaly recognized by its characteristic systolic compression of a discrete coronary segment during angiography. The myocardial bridge usually involves the left anterior descending coronary artery and comprises myocardial fibers that run perpendicular to the coronary artery. 3 AI-
198
January 1996 American Heart Journal
Levin et al.
though first described more than 40 years ago, controversy continues to exist over the clinical significance of myocardial bridging. A large angiographic study 4and two necropsy studies 2, 5 have found little or no atherosclerotic plaque formation at the site of the bridge. Therefore it is believed that the myocardial bridge may protect the coronary artery from significant atherosclerosis by limiting its exposure to the forces of the systolic pulse wave and potentially rainimizing endothelial trauma. However, several reports 69 have disputed this finding, and recent evidence now questions the protective effect afforded by a myocardial bridge. To our knowledge only three case reports 79 have described significant coronary artery stenosis at the site of a myocardial bridge documented by angiography. Two cases 7, 8 similar to our patient were found after angioplasty of the coronary artery stenosis was performed. One case involved the left anterior descending coronary artery 7 and the other the right coronary artery, s The third patient 9 underwent coronary artery bypass graft surgery because of multivessel disease after a myocardial bridge was discovered in the left anterior descending coronary artery. In the case described previously the culprit stenosis was at the proximal portion of a myocardial bridge in the left anterior descending coronary artery, and the patient had a similar clinical presentation with chest pain and ST segment elevation on the ECG. Myocardial bridging of the coronary segment was not discovered in our case, as in two previous cases, until angioplasty was performed, possibly because of the fixed underlying atherosclerotic stenosis limiting coronary inflow and masking systolic compression. Once angioplasty was performed, the characteristic "milking effect" consistent with myocardial bridging was noted. Transient coronary occlusion caused by plaque rupture and thrombotic occlusion or vasospasm may have been responsible for this patients' event. Fortunately a significant myocardial infarction was aborted, and subsequent angina was relieved with conventional angioplasty. Currently the patient has no symptoms. Myocardial bridging has been associated with angina, myocardial infarction, and sudden death. 3 These clinical events have been attributed to transient coronary occlusion (thrombotic or vasospastic) at the site of the myocardial bridge when myocardial bridging is the only coronary abnormality present on angiography. Noninvasive clinical studies have shown mixed results ranging from normal exercise treadmill testing to fLxed or reversible defects found on thallium-201 scintigraphy. 3 One invasive report 8 has described coronary vasospasm induced by intracoronary acetylcholine at the site of the myocardial bridge, indicating endothelial dysfunction. Apparently "kinking" of the entrapped vessel during systole may cause intimal trauma, endothelial damage, or both. Recently Ge et al. 1° reported the presence of atherosclerosis in the coronary segment proximal to the myocardial bridge by intravascular ultrasound and reduced coronary flow reserve by Doppler flow wire. In all reported cases of atherosclerotic narrowing at the site of a myocardial bridge including our own, the initial result was a success; however, optimal therapy of this con-
dition is not known. Until further data are available, treatment should be aimed at relief of symptoms, and clinical decisions regarding patients with symptoms and critical stenoses should be made in the standard fashion. Therapeutic decisions in patients with noncritical stenoses may be aided by the use of intravascular ultrasound and intracoronary Doppler flow wire, although this has yet to be proven. In conclusion, we report a rare case of coronary artery stenosis at the site of a myocardial bridge that was apparent only after angioplasty. It is evident from this report and others that the presence of myocardial bridging does not necessarily offer protection from significant coronary artery disease. REFERENCES
1. Stolte M, Weis P, Prestele H. Muscle bridges over the left anterior descending coronary artery: their influence on arterial disease. Virchows Arch Pathol Anat 1977;375:23-36. 2. Lee SS, Wu TL. The role of mural coronary artery in prevention ofcoronary atherosclerosis. Arch Pathol 1972;93:32-5. 3. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75-88. 4. Channer KS, Bukis E, Hartnell G, Rees JR. Myocardial bridging of the coronary arteries. Clin Radiol 1989;40:355-9. 5. Ishii T, Asuwa N, Masuda S, Ishikawa Y, Kiguchi H, Shimada K. Atherosclerosis suppression in the lei~ anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. Mod Pathol 1991;4:424-31. 6. Edwards JC, Burnsides CN, Swarm RL, Lansing AI. Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-42. 7. Laifer LI, Weiner BH. Percutaneous transtuminal coronary angloplasty of a coronary stenosis at the site of myocardial bridging. Cardiology 1991;79:245-8. 8. Munakata K, Sato N, Sasaki Y, Yasutake M, Kusama Y, Takayama M, Kishida H, Hayakawa H. Two cases of variant form angina pectoris associated with myocardial bridge: a possible relationship among coronary vasospasm, atherosclerosis and myocardial bridge. Jpn Circ J 1992;56:1248-52. 9. Parashara DK, Ledley GS, Kotler MN,,Yazdanfar S. The combined presence of myocardial bridging and fixed coronary artery stenosis. AM HEARTJ 1993;125:1170-2. 10. Ge J, Erbel R, Rupprecht H J, Koch L, Kearney P, George G, Haude M, Meyer J. Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging. Circulation 1994;89:1725-32.
Cardiac tamponade without pericardial effusion after blunt chest trauma Steven Levin, MD, Ivan Maldonado, MD, Christina Rehm, MD, Steven Ross, MD, and Richard L. Weiss, MD Camden, N.J. Tension pneumopericardium is an unusual complication in the patient undergoing critical care and may carry a high From the Department of Surgery and Medicine, Cooper Hospital/University Medical Center; the University of Medicine and Dentistry of New Jersey; and the Robert Wood Johnson Medical School at Camden. Reprint requests: Richard L. Weiss, MD, One Cooper Plaza, Camden, NJ 08103. AM HEARTJ 1996;131:198-200. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4J4J68069
196 Colleran et al. mitral valve area was 0.8 cm2, and the left atrial dimension was enlarged at 56 mm. No thrombi were seen in any of the cardiac chambers. Color-Doppler echocardiography revealed severe mitral regurgitation and moderate aortic regurgitation. Transesophageal echocardiography disclosed spontaneous echocardiographic contrast through the entire left atrium. A second cardiac catheterization was performed 3 weeks after the patient's admission. Left ventriculography showed global reduction in wall motion with akinesis of the anterolateral wall. Coronary arteriography revealed complete recanalization of the three lesions (Fig. 2). Coronary thromboemboli complicating valvular heart disease rarely have been documented by emergent coronary arteriography. In particular, simultaneous and multiple emboli in the coronary arteries have not been reported. The mechanism for the multiple coronary thromboemboli in the absence of systemic embolization may be explained as follows. A relatively large thrombus may have been disrupted during passage through the left main trunk, resulting in the occlusion of the different branches of the left coronary artery. This occurrence is more probable than the likelihood of consecutive coronary thromboemboli occurring in the different coronary branches during a short time. Although thrombolytic therapy is considered to be efficacious treatment for a coronary thromboembolism, intracoronary thrombolysis has been reported to be unsuccessful for recanalization of embolic lesions. 4"6A potential reason for the unsuccessful thrombolysis may be related to the age of the thrombus. In this case intracoronary thrombolysis was ineffective. However, crossing a guide wire over the occluded D2 resulted in recanalization of the artery. Disruption of the thrombus by the guide wire thus facilitated recanalization of the D2. Balloon angioplasty of the left circumflex coronary artery has been ineffective probably because of its small diameter. To our knowledge this report is the first to demonstrate multiple coronary thromboemboli for which coronary intervention therapy was performed. Our results suggest that for coronary thromboemboli the disruption of the thrombus by a guide wire should be attempted after unsuccessful thrombolysis. Further studies are required to establish the optimal reperfusion strategies for patients with coronary thromboemboli. REFERENCES
1. Coulshed N, Epstein EJ, McKendrick CS, Walker E. Systemic embolism in mitral valve disease. Br Heart J 1970;32:26-34. 2. Abernathy WS, Willis PW. Thromboembolic complication ofrheumatic heart disease. Cardiovasc Clin 1973;5:131-75. 3. Hwang J, Kuan P, Lin S, Chen W, Lei M, Ko Y, Cheng J, Lin J, Chen J, Lien W. Reappraisal by transesophageal echocardiography of the significance of left atrial thrombi in the prediction of systemic arterial embolization in rheumatic mitral valve disease. Am J Cardiol 1992; 70:769-73. 4. Nakao T, Kanaya H, Namura M, Ohsato K, Araki T, Ohka T, Seki M. A case of mitral stenosis associated with myocardial infarction, demonstrating coronary emboli and giant left atrial thrombus in acute phase [in Japanese]. Heart 1990;22:1303-08. 5. Funayama N, Terai H, Yazaki K. A case of mitral stenosis associated
American Heart Journal
with acute myocardial infarction induced by lei~ atrial thrombus [in Japanese]. Coronary 1991;8:56-60. 6. Kamishirado H, Yamanaka T, Morooka S, Takayanagi K, Sasaki T, Koshikawa K, Matsunaga R, Maekawa Y, Takabatake Y. A case of coronary artery embolism associated with combined valvular heart disease [in Japanese]. Kokyu To Junkan 1993;41:81-4.
Angiographic presence of myocardial bridge after successful percutaneous transluminal coronary angioplasty John A. Colleran, DO, John P. Tierney, RN, Richard Prokopchak, MD, Daniel J. Diver, MD, and Jeffrey A. Breall, MD, PhD Washington, D.C. It has previously been reported that portions of epicardial coronary arteries within segments of myocardial bridging are free of significant atherosclerosisfl 2 Although the mechanism of coronary protection in these segments is not known, it has been postulated that the coronary arteries coursing through the myocardium are not exposed to the pulsatile blood flow; thus the mechanical stress placed on the vessel is limited. 3 We report an unusual case of left anterior descending coronary artery stenosis at the site of a myocardial bridge, which was not evident until successful percutaneous transluminal coronary angioplasty was performed. A 44-year-old black man with a history of hypertension and cigarette smoking came to a local emergency department with acute onset of substernal chest pressure. The electrocardiogram (ECG) revealed 2 mm ST segment eleVation in the precordial leads consistent with an acute anterior myocardial infarction, and he was therefore treated with thrombolytic therapy, intravenous heparin, and nitroglycerin. Subsequently his symptoms subsided, and the ECG abnormalities resolved. No evidence of myocardial necrosis by serial cardiac enzymes (creatine kinase, creatine kinase-MB) was found. Several days later an exercise scintigraphy with technetium sestamibi was performed according to the Bruce protocol. The patient achieved a work level of 10 METs with a maximal heart rate of 144 (82% peak maximal heart rate) and a peak blood pressure of 156/104 mm Hg. Exercise was limited by fatigue; otherwise the patient had no symptoms. No evidence ofischemia was seen on ECG. The scintigram revealed a mild inferior reversible defect that was believed to be attenuation rather than ischemia. The anterior wall appeared normal. The patient was discharged on a medical regimen including From the Institute for Cardiovascular Sciences, Division of Cardiology, Department of Medicine, Georgetown University Medical Center. Reprint requests: Jeffrey A. Breall, MD, PhD, Division of Cardiology, 4 North M4217, Georgetown University Medical Center, 3800 Reservoir Rd. N.W., Washington, D.C. 20007. AM HEARTJ 1996;131:196-8. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4/4168066
Volume 131, Number 1 American Heart Journal
Colleran et al.
197
Fig. 1. A, Coronary angiogram in left anterior oblique view showing discrete 70% stenosis (arrow) with hazy appearance in mid-left anterior descending coronary artery during diastole. B, No significant change is noted in mid-left anterior descending coronary artery stenosis (arrow) during systole.
Fig. 2. A, After angioplasty of mid-left anterior descending coronary artery is performed, minimal residual stenosis (arrow) is noted during diastole. B, Same view during systole demonstrates compression of vessel (between arrows) consistent with myocardial bridge. aspirin and a calcium channel antagonist; however, I week later he had episodes of progressive exertional angina. He was therefore readmitted to our hospital for diagnostic cardiac catheterization. Right-sided and left-sided hemodynamic parameters were normal. Left ventriculography demonstrated normal left ventricular systolic function with a calculated ejection fraction of 66%. Coronary angiography revealed a discrete 70% stenosis in the mid-left anterior descending coronary artery that was very hazy in appearance and persisted after intracoronary nitroglycerin was administered. Because of this patient's history and recurring angina it was elected to perform percutaneous transluminal coronary angioplasty. After serial nominal inflations of a 3.0 × 20 mm perfusion balloon (Stack
perfusion balloon, Advanced Cardiovascular Systems Inc., Temecula, Calif.) were performed, a 10% to 20% residual stenosis with brisk antegrade flow and no evidence of dissection was noted during diastole (Fig. 1). However, significant compression consistent with a myocardial bridge was then obvious during systole (Fig. 2); this compression had not been apparent before the angioplasty was performed. The myocardial bridge is a relatively common congenital anomaly recognized by its characteristic systolic compression of a discrete coronary segment during angiography. The myocardial bridge usually involves the left anterior descending coronary artery and comprises myocardial fibers that run perpendicular to the coronary artery. 3 AI-
198
January 1996 American Heart Journal
Levin et al.
though first described more than 40 years ago, controversy continues to exist over the clinical significance of myocardial bridging. A large angiographic study 4and two necropsy studies 2, 5 have found little or no atherosclerotic plaque formation at the site of the bridge. Therefore it is believed that the myocardial bridge may protect the coronary artery from significant atherosclerosis by limiting its exposure to the forces of the systolic pulse wave and potentially rainimizing endothelial trauma. However, several reports 69 have disputed this finding, and recent evidence now questions the protective effect afforded by a myocardial bridge. To our knowledge only three case reports 79 have described significant coronary artery stenosis at the site of a myocardial bridge documented by angiography. Two cases 7, 8 similar to our patient were found after angioplasty of the coronary artery stenosis was performed. One case involved the left anterior descending coronary artery 7 and the other the right coronary artery, s The third patient 9 underwent coronary artery bypass graft surgery because of multivessel disease after a myocardial bridge was discovered in the left anterior descending coronary artery. In the case described previously the culprit stenosis was at the proximal portion of a myocardial bridge in the left anterior descending coronary artery, and the patient had a similar clinical presentation with chest pain and ST segment elevation on the ECG. Myocardial bridging of the coronary segment was not discovered in our case, as in two previous cases, until angioplasty was performed, possibly because of the fixed underlying atherosclerotic stenosis limiting coronary inflow and masking systolic compression. Once angioplasty was performed, the characteristic "milking effect" consistent with myocardial bridging was noted. Transient coronary occlusion caused by plaque rupture and thrombotic occlusion or vasospasm may have been responsible for this patients' event. Fortunately a significant myocardial infarction was aborted, and subsequent angina was relieved with conventional angioplasty. Currently the patient has no symptoms. Myocardial bridging has been associated with angina, myocardial infarction, and sudden death. 3 These clinical events have been attributed to transient coronary occlusion (thrombotic or vasospastic) at the site of the myocardial bridge when myocardial bridging is the only coronary abnormality present on angiography. Noninvasive clinical studies have shown mixed results ranging from normal exercise treadmill testing to fLxed or reversible defects found on thallium-201 scintigraphy. 3 One invasive report 8 has described coronary vasospasm induced by intracoronary acetylcholine at the site of the myocardial bridge, indicating endothelial dysfunction. Apparently "kinking" of the entrapped vessel during systole may cause intimal trauma, endothelial damage, or both. Recently Ge et al. 1° reported the presence of atherosclerosis in the coronary segment proximal to the myocardial bridge by intravascular ultrasound and reduced coronary flow reserve by Doppler flow wire. In all reported cases of atherosclerotic narrowing at the site of a myocardial bridge including our own, the initial result was a success; however, optimal therapy of this con-
dition is not known. Until further data are available, treatment should be aimed at relief of symptoms, and clinical decisions regarding patients with symptoms and critical stenoses should be made in the standard fashion. Therapeutic decisions in patients with noncritical stenoses may be aided by the use of intravascular ultrasound and intracoronary Doppler flow wire, although this has yet to be proven. In conclusion, we report a rare case of coronary artery stenosis at the site of a myocardial bridge that was apparent only after angioplasty. It is evident from this report and others that the presence of myocardial bridging does not necessarily offer protection from significant coronary artery disease. REFERENCES
1. Stolte M, Weis P, Prestele H. Muscle bridges over the left anterior descending coronary artery: their influence on arterial disease. Virchows Arch Pathol Anat 1977;375:23-36. 2. Lee SS, Wu TL. The role of mural coronary artery in prevention ofcoronary atherosclerosis. Arch Pathol 1972;93:32-5. 3. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75-88. 4. Channer KS, Bukis E, Hartnell G, Rees JR. Myocardial bridging of the coronary arteries. Clin Radiol 1989;40:355-9. 5. Ishii T, Asuwa N, Masuda S, Ishikawa Y, Kiguchi H, Shimada K. Atherosclerosis suppression in the lei~ anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. Mod Pathol 1991;4:424-31. 6. Edwards JC, Burnsides CN, Swarm RL, Lansing AI. Arteriosclerosis in the intramural and extramural portions of coronary arteries in the human heart. Circulation 1956;13:235-42. 7. Laifer LI, Weiner BH. Percutaneous transtuminal coronary angloplasty of a coronary stenosis at the site of myocardial bridging. Cardiology 1991;79:245-8. 8. Munakata K, Sato N, Sasaki Y, Yasutake M, Kusama Y, Takayama M, Kishida H, Hayakawa H. Two cases of variant form angina pectoris associated with myocardial bridge: a possible relationship among coronary vasospasm, atherosclerosis and myocardial bridge. Jpn Circ J 1992;56:1248-52. 9. Parashara DK, Ledley GS, Kotler MN,,Yazdanfar S. The combined presence of myocardial bridging and fixed coronary artery stenosis. AM HEARTJ 1993;125:1170-2. 10. Ge J, Erbel R, Rupprecht H J, Koch L, Kearney P, George G, Haude M, Meyer J. Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging. Circulation 1994;89:1725-32.
Cardiac tamponade without pericardial effusion after blunt chest trauma Steven Levin, MD, Ivan Maldonado, MD, Christina Rehm, MD, Steven Ross, MD, and Richard L. Weiss, MD Camden, N.J. Tension pneumopericardium is an unusual complication in the patient undergoing critical care and may carry a high From the Department of Surgery and Medicine, Cooper Hospital/University Medical Center; the University of Medicine and Dentistry of New Jersey; and the Robert Wood Johnson Medical School at Camden. Reprint requests: Richard L. Weiss, MD, One Cooper Plaza, Camden, NJ 08103. AM HEARTJ 1996;131:198-200. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4J4J68069