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Evaluation of pseudoaneurysm of the left ventricle by echocardiography and pulsed Doppler
Jun.1987 1508
Brief Communications
Amorlcan
Heart
Journal
Fig. 3. Cross-sectional view of stenotic human coronary artery following balloon angioplasty. Note the roughened intraluminal surface with intimal flaps (krrge arrows) and intimal tear (small arrow). Fig. 4. Magnified cross-sectionalview of atherosclerotic human coronary arterial wall after balloon angioplasty is followed by treatment with the Unicorn Cap-TM. Note the dark band of protein denaturation (large arrow) caused by the thermal effect adjacent to the stenotic channel. Intimal flap also appearsto be tacked down by the thermal process(small arrow).
human atherosclerotic disease by fiberoptic laser-heated metal cautery cap. AM HEART J 19&1,107:777. 2. Lee G. ReisRL. Ghan MC. Boaan MD. Lee MH. Low RI. Arge& A, Han&h H, Mason I%‘. Clinical laser r&anal& tion of coronary obstruction-angioecopic and angiographic - - . documentation; Chest 1986;90:776. 3. Lee G, Garcia JM, Chan MC, Corso PJ, Bacos J, Lee MH, Pichard A, Reis RL, Mason DT. Clinically successful longterm laser coronary recanahzation. AM HEART J 1986; 1129323.
4. Lee G, Reis RL, Boggan MD, Chan MC, Lee MH, Low RI, Hannah H. Mason DT. Laser recanalixation in severe endstage peripheral vascular disease. Am J Cardiol 1987; 59386. 5. Lee G, Ikeda RM, Chan MC, Lee MH, Riik JL, Reis RL, Theis JH, Low RI, Bommer WJ, Kung AH, Hanna ES, Mason DT. Limitations, risks, and complications of laser recanalixation: A cautious approach warranted. Am J Cardiol 1985;56:181. 6. Lee G, Ghan MC, Ikeda RM, Rink JL, Dukich J, Peterson L, Lee K, Reis RL, Mason DT. Applicability of laser to assist coronary halloon angioplasty. AM m J 1985; 110~1233.
Evahmtion of paeu&anwyem ventricle by Doppler William
E. Smeal, M.D.,
of We left
Sinda B. Dianxumba,
M.D.,
and Claude R. Joyner, M.D. Pittsburgh, Pa.
From the Department of Medicine (The Non-Invasive Laboratory), Allegheny General Hospital and the Univeraity of Pittsburgh. Reprint requests William E. SmeaI, M.D., The Non-Invasive Laboratory, Dept. of Medicine, AIIegheny General Hospital, 320 East North Ave., Pittsburgh, PA 15212.
Pseudoaneurysmsof the left ventricle result from a localized perforation in the ventricular myocardium. DifIerentiation from a true aneurysmmust be madebecauseof the significant potential of a pseudoaneurysm to rupture. Evidence supporting the diagnosisof a pseudoaneurysm may be obtained from ventriculography,’ echocardiography: 3 pulsed Doppler,+6 and gated radionuclide blood pool imaging.6Thesedifferent proceduresare complementary. In a given patient one procedure may give more specific evidencethan others to support the diagnosisof a pseudoaneurysm.This report presents a patient with a left ventricular pseudoaneurysm.The diagnosiswasmade by two-dimensional echocardiography and pulsed Doppler. A ‘IQyear-old white woman suddenly slumpedover and becameunresponsivewhile taIking to her daughter. She had been dischargedfrom the hospital 2 days previously, after having beenhospitalixed for an uncomplicated lateral wall my-dial infarction. Initial physical examination revealed a very lethargic woman who was only able to follow simple commands.Her systolic blond pressurewas 70 mm Hg. She had jugular venous distensionto the angle of the jaw at 30 degreesand a few posterior basilar rales. Cardiac exam& tion was unremarkable. Electrolytes, blood urea nitrogen, glucose,and hemoglobin were unremarkable. Cheat x-ray examination showed cardiac enlargementwithout signsof congestiveheart failure. The ECG showed sinus t@yoardia at 110 per minute and nonspecific ST segment and T wave changesin leads I, aV,, and V,. She was initially treated with dopamine and her blood pressureimproved. Her subsequentchest x-ray films and physical examination showedgradual development of congestive heart failure, which responded to diuresis. Serial ECGs over the next 2 weeks were unre-
markable, except for decreasingvoltage and nonspecificT
Volume Number
113 6
Brief Communications
Fig. 1. Panel A, Still frame from the two-dimensional echocardiogramof the pseudoaneurysm(PSI. Panel B, Pulsed Doppler interrogation with the samplevolume positioned in the neck of the pseudoaneurysm, with Doppler profile (DPj demonstrating both systolic and diastolic flow. Panel C, Left ventriculogram in the right anterior oblique projection (systolic frame) showing the aneurysm (AN) overlapping the inferior wall (arrowheads). Panel D, Schematic drawing of the pseudoaneurysm(PS). A0 = aortic root; C = mitral chordae tendineae; LA = left atrium: LV = left ventricle; N = neck of the pseudoaneurysm;S = samplevolume; RV = right ventricle.
Fig. 2. Left panel, Gross specimen and corresponding drawing of the heart with an incision made through the anterior wall, apex, and diaphragmatic wall in a plane parallel to the septum. Right panel, Gross specimen and drawing of the interior of the left ventricular wall at the site of perforation. a = posterior wall of the left ventricle; b = probe exiting the neck of the pseudoaneurysm;c = fresh thrombus in the pericardial cavity; d = left ventricular cavity; e = pericardium; f = posterior mitral leaflet; g = probe entering neck of the pseudoaneurysm.
1509
1510
Brief
Communications
wave changes in leads V5 and V,. Holter monitor was unremarkable. Serial hemoglobulin measurementswere stable despite occult blood in her stools. Upper gastrointestinal seriesand barium enemawere normal. Echocardiogram performed 21 days after hospitalization showeda pseudoaneurysm,at which time she was transferred to Allegheny General Hospital. The two-dimensionalechocardiogramwasrepeated and showed a defect in the posterior-lateral wall of the left ventricle leading into a pseudoaneurysm(Fig. 1, A). There wasa small areaof hypokinesis in the left ventricular wall adjacent to the pseudoaneurysm.Left and right ventricular function was otherwise normal. There wasa moderate pericardial effusion. Doppler examination showedturbulent systolic and diastolic flow within the neck of pseudoaneurysm (Fig. 1, B). Cardiac catheterization was performed. Pertinent findings on coronary angiography included minimal and delayed filling of an obtusemarginal branch of the circumflex artery, total occlusion of the proximal right coronary artery, and a left coronary artery dominance system. The left ventriculogram in the left anterior oblique projection showeda smallarea of akinesis in the posterior lateral wall. The left ventriculogram in the right anterior oblique projection (Fig. 1, C) during systole showedan area in the region of the posterior lateral wall that was akinetic and overlapped the inferior wall. Both projections failed to define the neck (Fig. 1, D) of the pseudoaneurysm.Unfortunately, on the second hospital day at Allegheny General Hospital the pseudoaneurysm ruptured and the patient died. Autopsy showed a tense bloody pericardial effusion with fresh thrombus, perforation in the posterior-lateral wall of the left ventricle, and organized thrombus on the epicardium around the site of the perforation (Fig. 2). There wasevidence of a localized posterior-lateral myocardial infarction and infarction of a papillary musclein the right ventricle. The differentiation between a true aneurysm and a pseudoaneurysmis of critical importance. The wall of a true aneurysm contains infarcted musclewhich, although damaged, has considerably more resistance to rupture than that of a pseudoaneurysm.The wall of a pseudoaneurysm is madeof organized thrombus and overlying adherent pericardium. The other distinction between a true aneurysmand a pseudoaneurysmis the size of the communication between the ventricular cavity and the aneurysm itself. In a pseudoaneurysm,the communication is considerably smaller, and is a localized perforation of the ventricular wall in an area of infarction or trauma. Cardiac catheterization may not define the neck of a pseudoaneurysm. This may be secondary to the wall of the pseudoaneurysm abutting on that of the ventricular cavity (Fig. 1, D). The pseudoaneurysmmay curve around the ventricle in such a way that the contrast material in the pseudoaneurysm and that in the ventricle blend together. This may make the communication between the ventricular cavity and the pseudoaneurysmappear much larger, thus misleading the observer into interpreting the angiogram as showing a true aneurysm. As has been previously described: this case illustrates that two-dimensional
American
June 1987 Heart Journal
echocardiographymay prove, in somepatients, to be more helpful than the ventriculogram in making the diagnosis of left ventricular pseudoaneurysm.It may define the neck of the pseudoaneurysmmore clearly. Furthermore, pulsed Doppler can demonstrate turbulent flow in the neck and help to exclude artifact such as echo drop-out. REFERENCES
1. HigginsCG,Lipton MJ. JohnsonAD, PetersonKL, Viewex Wiik. Falsean&rrysmsof the left ventricle.Identificationof distinctive clinical radiographicand angiographicfeatures. Radiology1978;127:21. 2. Catherweod E, Mintz GS,Kotler MN, Parry WR, SegaIBL. Two-dimensional echocardiographic recognitionof left ventricular pseudoaneurysm. Circulation1980;62:294. 3. RoelsndtJ, van denBrand M, Vletter WB, NautaJ, Hugenholtz PG.Echocardiographic diagnosis of pseudoaneurysm of the left ventricle.Circulation1975:52:466. 4. GrubeE, RedelD, Janson R. Non-invasivediagnosis of a false left ventricular aneurysmby echocardiography and pulsed Dopplerechocardiography. Br Heart J 1980,43:232. 5. Wendel CH. CornmanCR. DianzumbaSB. Diaxnosisof pseudoaneurysm of the ascending aorta by pulsed-Doppler crosssectionalechocardiography. Br Heart J 1985;53:567. 6. Botvinick EH, Shames D, HutchinsonJC, RoeBB, Fitzpatrick M. Noninvasivediagnosisof a false left ventricular aneurysmwith radioisotopegatedcardiacbloodpool imaging. Differentiation from true aneurysm.Am J Cardiol 1976;37:1089. I. SearsTD, OngYS, StarkeH, Forker AD. Ventricular pseudoaneurysm identified by cross-sectional echocardiography. Ann Intern Med 1979;90:935.
Thrombosed aorta resuttkrg in &einal cord ischemia and paraplegia in ischemic cardiomyopathy Gurpreet Kochar, M.D., Morris N. Kotler, M.D., John Hartman, M.D.,* * Steven E. Goldberg, M.D., Wayne Parry, R. Parameswaran,M.D., and Mary Scanlon, M.D.* Philadelphia, Pa.
A number of complications have been associatedwith left ventricular dysfunction, including low cardiac output, pulmonary edema,and mural thrombi in the left ventricle with embolization to the peripheral or central vessels.We describe a patient with ischemic cardiomyopathy who developed anterior spinal artery syndrome secondary to &hernia of the great anterior medullary artery of Adamkiewicz as a result of mural thrombus of the abdominal aorta. A 66-year-old black man with a past history of anterolateral myocardial infarction, ischemic cardiomyopathy, From the Department and the **Pathology cal Center, Northern
of Medicine-Division of Cardiovascular Disease, and *Radiology Departments, Albert, Einstein MediDivision, Temple University School of Medicine.
Reprint requests: Morris N. Kotler, M.D., Albert Einstein York & Tabor Rds., 3rd Floor, Klein Bldg., Philadelphia,
Medical Center, PA 19x41.
Brief Communications
Amorlcan
Heart
Journal
Fig. 3. Cross-sectional view of stenotic human coronary artery following balloon angioplasty. Note the roughened intraluminal surface with intimal flaps (krrge arrows) and intimal tear (small arrow). Fig. 4. Magnified cross-sectionalview of atherosclerotic human coronary arterial wall after balloon angioplasty is followed by treatment with the Unicorn Cap-TM. Note the dark band of protein denaturation (large arrow) caused by the thermal effect adjacent to the stenotic channel. Intimal flap also appearsto be tacked down by the thermal process(small arrow).
human atherosclerotic disease by fiberoptic laser-heated metal cautery cap. AM HEART J 19&1,107:777. 2. Lee G. ReisRL. Ghan MC. Boaan MD. Lee MH. Low RI. Arge& A, Han&h H, Mason I%‘. Clinical laser r&anal& tion of coronary obstruction-angioecopic and angiographic - - . documentation; Chest 1986;90:776. 3. Lee G, Garcia JM, Chan MC, Corso PJ, Bacos J, Lee MH, Pichard A, Reis RL, Mason DT. Clinically successful longterm laser coronary recanahzation. AM HEART J 1986; 1129323.
4. Lee G, Reis RL, Boggan MD, Chan MC, Lee MH, Low RI, Hannah H. Mason DT. Laser recanalixation in severe endstage peripheral vascular disease. Am J Cardiol 1987; 59386. 5. Lee G, Ikeda RM, Chan MC, Lee MH, Riik JL, Reis RL, Theis JH, Low RI, Bommer WJ, Kung AH, Hanna ES, Mason DT. Limitations, risks, and complications of laser recanalixation: A cautious approach warranted. Am J Cardiol 1985;56:181. 6. Lee G, Ghan MC, Ikeda RM, Rink JL, Dukich J, Peterson L, Lee K, Reis RL, Mason DT. Applicability of laser to assist coronary halloon angioplasty. AM m J 1985; 110~1233.
Evahmtion of paeu&anwyem ventricle by Doppler William
E. Smeal, M.D.,
of We left
Sinda B. Dianxumba,
M.D.,
and Claude R. Joyner, M.D. Pittsburgh, Pa.
From the Department of Medicine (The Non-Invasive Laboratory), Allegheny General Hospital and the Univeraity of Pittsburgh. Reprint requests William E. SmeaI, M.D., The Non-Invasive Laboratory, Dept. of Medicine, AIIegheny General Hospital, 320 East North Ave., Pittsburgh, PA 15212.
Pseudoaneurysmsof the left ventricle result from a localized perforation in the ventricular myocardium. DifIerentiation from a true aneurysmmust be madebecauseof the significant potential of a pseudoaneurysm to rupture. Evidence supporting the diagnosisof a pseudoaneurysm may be obtained from ventriculography,’ echocardiography: 3 pulsed Doppler,+6 and gated radionuclide blood pool imaging.6Thesedifferent proceduresare complementary. In a given patient one procedure may give more specific evidencethan others to support the diagnosisof a pseudoaneurysm.This report presents a patient with a left ventricular pseudoaneurysm.The diagnosiswasmade by two-dimensional echocardiography and pulsed Doppler. A ‘IQyear-old white woman suddenly slumpedover and becameunresponsivewhile taIking to her daughter. She had been dischargedfrom the hospital 2 days previously, after having beenhospitalixed for an uncomplicated lateral wall my-dial infarction. Initial physical examination revealed a very lethargic woman who was only able to follow simple commands.Her systolic blond pressurewas 70 mm Hg. She had jugular venous distensionto the angle of the jaw at 30 degreesand a few posterior basilar rales. Cardiac exam& tion was unremarkable. Electrolytes, blood urea nitrogen, glucose,and hemoglobin were unremarkable. Cheat x-ray examination showed cardiac enlargementwithout signsof congestiveheart failure. The ECG showed sinus t@yoardia at 110 per minute and nonspecific ST segment and T wave changesin leads I, aV,, and V,. She was initially treated with dopamine and her blood pressureimproved. Her subsequentchest x-ray films and physical examination showedgradual development of congestive heart failure, which responded to diuresis. Serial ECGs over the next 2 weeks were unre-
markable, except for decreasingvoltage and nonspecificT
Volume Number
113 6
Brief Communications
Fig. 1. Panel A, Still frame from the two-dimensional echocardiogramof the pseudoaneurysm(PSI. Panel B, Pulsed Doppler interrogation with the samplevolume positioned in the neck of the pseudoaneurysm, with Doppler profile (DPj demonstrating both systolic and diastolic flow. Panel C, Left ventriculogram in the right anterior oblique projection (systolic frame) showing the aneurysm (AN) overlapping the inferior wall (arrowheads). Panel D, Schematic drawing of the pseudoaneurysm(PS). A0 = aortic root; C = mitral chordae tendineae; LA = left atrium: LV = left ventricle; N = neck of the pseudoaneurysm;S = samplevolume; RV = right ventricle.
Fig. 2. Left panel, Gross specimen and corresponding drawing of the heart with an incision made through the anterior wall, apex, and diaphragmatic wall in a plane parallel to the septum. Right panel, Gross specimen and drawing of the interior of the left ventricular wall at the site of perforation. a = posterior wall of the left ventricle; b = probe exiting the neck of the pseudoaneurysm;c = fresh thrombus in the pericardial cavity; d = left ventricular cavity; e = pericardium; f = posterior mitral leaflet; g = probe entering neck of the pseudoaneurysm.
1509
1510
Brief
Communications
wave changes in leads V5 and V,. Holter monitor was unremarkable. Serial hemoglobulin measurementswere stable despite occult blood in her stools. Upper gastrointestinal seriesand barium enemawere normal. Echocardiogram performed 21 days after hospitalization showeda pseudoaneurysm,at which time she was transferred to Allegheny General Hospital. The two-dimensionalechocardiogramwasrepeated and showed a defect in the posterior-lateral wall of the left ventricle leading into a pseudoaneurysm(Fig. 1, A). There wasa small areaof hypokinesis in the left ventricular wall adjacent to the pseudoaneurysm.Left and right ventricular function was otherwise normal. There wasa moderate pericardial effusion. Doppler examination showedturbulent systolic and diastolic flow within the neck of pseudoaneurysm (Fig. 1, B). Cardiac catheterization was performed. Pertinent findings on coronary angiography included minimal and delayed filling of an obtusemarginal branch of the circumflex artery, total occlusion of the proximal right coronary artery, and a left coronary artery dominance system. The left ventriculogram in the left anterior oblique projection showeda smallarea of akinesis in the posterior lateral wall. The left ventriculogram in the right anterior oblique projection (Fig. 1, C) during systole showedan area in the region of the posterior lateral wall that was akinetic and overlapped the inferior wall. Both projections failed to define the neck (Fig. 1, D) of the pseudoaneurysm.Unfortunately, on the second hospital day at Allegheny General Hospital the pseudoaneurysm ruptured and the patient died. Autopsy showed a tense bloody pericardial effusion with fresh thrombus, perforation in the posterior-lateral wall of the left ventricle, and organized thrombus on the epicardium around the site of the perforation (Fig. 2). There wasevidence of a localized posterior-lateral myocardial infarction and infarction of a papillary musclein the right ventricle. The differentiation between a true aneurysm and a pseudoaneurysmis of critical importance. The wall of a true aneurysm contains infarcted musclewhich, although damaged, has considerably more resistance to rupture than that of a pseudoaneurysm.The wall of a pseudoaneurysm is madeof organized thrombus and overlying adherent pericardium. The other distinction between a true aneurysmand a pseudoaneurysmis the size of the communication between the ventricular cavity and the aneurysm itself. In a pseudoaneurysm,the communication is considerably smaller, and is a localized perforation of the ventricular wall in an area of infarction or trauma. Cardiac catheterization may not define the neck of a pseudoaneurysm. This may be secondary to the wall of the pseudoaneurysm abutting on that of the ventricular cavity (Fig. 1, D). The pseudoaneurysmmay curve around the ventricle in such a way that the contrast material in the pseudoaneurysm and that in the ventricle blend together. This may make the communication between the ventricular cavity and the pseudoaneurysmappear much larger, thus misleading the observer into interpreting the angiogram as showing a true aneurysm. As has been previously described: this case illustrates that two-dimensional
American
June 1987 Heart Journal
echocardiographymay prove, in somepatients, to be more helpful than the ventriculogram in making the diagnosis of left ventricular pseudoaneurysm.It may define the neck of the pseudoaneurysmmore clearly. Furthermore, pulsed Doppler can demonstrate turbulent flow in the neck and help to exclude artifact such as echo drop-out. REFERENCES
1. HigginsCG,Lipton MJ. JohnsonAD, PetersonKL, Viewex Wiik. Falsean&rrysmsof the left ventricle.Identificationof distinctive clinical radiographicand angiographicfeatures. Radiology1978;127:21. 2. Catherweod E, Mintz GS,Kotler MN, Parry WR, SegaIBL. Two-dimensional echocardiographic recognitionof left ventricular pseudoaneurysm. Circulation1980;62:294. 3. RoelsndtJ, van denBrand M, Vletter WB, NautaJ, Hugenholtz PG.Echocardiographic diagnosis of pseudoaneurysm of the left ventricle.Circulation1975:52:466. 4. GrubeE, RedelD, Janson R. Non-invasivediagnosis of a false left ventricular aneurysmby echocardiography and pulsed Dopplerechocardiography. Br Heart J 1980,43:232. 5. Wendel CH. CornmanCR. DianzumbaSB. Diaxnosisof pseudoaneurysm of the ascending aorta by pulsed-Doppler crosssectionalechocardiography. Br Heart J 1985;53:567. 6. Botvinick EH, Shames D, HutchinsonJC, RoeBB, Fitzpatrick M. Noninvasivediagnosisof a false left ventricular aneurysmwith radioisotopegatedcardiacbloodpool imaging. Differentiation from true aneurysm.Am J Cardiol 1976;37:1089. I. SearsTD, OngYS, StarkeH, Forker AD. Ventricular pseudoaneurysm identified by cross-sectional echocardiography. Ann Intern Med 1979;90:935.
Thrombosed aorta resuttkrg in &einal cord ischemia and paraplegia in ischemic cardiomyopathy Gurpreet Kochar, M.D., Morris N. Kotler, M.D., John Hartman, M.D.,* * Steven E. Goldberg, M.D., Wayne Parry, R. Parameswaran,M.D., and Mary Scanlon, M.D.* Philadelphia, Pa.
A number of complications have been associatedwith left ventricular dysfunction, including low cardiac output, pulmonary edema,and mural thrombi in the left ventricle with embolization to the peripheral or central vessels.We describe a patient with ischemic cardiomyopathy who developed anterior spinal artery syndrome secondary to &hernia of the great anterior medullary artery of Adamkiewicz as a result of mural thrombus of the abdominal aorta. A 66-year-old black man with a past history of anterolateral myocardial infarction, ischemic cardiomyopathy, From the Department and the **Pathology cal Center, Northern
of Medicine-Division of Cardiovascular Disease, and *Radiology Departments, Albert, Einstein MediDivision, Temple University School of Medicine.
Reprint requests: Morris N. Kotler, M.D., Albert Einstein York & Tabor Rds., 3rd Floor, Klein Bldg., Philadelphia,
Medical Center, PA 19x41.