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Intravascular ultrasound identification of calcified intraluminal lesions misdiagnosed as thrombi by coronary angiography
Volume 132, Number 3 American Heart Journal
Duissaillant et al.
687
Intravascular ultrasound identification of calcified intraluminal lesions misdiagnosed as thrombi by coronary angiography Gaston R. Duissaillant, MD, Gary S. Mintz, MD, Augusto D. Pichard, MD, Kenneth M. Kent, MD, PhD, Lowell F. Satler, MD, Jeffrey J. Popma, MD, Jennifer Griffin, BS, and Martin B. Leon, MD
Washington, D.C. Accurate identification of coronary atherosclerotic plaque composition is important for optimum patient management and transcatheter therapy. In particular, the presence ofthrombus typically leads to protracted hospitalization, intravenous or intracoronary thrombolysis, prolonged systemic anticoagulation, and the use oftranscatheter devices designed to remove thrombi. Furthermore, thrombi may be implicated in poor outcome after transcatheter therapy. Intraluminal filling defects are believed to be the most specific angiographic markers of thrombus. We report three patients with intracoronary filling defects initially diagnosed as thrombus; however, intravascular ultrasound (IVUS) imaging showed that these filling defects represented calcified nodules. IVUS studies were performed with one of two commercially available systems. The first (Cardiovascular Imaging Systems Inc./InterTherapy Inc., Sunnyvale, Calif.) incorporated a single element 25-MHz transducer and an angled mirror mounted on the tip of a flexible shaft that was rotated at 1800 rpm within a 3.9F short monorail polyethylene imaging sheath to form planar cross-sectional images in real time. The second (Cardiovascular Imaging Systems) incorporated a single element 30-MHz beveled transducer within either a 2.9F long monorail imaging catheter having a common distal lumen design (the distal lumen alternatively accommodates the imaging core or the guide wire, but not both) or within a 3.2F short monorail imaging catheter. With both systems the imaging catheter was advanced 5 to 10 mm beyond the target lesion and the transducer was withdrawn automatically at 0.5 mm/sec within the imaging sheath to perform the imaging sequence. IVUS studies were recorded on ~-inch high resolution s-VHS tape for offiine analysis. Patient 1. A 78-year-old white man with a history of pneumoconiosis, gastrectomy for stomach cancer, congestive heart failure from dilated cardiomyopathy, and coronary artery disease was seen for progressive angina. A From the Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, Washington Hospital Center. Supported in part by the Cardiology Research Foundation, Washington, D.C. Reprint requests: Martin B. Leon, MD, Washington Cardiology Center, 110 Irving St., NW, 4B-1, Washington, DC 20010. Am Heart J 1996;132:687-9. Copyright © 1996 by Mosby-Ye~r Book, Inc. 0002-8703/96/$5.00 + 0 4/4/71990
Fig. 1. Proximal right coronary artery filling defect (arrow) was initially thought to represent intracoronary thrombus. Patient was treated with prolonged system anticoagulation, intracoronary thrombolysis, and extraction atherectomy. IVUS imaging showed that filling defect was, in fact, calcified lesion protruding into lumen.
Fig. 2. Mid-right coronary artery filling defect (arrow) was initially thought to represent intracoronary thrombus. Patient was also treated with prolonged systemic anticoagulation. IVUS imaging showed that filling defect was, in fact, calcified lesion protruding into the lumen. Because of limited device availability, patient was referred for bypass graft surgery. coronary angiogram showed a 95% ostial fight coronary artery lesion with a round filling defect highly suggestive ofthrombus. He was treated with heparin and sent home taking coumadin to dissolve the thrombus. However, he returned with worsening angina; coronary angiography still showed a large filling defect almost completely occluding the right coronary artery (Fig. 1). He was initially treated with an intracoronary urokinase infusion of 250,000 U followed by the use of a 2.2-mm transluminal extraction atherectomy cutter (Interventional Technologies, Inc., San Diego, Calif.) and 3.5-ram adjunct balloon
688
September 1996 American Heart Journal
Duissaillant et al.
Fig. 3. Proximal left anterior descending coronary artery filling defect (large arrow, left) was initially thought to represent intracoronary thrombus. Patient was treated with prolonged systemic anticoagulation and was scheduled for laser thrombolysis. IVUS imaging (right) showed that filling defect was, in fact, calcified lesion. IVUS illustration is series of four cross-sectional image slices taken 2 mm apart. Double arrows indicate leading edge of calcium protruding into lumen on each of four slices. Patient was treated with rotational atherectomy followed by endovascular stent placement. inflation. A residual hazy 35% stenosis remained. IVUS imaging performed to assess the angioplasty result revealed a heavily calcified proximal right coronary artery and a markedly eccentric plaque that protruded from the arterial wall into the lumen corresponding to the anglographic falling defect. After final dilatation with a 4.0-ram balloon, a 23% residual stenosis remained. Patient 2. A 72-year-old white man with a history of myocardial infarction underwent preoperative assessment for radical prostate surgery. A thallium scan disclosed myocardial ischemia. Cardiac catheterization showed 3+ mitral regurgitation, left anterior descending artery occlusion receiving good collateral flow from the right coronary artery, and a large filling defect in the mid-right coronary artery consistent with thrombus (Fig. 2). He was consequently treated with heparin for 2 weeks. However, repeat coronary angiography showed persistence of the right coronary artery filling defect. IVUS revealed circumferential calcium as well as a calcified, eccentric, atherosclerotic lesion protruding into the lumen corresponding to the angiographic filling defect. In the absence of a transcatheter device designed to treat calcific lesions (the Rotablator, Heart Technology, Bellevue, Wash, had been recalled and was not available), the patient underwent elective cardiac surgery before radical prostatectomy. Patient 3. An 84-year-old woman was seen with prolonged chest pain and creatinine kinase elevation consistent with non-Q-wave myocardial infarction. Because of recurrent chest pain, coronary angiography was performed and showed a severe proximal left anterior descending stenosis with filling defects indicative of thrombus (Fig. 3A). She was treated with intravenous heparin for 5 days without evidence of angiographic thrombus dissolution. A laser thrombolysis (Palomar Medical, Portland, Ore.) procedure was scheduled. However, IVUS imaging showed abundant and heavily calcified atherosclerotic material with rounded contours protruding into the lumen corresponding to the filling defects (Fig. 3, right). Consequently,
the angioplasty strategy was changed. After rotational atherectomy a Palmaz-Schatz stent (Johnson and Johnson Interventional Systems, Warren, N.J.) was implanted with a 4% residual diameter stenosis. Coronary angioplasty of thrombus-containing lesions is associated with higher complication rates than non-thrombus-containing lesions. 1,2 Potential complications include abrupt vessel closure, distal embolization, and no reflow leading to myocardial infarction, emergent coronary artery bypass surgery, or death. As a result, treatment strategies of thrombus-containing lesions typically include the use of prolonged preprocedural anticoagulants, intraprocedural thrombolytics, or extraction atherectomy. Newer catheter treatment strategies being tested include laser thrombolysis and the rheolytic thrombectomy catheter (Possis Medical Inc., Minneapolis, Minn.). Angiographic criteria to identify intracoronary thrombus include discrete intraluminal filling defects, particularly if seen in various projections or if mobile, total occlusions with convex contours, and the presence of contrast media staining. 1,2 When angioscopy is used as the gold standard, the reported specificity of angiography for identifying thrombus is 100%.3 We present three patients with classical angiographic features ofintracoronary thrombus in whom IVUS imaging showed that the filling defects were not thrombi, but calcified (presumably atherosclerotic) masses. IVUS has proven usefifl in identifying the composition of atherosclerotic plaque. It is especially sensitive in detecting and localizing calcification as bright dense echoes associated with acoustic shadowing. 4 In conclusion, angiographic images of filling defects in the coronary arteries do not invariably indicate the presence of thrombus. Preintervention 1VUS imaging is usehfl in detecting the calcific nature of intracoronary filling defects. REFERENCES
1. PopmaJJ and BashoreTM.Qualitativeand quantitative angiography. In: Topo]EJ, editor. Textbookof interventional cardiology.Philadelphia: W.B.Saunders Co., 1994:1052-68.
Volume 132, Number 3 American Heart Journal
2. Mabin TA, Holmes DR, Smith HC, Vliestra RE, Bobe AA, Reeder GS, et al. Intracoronary thrombus: role in coronary occlusion complicating percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1985;5:198-202. 3. den Heijer P, Foley DP, Escaned J, Hillege HL, van Dijk RB, Serruys PW, et al. Angioscopic versus angiographic detection ofintimal dissection and intracorenary thrombus. J Am Coll Cardio] 1994;24:649-54. 4. Mintz GS, Douek P, Pichard AD, Kent KM, Satler LF, Popma J J, et al. Target lesion calcification in coronary artery disease: an intravascular ultrasound study. J Am Coll Cardiol 1992;20:1149-55.
Diagnosis of mitral valve aneurysms by transesophageal echocardiography Ariel Roguin, MD, a Diana Rinkevich, MD, a Simcha Milo, MD, b and Shimon A. Reisner, MD a
Haifa, Israel Mitral valve aneurysm (MVAN) is an infrequent complication most commonly associated with aortic valve infective endocarditis.l-2 The most probable mechanism for the formation of MVAN in these patients is destruction and infection of the anterior mitral valve leaflet by the highvelocity aortic regurgitation jet. 2 There have been rare reports of MVAN in patients with connective-tissue diseases such as Marfan syndrome 3 and in patients with mitral valve prolapse. 4 MVAN of the posterior mitral valve leaflet is exceptionally rare. 5-6 We report on three cases of MVAN from two different causes. Two patients had anterior mitral leaflet with documented aortic valve endocarditis, and one had MVAN of the posterior leaflet with no evidence of infective endocarditis. Case 1. A 38-year-old man with a 1-month history of dyspnea, fatigue, and low-grade fever was admitted to the hospital. Six years earlier the patient had had infective endocarditis with a residual mitral and aortic regurgitation. Blood pressure was 150/30 mm Hg, heart rate 100 beats/min, and regular and body temperature 37.4 ° C. The heart was enlarged. There was a grade 3/6 systolic murmur at the apex and a grade 2/4 aortic diastolic murmur. The lungs were clear, and there was no hepatomegaly. The spleen was palpable 1 cm below the left costal margin. The peripheral pulsations were Corrigan in type. Other findings of the examination were normal, and there were no other infective endocarditis signs. There was leukocytosis (ll,300/mm 3) with an elevated erythrocyte sedimentation rate (70 mm/hr). Blood cultures grew Staphylococcus epidermis. An ECG showed sinus rhythm, normal QRS axis, left atrial enlargement, and left ventricular hypertrophy. The chest radiographs confirmed the presence of cardiomegaly. Transesophageal echocardiography demonFrom the Departments of aCardiology and bCardiac Surgery, Rambam Medical Center, Technion Faculty of Medicine. Reprint requests: Shimon A. Reisner, MD, Department of Cardiology, Box 9602, Rambam Medical Center, Haifa 31096, Israel. Am Heart J 1996;132:689-91. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4]4/71999
Roguin et
al.
689
strated left ventricular enlargement with normal systolic function. An abscess was seen at the posterior part of the aortic root with left aortic valve cusp vegetations. In the anterior mitral valve leaflet another vegetation was seen with an aneurysm near its midpoint (Fig. 1). The aneurysm bulged toward the left atrium during systole. The Doppler examination revealed severe aortic regurgitation and a moderate mitral regurgitation. The aortic regurgitant jet struck the anterior mitral leaflet. The patient was initially treated with antibiotics but, because of aortic regurgitation aggravation and hemodynamic deterioration, he had aortic valve replacement with mitral valvuloplasty. The aneurysm of the anterior mitra] valve leaflet was confirmed during surgery. Histologic examination of the resected segments showed focal fibrin deposits and acute inflammation foci, with gram-positive colonies consistent with the diagnosis of infective endocarditis. The postoperative recovery was uneventful. Case 2. A 40-year-old man with a 2-month history of low-grade fever and fatigue was admitted to the hospital. Physical examination findings were normal except for a grade 3/6 systolic murmur at the apex. There was anemia (8.7 gm/dl) with an elevated erythrocyte sedimentation rate (86 mm/hr). Blood cultures grew Streptococcus viridans. Transthoracic echocardiography revealed vegetations in the left aortic valve cusp and in the anterior mitral valve leaflet. The patient was treated with antibiotics for 7 weeks. Transesophageal echocardiography in the follow-up clinic revealed an aneurysm in the anterior mitral valve leaflet near its midpoint. The patient refused surgery. Case 3. A 73-year-old man who had had a myocardial infarction and coronary artery bypass graft 8 years earlier underwent surgery for a small bowel Obstruction after sigmoidectomy. Complete atrioventricular block developed the night after the abdominal operation. Blood pressure was 156/72 mm Hg, heart rate 50 beats/min, and regular and body temperatures 36.4 ° C. There was a grade 3/6 systolic murmur over the precordium. On postoperative day 3, the patient's body temperature rose to 39 ° C. Transthoracic echocardiography was not conclusive of infective endocarditis findings. Transesophageal echocardiography demonstrated moderate left ventricular enlargement with preserved systolic function. In the posterior mitral valve leaflet an aneurysm was seen (Fig. 2). Both mitral leaflets appeared myxomatous. Doppler examination revealed moderate to severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary hypertension. The aortic valve was normal. Fever disappeared after 2 days. All blood cultures were negative. The patient was referred to the cardiology outpatient clinic. MVAN is an infrequent complication most commonly associated with aortic valve endocarditis. 1-2 As presented here in our first and second case reports, MVAN in patients with aortic valve infective endocarditis appears on the anterior mitral leaflet and probably results from the infected high-velocity blood jet of aortic regurgitation. As a result of a focal disease with otherwise normal mitral leaflet structure, MVAN in infective endocarditis is small and
Duissaillant et al.
687
Intravascular ultrasound identification of calcified intraluminal lesions misdiagnosed as thrombi by coronary angiography Gaston R. Duissaillant, MD, Gary S. Mintz, MD, Augusto D. Pichard, MD, Kenneth M. Kent, MD, PhD, Lowell F. Satler, MD, Jeffrey J. Popma, MD, Jennifer Griffin, BS, and Martin B. Leon, MD
Washington, D.C. Accurate identification of coronary atherosclerotic plaque composition is important for optimum patient management and transcatheter therapy. In particular, the presence ofthrombus typically leads to protracted hospitalization, intravenous or intracoronary thrombolysis, prolonged systemic anticoagulation, and the use oftranscatheter devices designed to remove thrombi. Furthermore, thrombi may be implicated in poor outcome after transcatheter therapy. Intraluminal filling defects are believed to be the most specific angiographic markers of thrombus. We report three patients with intracoronary filling defects initially diagnosed as thrombus; however, intravascular ultrasound (IVUS) imaging showed that these filling defects represented calcified nodules. IVUS studies were performed with one of two commercially available systems. The first (Cardiovascular Imaging Systems Inc./InterTherapy Inc., Sunnyvale, Calif.) incorporated a single element 25-MHz transducer and an angled mirror mounted on the tip of a flexible shaft that was rotated at 1800 rpm within a 3.9F short monorail polyethylene imaging sheath to form planar cross-sectional images in real time. The second (Cardiovascular Imaging Systems) incorporated a single element 30-MHz beveled transducer within either a 2.9F long monorail imaging catheter having a common distal lumen design (the distal lumen alternatively accommodates the imaging core or the guide wire, but not both) or within a 3.2F short monorail imaging catheter. With both systems the imaging catheter was advanced 5 to 10 mm beyond the target lesion and the transducer was withdrawn automatically at 0.5 mm/sec within the imaging sheath to perform the imaging sequence. IVUS studies were recorded on ~-inch high resolution s-VHS tape for offiine analysis. Patient 1. A 78-year-old white man with a history of pneumoconiosis, gastrectomy for stomach cancer, congestive heart failure from dilated cardiomyopathy, and coronary artery disease was seen for progressive angina. A From the Intravascular Ultrasound Imaging and Cardiac Catheterization Laboratories, Washington Hospital Center. Supported in part by the Cardiology Research Foundation, Washington, D.C. Reprint requests: Martin B. Leon, MD, Washington Cardiology Center, 110 Irving St., NW, 4B-1, Washington, DC 20010. Am Heart J 1996;132:687-9. Copyright © 1996 by Mosby-Ye~r Book, Inc. 0002-8703/96/$5.00 + 0 4/4/71990
Fig. 1. Proximal right coronary artery filling defect (arrow) was initially thought to represent intracoronary thrombus. Patient was treated with prolonged system anticoagulation, intracoronary thrombolysis, and extraction atherectomy. IVUS imaging showed that filling defect was, in fact, calcified lesion protruding into lumen.
Fig. 2. Mid-right coronary artery filling defect (arrow) was initially thought to represent intracoronary thrombus. Patient was also treated with prolonged systemic anticoagulation. IVUS imaging showed that filling defect was, in fact, calcified lesion protruding into the lumen. Because of limited device availability, patient was referred for bypass graft surgery. coronary angiogram showed a 95% ostial fight coronary artery lesion with a round filling defect highly suggestive ofthrombus. He was treated with heparin and sent home taking coumadin to dissolve the thrombus. However, he returned with worsening angina; coronary angiography still showed a large filling defect almost completely occluding the right coronary artery (Fig. 1). He was initially treated with an intracoronary urokinase infusion of 250,000 U followed by the use of a 2.2-mm transluminal extraction atherectomy cutter (Interventional Technologies, Inc., San Diego, Calif.) and 3.5-ram adjunct balloon
688
September 1996 American Heart Journal
Duissaillant et al.
Fig. 3. Proximal left anterior descending coronary artery filling defect (large arrow, left) was initially thought to represent intracoronary thrombus. Patient was treated with prolonged systemic anticoagulation and was scheduled for laser thrombolysis. IVUS imaging (right) showed that filling defect was, in fact, calcified lesion. IVUS illustration is series of four cross-sectional image slices taken 2 mm apart. Double arrows indicate leading edge of calcium protruding into lumen on each of four slices. Patient was treated with rotational atherectomy followed by endovascular stent placement. inflation. A residual hazy 35% stenosis remained. IVUS imaging performed to assess the angioplasty result revealed a heavily calcified proximal right coronary artery and a markedly eccentric plaque that protruded from the arterial wall into the lumen corresponding to the anglographic falling defect. After final dilatation with a 4.0-ram balloon, a 23% residual stenosis remained. Patient 2. A 72-year-old white man with a history of myocardial infarction underwent preoperative assessment for radical prostate surgery. A thallium scan disclosed myocardial ischemia. Cardiac catheterization showed 3+ mitral regurgitation, left anterior descending artery occlusion receiving good collateral flow from the right coronary artery, and a large filling defect in the mid-right coronary artery consistent with thrombus (Fig. 2). He was consequently treated with heparin for 2 weeks. However, repeat coronary angiography showed persistence of the right coronary artery filling defect. IVUS revealed circumferential calcium as well as a calcified, eccentric, atherosclerotic lesion protruding into the lumen corresponding to the angiographic filling defect. In the absence of a transcatheter device designed to treat calcific lesions (the Rotablator, Heart Technology, Bellevue, Wash, had been recalled and was not available), the patient underwent elective cardiac surgery before radical prostatectomy. Patient 3. An 84-year-old woman was seen with prolonged chest pain and creatinine kinase elevation consistent with non-Q-wave myocardial infarction. Because of recurrent chest pain, coronary angiography was performed and showed a severe proximal left anterior descending stenosis with filling defects indicative of thrombus (Fig. 3A). She was treated with intravenous heparin for 5 days without evidence of angiographic thrombus dissolution. A laser thrombolysis (Palomar Medical, Portland, Ore.) procedure was scheduled. However, IVUS imaging showed abundant and heavily calcified atherosclerotic material with rounded contours protruding into the lumen corresponding to the filling defects (Fig. 3, right). Consequently,
the angioplasty strategy was changed. After rotational atherectomy a Palmaz-Schatz stent (Johnson and Johnson Interventional Systems, Warren, N.J.) was implanted with a 4% residual diameter stenosis. Coronary angioplasty of thrombus-containing lesions is associated with higher complication rates than non-thrombus-containing lesions. 1,2 Potential complications include abrupt vessel closure, distal embolization, and no reflow leading to myocardial infarction, emergent coronary artery bypass surgery, or death. As a result, treatment strategies of thrombus-containing lesions typically include the use of prolonged preprocedural anticoagulants, intraprocedural thrombolytics, or extraction atherectomy. Newer catheter treatment strategies being tested include laser thrombolysis and the rheolytic thrombectomy catheter (Possis Medical Inc., Minneapolis, Minn.). Angiographic criteria to identify intracoronary thrombus include discrete intraluminal filling defects, particularly if seen in various projections or if mobile, total occlusions with convex contours, and the presence of contrast media staining. 1,2 When angioscopy is used as the gold standard, the reported specificity of angiography for identifying thrombus is 100%.3 We present three patients with classical angiographic features ofintracoronary thrombus in whom IVUS imaging showed that the filling defects were not thrombi, but calcified (presumably atherosclerotic) masses. IVUS has proven usefifl in identifying the composition of atherosclerotic plaque. It is especially sensitive in detecting and localizing calcification as bright dense echoes associated with acoustic shadowing. 4 In conclusion, angiographic images of filling defects in the coronary arteries do not invariably indicate the presence of thrombus. Preintervention 1VUS imaging is usehfl in detecting the calcific nature of intracoronary filling defects. REFERENCES
1. PopmaJJ and BashoreTM.Qualitativeand quantitative angiography. In: Topo]EJ, editor. Textbookof interventional cardiology.Philadelphia: W.B.Saunders Co., 1994:1052-68.
Volume 132, Number 3 American Heart Journal
2. Mabin TA, Holmes DR, Smith HC, Vliestra RE, Bobe AA, Reeder GS, et al. Intracoronary thrombus: role in coronary occlusion complicating percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1985;5:198-202. 3. den Heijer P, Foley DP, Escaned J, Hillege HL, van Dijk RB, Serruys PW, et al. Angioscopic versus angiographic detection ofintimal dissection and intracorenary thrombus. J Am Coll Cardio] 1994;24:649-54. 4. Mintz GS, Douek P, Pichard AD, Kent KM, Satler LF, Popma J J, et al. Target lesion calcification in coronary artery disease: an intravascular ultrasound study. J Am Coll Cardiol 1992;20:1149-55.
Diagnosis of mitral valve aneurysms by transesophageal echocardiography Ariel Roguin, MD, a Diana Rinkevich, MD, a Simcha Milo, MD, b and Shimon A. Reisner, MD a
Haifa, Israel Mitral valve aneurysm (MVAN) is an infrequent complication most commonly associated with aortic valve infective endocarditis.l-2 The most probable mechanism for the formation of MVAN in these patients is destruction and infection of the anterior mitral valve leaflet by the highvelocity aortic regurgitation jet. 2 There have been rare reports of MVAN in patients with connective-tissue diseases such as Marfan syndrome 3 and in patients with mitral valve prolapse. 4 MVAN of the posterior mitral valve leaflet is exceptionally rare. 5-6 We report on three cases of MVAN from two different causes. Two patients had anterior mitral leaflet with documented aortic valve endocarditis, and one had MVAN of the posterior leaflet with no evidence of infective endocarditis. Case 1. A 38-year-old man with a 1-month history of dyspnea, fatigue, and low-grade fever was admitted to the hospital. Six years earlier the patient had had infective endocarditis with a residual mitral and aortic regurgitation. Blood pressure was 150/30 mm Hg, heart rate 100 beats/min, and regular and body temperature 37.4 ° C. The heart was enlarged. There was a grade 3/6 systolic murmur at the apex and a grade 2/4 aortic diastolic murmur. The lungs were clear, and there was no hepatomegaly. The spleen was palpable 1 cm below the left costal margin. The peripheral pulsations were Corrigan in type. Other findings of the examination were normal, and there were no other infective endocarditis signs. There was leukocytosis (ll,300/mm 3) with an elevated erythrocyte sedimentation rate (70 mm/hr). Blood cultures grew Staphylococcus epidermis. An ECG showed sinus rhythm, normal QRS axis, left atrial enlargement, and left ventricular hypertrophy. The chest radiographs confirmed the presence of cardiomegaly. Transesophageal echocardiography demonFrom the Departments of aCardiology and bCardiac Surgery, Rambam Medical Center, Technion Faculty of Medicine. Reprint requests: Shimon A. Reisner, MD, Department of Cardiology, Box 9602, Rambam Medical Center, Haifa 31096, Israel. Am Heart J 1996;132:689-91. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4]4/71999
Roguin et
al.
689
strated left ventricular enlargement with normal systolic function. An abscess was seen at the posterior part of the aortic root with left aortic valve cusp vegetations. In the anterior mitral valve leaflet another vegetation was seen with an aneurysm near its midpoint (Fig. 1). The aneurysm bulged toward the left atrium during systole. The Doppler examination revealed severe aortic regurgitation and a moderate mitral regurgitation. The aortic regurgitant jet struck the anterior mitral leaflet. The patient was initially treated with antibiotics but, because of aortic regurgitation aggravation and hemodynamic deterioration, he had aortic valve replacement with mitral valvuloplasty. The aneurysm of the anterior mitra] valve leaflet was confirmed during surgery. Histologic examination of the resected segments showed focal fibrin deposits and acute inflammation foci, with gram-positive colonies consistent with the diagnosis of infective endocarditis. The postoperative recovery was uneventful. Case 2. A 40-year-old man with a 2-month history of low-grade fever and fatigue was admitted to the hospital. Physical examination findings were normal except for a grade 3/6 systolic murmur at the apex. There was anemia (8.7 gm/dl) with an elevated erythrocyte sedimentation rate (86 mm/hr). Blood cultures grew Streptococcus viridans. Transthoracic echocardiography revealed vegetations in the left aortic valve cusp and in the anterior mitral valve leaflet. The patient was treated with antibiotics for 7 weeks. Transesophageal echocardiography in the follow-up clinic revealed an aneurysm in the anterior mitral valve leaflet near its midpoint. The patient refused surgery. Case 3. A 73-year-old man who had had a myocardial infarction and coronary artery bypass graft 8 years earlier underwent surgery for a small bowel Obstruction after sigmoidectomy. Complete atrioventricular block developed the night after the abdominal operation. Blood pressure was 156/72 mm Hg, heart rate 50 beats/min, and regular and body temperatures 36.4 ° C. There was a grade 3/6 systolic murmur over the precordium. On postoperative day 3, the patient's body temperature rose to 39 ° C. Transthoracic echocardiography was not conclusive of infective endocarditis findings. Transesophageal echocardiography demonstrated moderate left ventricular enlargement with preserved systolic function. In the posterior mitral valve leaflet an aneurysm was seen (Fig. 2). Both mitral leaflets appeared myxomatous. Doppler examination revealed moderate to severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary hypertension. The aortic valve was normal. Fever disappeared after 2 days. All blood cultures were negative. The patient was referred to the cardiology outpatient clinic. MVAN is an infrequent complication most commonly associated with aortic valve endocarditis. 1-2 As presented here in our first and second case reports, MVAN in patients with aortic valve infective endocarditis appears on the anterior mitral leaflet and probably results from the infected high-velocity blood jet of aortic regurgitation. As a result of a focal disease with otherwise normal mitral leaflet structure, MVAN in infective endocarditis is small and