Transesophageal echocardiography in the detection of left ventricular pseudoaneurysm

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Fig. 2. Pathologic specimen.Histologic section of the papillary muscle,showingcompletecoagulative necrosisof the musclesurrounded by a fibrous wall. The fibrous wall is infiltrated by chronic inflammatory cells, but there is no neutrophilic infiltration. Note the absenceof nuclei and retention of cell outlines in the infarcted muscle.(Hematoxylin and eosin stain: original magnification x25.)

should be considered in patients with no other obvious causesin their history. It would appear that TEE is capable of providing a prompt and definitive diagnosisof papillary musclerupture, even when other associatedcardiac conditions may makethe echocardiographicinterpretation difficult.6 REFERENCES

Nishimura RA, et al. Papillary muscle rupture complicating acute myocardial infarction: analysis of 17 patients. Am J Cardiol 1983;51:373-7. 2. Mazzuco A, et al. Acute mitral regurgitation after blunt chest trauma. Arch Intern Med 1983:143:2326-g. 3. Garcia-Gallego F, Carratala J, Frutos A, Gamallo C, Mesa JM, Munoz JE. Rupture of the mitral posteromedial papillary muscle associated with myxomatous mitral valve. Rev Esp Cardiol 1989;42:693-6. (in Spanish) 4. Kinney EL, et al. Value of two-dimensional echocardiographic detection of incomplete mitral leaflet closure. AM HEART J

Transesophageal echocardiography the detection of left ventricular pseudoaneurysm

in

Marcus F. Stoddard, MD, Phillip R. Dawkins, MD, Rita A. Longaker, RCT, John Goad, MD, and Andrew Shih, MD Louisville, Ky.

1.

1985;109:87-90.

5. Pate1 AM, Miller FA Jr, Khandheria BK, Mullany CJ, Seward JB, Oh JK. Role of transesophageal echocardiography in the diagnosis of papillary muscle rupture secondary to myocardial infarction. AM HEART J 1989;118:1330-3. 6. Carpentier A. Cardiac valve surgery-the “French Correction.” J Thorac Cardiovasc Surg 1983;86:323-37. 7. Gula G, et al. Surgical correction of complete rupture of the anterior papillary muscle. Ann Thorac Surg 1981;32:88-91. 8. Gregory F Jr, et al. A new technique for repair of mitral insufficiency caused by ruptured chordae of the anterior leaflet. J Thorac Cardiovasc Surg 1988;96:765-8. 9. Lavie CJ. Gersch BJ. Mechanical and electrical comnlications of acute myocardial infarction. May Clin Proc 1990;65:709-30. 10. Adachi T, Kei J, Onuki T, Kawashima M, Yokoyama M, Nitta S. A case of mitral regurgitation caused by necrosis and total rupture of the papillary muscle. Nippon Kyobu Geka Gakkai Zasshi 1990;38:178-83.

Left ventricular pseudoaneurysm,in which a ventricular free wall rupture is locally contained by adherent pericardium, is a well-recognized complication of myocardial infarcti0n.l Other diverse causesof pseudoaneurysminclude intraoperative venting of the cardiac apex, penetrating trauma, and infection.2-4 Comparedwith a true left ventricular aneurysm a pseudoaneurysmhas a greater propensity to suddenly rupture, with catastrophic sequelae.4, 5 Pseudoaneurysmmay be surgically curable; a prompt and accurate diagnosisis thus essential.Left ventriculography by cardiac catheterization hasbeenthe procedure of choice in the diagnosisof pseudoaneurysm, but recently this method hasbeenchallengedby the emergenceof transthoracic two-dimensional and color-flow Doppler echocardiography.7-gIn technically difficult cases,however, transthoracic echocardiographymay fail to delineate the site of From the Cardiology Division, University of Louisville. Reprint requests: Marcus F. Stoddard, MD, Noninvasive Cardiology, University of Louisville, 550 S. Jackson St., Ambulatory Care Building, Louisville, KY 40202. AM HEARTJ 1993;125:534

Copyright ‘t* 1993 by Mosby-Year 0002-8703/93/$1.00 + .lO

Book, Inc. 4/4/42609

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myocardial rupture to confirm a pseudoaneurysm.The superior resolution of transesophageal echocardiography comparedwith transthoracic echocardiography suggestsa potential role for the transesophagealapproach in the diagnosisof pseudoaneurysm.To our knowledge, no cases have been reported of successfuldiagnosis with transesophageal echocardiography of an apical ventricular pseudoaneurysm.Sutherland et a1.gwere unable to delineate ventricular pseudoaneurysmsin two patients by transesophagealechocardiography; they attributed this result to the difficulty in imagingthe left ventricular apex by transesophagealechocardiography. We describe here the successfulimaging of an apical left ventricular pseudoaneurysm resulting from intraoperative venting through transesophagealechocardiography,which required a modified transgastric approach. Although further experienceis needed to definitively determine the role of transesophageal echocardiography in this setting, our case report demonstratesthe feasibility of the transesophagealtechnique in the diagnosisof ventricular pseudoaneurysm. A 75year-old man was admitted to the University of Louisville with complaints of progressivedyspneaon exertion during the previous 6 months, which had grown strikingly worse for 5 days. He denied chest pain. Additional pertinent complaints included progressivegeneralizedfatigue, arthralgias, myalgias, and a 37-pound weight loss during the previous 6 months. He denied night sweatsbut noted occasionaldiaphoresisand fever. Seven months previously he had sought treatment for unstable angina pectoris and underwent aortic valve replacement with a St. Jude Medical bileaflet tilting-disc prosthesis and threevesselcoronary artery bypassgraft surgery for critical aortic stenosis(aortic valve area of 0.43cm2by Gorlin method) and significant obstructive left main and triple-vessel coronary artery disease,respectively. During this surgical procedure, the left ventricle was vented from the apex. During that admissionthe patient’s postoperative course wascomplicated by atria1fibrillation, necessitatingdigoxin for rate control and procainamide for pharmacologiccardioversion. Fever and Staphyloccocus aureus bacteremia developedafter operation and transesophagealechocardiography wasdone to assess for prosthetic valve endocarditis. No vegetations or valvular abnormalities were found and left ventricular function wasnormal. Bacteremia was attributed to central venouslines and the fever abated after all lines were removed and the patient wastreated for 14 days with piperacillin and vancomycin. He was dischargedon a therapeutic regimenof digoxin, procainamide, and warfarin. Pertinent history included hereditary pyropoikilocytosis, treated 40 years previously with splenectomy. As a result of this hematologic illness, resulting in heat-sensitive erythrocyte hemolysis,the patient’s hemoglobin level wasusually 9.6 to 10.0 gm/dl. On physical examination the patient wasfound to be an elderly cachexic black man in mild respiratory distress with a blood pressureof 140/70mm Hg, a regular pulseof 98 beats/min, respiratory rate of 24 breaths/min, and an oral temperature

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of 99.8O F. Chest examination showed normal breath soundsand no rales.The cardiac point of maximal impulse was diffuse and displaced to the anterior axillary line. Crisp, metallic heart soundswere audible. A 2/6 systolic ejection murmur and a l/6 holosystolic murmur were audible over the third left intercostal spaceand apex, respectively. Both murmurs were nonradiating and did not appreciably changewith hand-grip or Valsalva maneuvers. Peripheral edemawasabsent. Laboratory studiesshowed a hemoglobinlevel of 7.9gm/dl and a white blood cell count of 21,000cells/mm3with 4 band cells,79 segmentalcells,14 lymphocytes, 2 monocytes, and 1 eosinophil on peripheral smear. Platelet count was 839,000cells/mm3.Peripheral smearwasnotable for marked anisocytosis,poikilocytosis, microcytosis, and schistocytosis.Erythrocyte sedimentation rate was 103mm/hr. A chest radiograph showedmild cardiomeagaly,prominent pulmonary vasculature, and an aortic valve prosthesis. The ECG showed normal sinus rhythm and nonspecific ST-T changesbut showedno evidence of conduction abnormalities. Prosthetic valvular endocarditis was suspected.Transthoracic two-dimensional and color-flow Doppler echocardiographic studies were performed and failed to demonstrate prosthetic valve vegetation or dysfunction; they did show, however, a cystic area in proximity of the left ventricular apex. To assess for prosthetic valve vegetation, a transesophagealechocardiographicstudy wasmadewith a 50 MHz monoplanescope(Hewlett-Packard Co., Medical Products Group, Andover, Mass.). No vegetations were seen.Two-dimensional and color-flow Doppler echocardiography demonstrated continuity of the cystic area noted on transthoracic echocardiographywith the left ventricular apex through a narrow-necked communication;this was considereddiagnostic of a pseudoaneurysm.The pseudoaneurysm was complex and had an apparent smaller chamber in direct continuity with the left ventricle and a larger chamber in continuity with the smaller chamber (Figs. 1 through 3). The pseudoaneurysmwasnot seenwith the standard transgastric short-axis views of the left ventricle and wasonly poorly visualized from the transesophagealfour-chamber view. A modified transgastric approach was necessaryto delineate the pseudoaneurysm;this required alining the transverseplane of the monoplanescope along the longitudinal axis of the left ventricle from a transgastric window. This wasaccomplishedby flexing the tip of the scopeto the patient’s left and maintaining contact with the gastric mucosaby anteflexing the transducer and rotating the scopecounterclockwise.Once a longitudinal plane wasachieved, the scopewasadvanced to the left ventricular apex and color-flow Doppler echocardiography wassuccessfullyusedasan aid to searchfor continuity between the left ventricle and the pseudoaneurysm.Pulsed Doppler echocardiography performed during transesophagealechocardiography demonstrated turbulent flow (aliasing) at the site of communication between the left ventricle and the apparent smallerpseudoaneurysmchamber. Pulsed Doppler echocardiography at the communication

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Fig. 1. Transesophagealtwo-dimensional imagewith a modified transgastric longitudinal view demon-

strating a pseudoaneurysm.The pseudoaneurysmhad a smallerchamber (I) in continuity with the apex (arrow) of the left ventricle (LV), and a larger chamber (2) in continuity with the smaller chamber.

between the apparent smallerand larger pseudoaneurysm chambersshowedmultiphasic flow with systolic and diastolic components (Fig. 4). Results of contrast (agitated saline solution) and color-flow Doppler transesophageal echocardiographic interrogation of the interventricular septum were unremarkable for ventricular septal defect. Subsequent continuous-wave Doppler with the nonimaging transducer demonstrated a bidirectional systolic and diastolic flow pattern with a peak systolic velocity of 4 m/set, consistentwith a 64 mm Hg peak gradient from the left ventricle into the pseudoaneurysm(Fig. 5). The pseudoaneurysmwasfurther confirmed by cardiaccatheterization during the levophaseof a pulmonary artery contrast injection. However, the continuity of two chambersapparent on transesophagealechocardiography was not appreciable. Nine sets of blood cultures during 11 days showed no growth, and drug-induced lupus was subsequently diagnosedfrom a positive antinuclear antibody test at a 20,480 dilution and a positive single-stranded deoxyribonucleic acid test. Symptoms and recurrent fever resolved 3 weeks after procainamidewasdiscontinued. Surgery wasdeferred becauseof the patient’s multiple medical illnessesand malnourished state. To our knowledge this is the first casereport demonFig. 2. Transesophagealcolor-flow Doppler image from analogousview asshownin Fig. 1 demonstrating systolic jet entering the smaller pseudoaneurysmchamber (1) from site of continuity (arrow) with left ventricle. 2, Larger chamber.

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Fig. 3. Color-flow transesophagealimagesimilar to Fig. 1 demonstrating systolic (A) and diastolic (B) flow between the smaller (1) and larger (2) pseudoaneurysmchambers.Arrow depicts color-flow jet.

strating the feasibility of transesophagealechocardiography in the diagnosisof an apical left ventricular pseudoaneurysm. With transesophagealechocardiography, Perrella et aLlowere able to delineatea pseudoaneurysmof the aortic root. Ballal et al.ll diagnoseda left atria1 pseudoaneurysmwith transesophagealechocardiography.Alam et a1.12demonstrated pseudoaneurysmsat the basilar portions of the left ventricle. Transesophagealechocardiography consistently allowsideal imagingof the aortic root, left atrium, and basilar left ventricular walls; it is therefore not unexpected for it to allow diagnosisof pseudoaneurysmat these sites.However, the left ventricular apex may be difficult to image with standard transesophagealviews. In addition, previous investigators were unable to visualize apical ventricular pseudoaneurysmswith transesophageal echocardiography.gThe role of transesophagealechocardiography in the diagnosisof left ventricular pseudoaneurysm arising from the apex is therefore in question. Our case report demonstrates the feasibility of using transesophagealechocardiographyin diagnosingthis entity and underscoresthe importance of employing a modified transgastric approach with a monoplane scope.This approach achievesa longitudinal plane of the heart. We employ this modified view routinely during transesophagealechocardiography. Occasionally, however, a transgastric longitudinal plane cannot be obtained with a monoplanescope.It

is probable that the longitudinal plane of a biplane transesophagealscope in a transgastric-apical position will greatly simplify this diagnosis. Color-flow Doppler echocardiography has been previously shown to be an invaluable adjunct to transthoracic two-dimensional imaging in documenting communication betweena pseudoaneurysmand the left ventricle.g Despite the inherent superior resolution of two-dimensionaltransesophagealechocardiography as opposedto transthoracic echocardiography, color-flow Doppler echocardiography greatly simplified the diagnosisof pseudoaneurysmin this case.This further confirms the importance of coupling color-flow Doppler echocardiography with two-dimensional transesophagealechocardiographywhen attempting to diagnosea pseudoaneurysm.Roelandt et a1.13described a characteristic continuous-waveDoppler flow pattern of left ventricular pseudoaneurysm. In our case, this specific diagnostic flow pattern was seen;it was characterized as bidirectional flow into the pseudoaneurysmduring ventricular systole and atria1 contraction and flow from the pseudoaneurysminto the left ventricle beginning in late ventricular systole and continuing throughout early to mid diastole. Maximal velocity occurs during ventricular systole; it was higher in this case(4.0 m/set) than in previous reported cases(2.16 m/sec).13 It is intriguing to speculate on the possible role of

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Fig. 4. Pulsed Doppler echocardiography at site of communication between pseudoaneurysm chambers depicted in Fig. 3 demonstrating bidirectional flow between chambers in systole (S) and diastole (0). Velocities above and below Doppler baseline represent flow into and out of larger chamber, respectively. Vertical velocity marks along left side of figure represent 20 cm/set increments in velocity.

Fig. 5. Continuous-wave Doppler at site of communication between left ventricle and pseudoaneurysm demonstrating flow into pseudoaneurysm during atrial (A) and ventricular (S) systole and out of pseudoaneurysm into left ventricle during ventricular diastole (0). Note merging of atrial and ventricular systolic components. Peak systolic velocity was 4.0 m/set, consistent with a 64 mm Hg gradient.

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pseudoaneurysm in causing intravascular hemolysis. In our case, the patient’s intravascular hemolysis had worsened and was not fully explained. Perhaps hemolysis occurs in some patients with a high pressure gradient into a pseudoaneurysm. Although the role of transesophageal echocardiography in the diagnosis of left ventricular pseudoaneurysm is not established, this case report confirms the feasibility of the transesophageal technique when a modified approach is used. We suggest that transesophageal echocardiography may be a useful adjunct to transthoracic echocardiography when the latter technique fails to confirm the diagnosis of ventricular pseudoaneurysm.

2.

3.

Martin RH, Almond CH, Saab S, Watnon LE. True and false aneurysms of the left ventricle following myocardial infarction. Am J Med 1977;62:418. Weesner KM, Byrum C, Rosenthal A. Left ventricular aneurysms associated with intraoperative venting of the cardiac apex in children. AM HEART J 1981;101:622. Higgins CB, Lipton MJ, Johnson AD, Peterson KL, Vieweg WVR. False aneurysms of the left ventricle. Radiology 1978;127:21.

Davidson KH, Parisi AF, Harrington JJ, Barasamian EM, Fishbein MC. Pseudoaneurysm of the left ventricle: an unusual echocardiographic presentation: review of the literature. Ann Intern Med 1977;86:430. 5. Vlodaver Z, Coe JI, Edwards JE. True and false aneurysms propensity of the later to rupture. Circulation 1975;51:567. 6. Higgins CB, Lipton MJ, Johnson AD, Peterson KL, Vieweg WVR. False aneurysms of the left ventricle: identification of distinctive clinical, radiographic and angiographic features. Radiology 1978;127:21. I. Roelandt J, Brand MVD, Vletter WB, Nauta J, Hugenholtz PG. Echocardiographic diagnosis of pseudoaneurysm of the left ventricle. Circulation 1975;52:466. 8. Catherwood E, Mintz GS, Kotler MN, Parry WR, Segal BL. Two-dimensional echocardiographic recognition of left ventricular pseudoaneurysm. Circulation 1980;62:294. 9. Sutherland GR, Smyllie JH, Roelandt JRTC. Advantages of colour flow imaging in the diagnosis of left ventricular pseudoaneurysm. Br Heart J 1989;61:59. 10. Perrella MA, Smith HC, Khandheria BK. Pseudoaneurysm of the aortic root diagnosed by noninvasive imaging: report of a case. J Am Sot Echocardiogr 1991;4:499. 11. Ballal R, Nanda NC, Sanyal R. Intraoperative transesophageal echocardiographic diagnosis of left atrial pseudoaneurysm. AM HEART J 1992;123:217. 12. Alam M, Glick C, Garcia R, Lewis JW. Transesophageal echocardiographic features of left ventricular pseudoaneurysm resulting after mitral valve replacement surgery. AM 4.

HEART

J 1992;123:226.

13. Roelandt JRTC, Sutherland GR, Yoshida K, Yoshikawa J. Improved diagnosis and characterization of left ventricular pseudoaneurysm by Doppler color flow imaging. J Am Co11 Cardiol 1988;12:867.

Myocardial perfusion imaging during stress-induced sustained ventricular tachyarrhythmia Thomas C. Hilton, MD, Gordon H. Ira, Jr., MD, Wanda Bolena, CNNT, and Stephen A. Stowers, MD Jacksonville,

Exercise-inducedsustainedventricular tachyarrhythmia is rare and may occur in patients with or without coronary artery disease.lw4 Acute detection of myocardial ischemiaat onset of ventricular arrhythmia is difficult becausethe ischemia may be “silent,“3 the ECG may be nondiagnostic, and conventional myocardial perfusion imagingwith thallium-201 is frequently not possible becauseof acute hemodynamic instability, which necessitatestransfer of patients from the stress laboratory

to an intensive

care unit. Tech-

netium-99M methoxy isobutyl isonitrile (ggmTc-sestamibi) is now approved as an alternative myocardial perfusion exhibits minimal redistriimaging agent. ggmTc-sestamibi bution over time, and imaging can be performed up to 4 hours after injection. Unlike thallium-201, Tc-sestamibi

REFERENCES 1.

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Fla.

allows a time window for subsequentmyocardial imaging in patients who are acutely unstable. In the present case, we describea patient with exercise-inducedpolymorphic ventricular tachyarrhythmia and hemodynamiccollapsein whom ggmTc-sestamibiwas injected immediately before the onset of ventricular tachyarrhythmia. Resultsof imaging with ggmTc-sestamibi were critical to patient management and expandedour current understandingof exerciseinduced ventricular tachyarrhythmia. A 72-year-old man waswell until 2 years before admission to the hospital, at which time he was evaluated for frequent premature ventricular contractions. He was treated with flecainide 100mg two times daily, and he experienced significant symptomatic improvement. He did well until the day that he wasadmitted to the hospital for treatment of uncontrolled hypertension (200/100mm Hg) with angina and mild congestiveheart failure. Blood pressure was controlled, and symptoms resolved with additional antihypertensive therapy. Serial ECGs and cardiac enzymesrevealed no evidenceof myocardial infarction. On the third hospital day, the patient underwent stresstesting. Rest single photon emissioncomputed tomography thallium-201 imagingwasperformed with a 15-inchfield of view and a %-inch crystal (SiemensOrbitrer, Chicago,Ill.) (Fig. 1). The patient underwent imaging in a 180-degree arc, 40 secondsper view, from the left posterior oblique projection to right anterior oblique projection. Becauseof perceived exerciselimitations, 40 mg of dipyridamole was infused over 4 minutes before exercise to achieve peak stress. The patient then exercised for 4.5 minutes (1.5 minutes into stageII of the Bruce protocol). Thirty millicuries of gg”Tc-sestamibiwas injected at 3 minutes; after 4.5 minutes of exercise,polymorphic, sustainedventricular tachycardia with hemodynamiccollapsedeveloped(Fig. 2). Successfulconversionto normal sinusrhythm wasachieved after cardiac resuscitation including direct-current cardioversion (three times). The patient was transferred to an intensive care unit where his rhythm stabilized. Three hours later, stressggmTc-sestamibi imagingwasperformed with a Technicare 420 mobile camera (Techicare, Solon, Ohio) and an ADAC 3300 computer (ADAC, Milipitas,

From

the Division

of Cardiology,

Reprint requests: Thomas Jacksonville, FL 32216. AM HEART

St. Luke’s

C. Hilton,

Hospital,

MD,

4205

Jacksonville, Belfort

Rd,

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