November 1990

i 220 Brief Communications American Heart Journal

presumably secondary to compression of the left pulmo- nary artery. Calcification of well-organized thrombus in an aortic pseudoaneurysm also has not been previously de- scribed. Prosthetic aortocoronary grafts are seldom re- quired, and this is the first report of a pseudoaneurysm in- volving a polytetrafluoroethylene aortocoronary graft.

Rupture of an aortocoronary graft should be considered in the differential diagnosis of patients who present with an anterior mediastinal mass or a new murmur following cor- onary artery bypass surgery. The diagnosis can usually be established by contrast-enhanced CT in combination with selective graft angiography. 2, 3 It may be difficult to distin- guish a large saphenous vein graft aneurysm7,* from a ruptured graft even with these techniques. Biplane transe- sophageal echocardiography provides excellent visualiza- tion of the ascending aorta and has the obvious advantages of being noninvasive and not requiring contrast medium. It is a useful imaging modality in patients with proximal de- hiscence of an aortocoronary graft, as in the second case described.

A review of the literature reveals six previously reported cases of ruptured aortocoronary saphenous vein graftslm6 (Table I). Only two reported cases,ls5 including one of in- fective mediastinitis, involved dehiscence of the proximal aortocoronary anastomosis similar to the cases in this re- port. The incidence of perioperative myocardial infarction or death in patients with ruptured aortocoronary grafts undergoing surgery is high. Surgical repair of ruptured aortocoronary grafts is complicated by the extensive perivascular fibrosis and mediastinal adhesions. These pa- tients commonly have severe multivessel coronary artery disease and depressed left ventricular systolic function.

Surgical management of ruptured aortocoronary grafts should include the establishment of femoral-femoral car- diopulmonary bypass prior to sternotomy and possibly even prior to anesthetic induction and positive pressure ventilation. A mediastinal mass compressing the pulmo- nary artery in conjunction with positive pressure ventila- tion and the gravitational effect of the mass in the supine position may result in a significant increase in right ventricular afterload with circulatory collapse.g Systemic cooling to 28’ C prior to sternotomy with further cooling to 18” C if difficulty is encountered during mediastinal dissection will allow cardiac arrest and decrease bleeding if the aorta is accidentally entered. Dissection of the aorta distal to the aneurysm should be performed prior to manipulation of the aneurysm. To avoid coronary embo- lization from a partially occluded graft, the distal end of the saphenous vein graft should be ligated before cross-clamp- ing the aorta. After aortic cross-clamping, cardioplegic so- lution should be instilled into the coronary arteries as well as into the coronary sinus to improve myocardial preserva- tion. Ideally, complete revascularization should be per- formed with new grafts. Percutaneous graft occlusion may be an alternative to surgical intervention for ruptured sa- phenous vein grafts if the site of rupture is not at the aor- tic anastomosis2

Anastomotic aneurysms occur most commonly when a prosthetic vascular graft is used, as in the second case de-

scribed. GaylislO found that weakness of the arterial wall, with sutures pulling out, was the most common cause of pseudoaneurysm formation involving prosthetic vascular grafts. In our second case, a polytetrafluoroethylene graft was used and the aortic wall was noted to be extremely fri- able. Thrombolytic therapy likely also contributed to poor healing at the aortic anastomotic site. All six peripheral vein graft aneurysms reported by GaylislO occurred in the juxta-anastomotic position with intact suture lines. This is similar to most of the ruptured aortocoronary saphenous vein grafts described. Possible factors leading to saphenous vein rupture remote from the proximal anastomosis in- clude vein graft weakness, trauma during harvesting or implantation, and hypertension.

REFERENCES

1. Stone IM, Aranda JM, Thurer RJ, Clark R, Befeler B. Disruption of proximal aorto-saphenous vein anastomosis. Chest 1977;71:544-6.

2. Shapeero LG, Guthaner DF, Swerdlow CD, Wexler L. Rupture of a coronary bypass graft aneurysm: CT evaluation and coil occlusion therapy. AJR 1983;14i:1060-2.

3. Yousem D. Scott W. Fishman EK. Watson AJ. Trail1 T. Gimenez L: Saphenouk vein graft aneurysms demonstrated by computed tomography. J Comput Assist Tomogr 1986;lO: 526-8.

4. Murphy JP, Shabb B, Nishikawa A, Adams PR, Walker WE. Rupture of an aortocoronary saphenous vein graft aneurysm. Am J Cardiol 1986;58:555-7.

5. Douglas BP, Bulkley BH, Hutchins GM. Infected saphenous vein coronary artery bypass graft with mycotic aneurysm. Chest 1979;75:76-7.

6. Nielsen JF, Stentoft J, Aunsholt NA. Hemoptysis caused by aneurysm of saphenous bypass graft to a coronary artery. Stand J Thorac Cardiovasc Surg 1988;22:189-91.

7. Taliercio CP, Smith HC, Pluth JR, Gibbons RJ. Coronary ar- tery venous bypass graft aneurysm with symptomatic coro- narv artery emboli. J Am Co11 Cardiol 1986;7:435-7.

8. Lopez-Velarde P, Hallman GL. Treistman B. Aneurysm of an aortocoronary saphenous vein bypass graft presenting as an anterior mediastinal mass. Ann Thorac Surg 1988;46:349-50.

9. Pullerits J, Holzman R. Anaesthesia for patients with medias- tinal masses. Can J Anaesth 1989;36:681-8.

10. Gaylis H. Pathogenesis of anastomotic aneurysms. Surgery 1981;90:509-15.

Idiopathic multiple left ventricular aneurysms

Abraham Gonzalez, MD, Philip T. Sager, MD, Shahbudin H. Rahimtoola, MB, FRCP, and Anil K. Bhandari, MD. Los Angeles, Calif.

From the Division of Cardiology, Department of Medicine, Los Angeles County and USC Medical Center, University of Southern California School of Medicine.

Reprint requests: Abraham Gonzalez, MD, Los Angeles County and USC Medical Center, Division of Cardiology, 2025 Zonal Ave., Los Angeles, CA 9003.3.

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Number 5 Brief Communications 122 1

Fig. 1. Left ventriculogram in right anterior oblique projection showing inferobasal, apical septal, and distal anterolateral wall aneurysms fat-rows).

Coronary artery disease is the most common cause of left ventricular aneurysms and is found in at least 75% of pa- tients with aneurysms1 Less common causes have included cardiac trauma, infective endocarditis, congenital heart disease, syphilis, tuberculosis with cardiac involvement, and Chagas’ disease. Rarely, no apparent etiology can be elucidated, and the aneurysms have been labeled as idio- pathic in origin. 2-5 In the reported patients with idiopathic aneurysms, they have always involved a single cardiac lo- cation. To the best of our knowledge, there has been no re- port of a patient with idiopathic multiple left ventricular aneurysms. We report a patient with three well-defined idiopathic left ventricular aneurysms in whom recurrent sustained ventricular tachycardia was the clinical presen- tation.

A 56-year-old Salvadoran woman presented in January 1987 with sustained monomorphic ventricular tachycardia. For 4 years prior to admission, she had symptoms of exer- tional dyspnea, and she was diagnosed as having mild con- gestive heart failure. She denied history of prior palpita- tions, syncope, diabetes mellitus, chest pain, myocardial infarction, rheumatic heart disease, hypertension, or tu- berculosis. She also denied any history of chest trauma. Physical examination demonstrated an apical gallop rhythm but no murmurs. The remainder of the examina- tion was normal. The 12-lead ECG showed sustained ven- tricular tachycardia at a rate of 200 beats/min, and the QRS complexes had a morphologic configuration of left bundle branch block and superior frontal axis. Following cardio- version, the ECG showed sinus rhythm at a rate of 84 with a PR interval of 184 msec and QRS duration of 108 msec; T waves were inverted in the inferior and anterolateral leads. The chest x-ray film showed mild cardiomegaly without abnormal bulging of the cardiac silhouette, and the lung fields were clear. Laboratory examination was unre-

markable. Multiple serologic tests for Chagas’ disease were negative. She was found to have an abnormal titer (1:8) for venereal disease research laboratory test and positive mi- crohemagglutinins to Treponema pallidurn. Cerebrospinal fluid examination was normal. The patient denied any prior history suggestive of syphilis, and the physical exam- ination revealed no stigmata of syphilis. She received a 4- week course of erythromycin because of a history of allergy to penicillin. Cardiac catheterization and coronary angiog- raphy showed normal coronary arteries and a diminished left ventricular ejection fraction of 0.36. Left ventriculog- raphy disclosed the presence of generalized hypokinesis and three discrete aneurysms involving the inferobasal, apical septal, and distal anterolateral walls of the left ven- tricle (Fig. 1). The aneurysms measured 2.9,2.7, and 2.3 cm in width, and 1.4,1.5, and 1.0 cm in depth, respectively. All were rounded protuberances with broad necks. No intra- cardiac thrombus was detected. Programmed ventricular stimulation studies induced three sustained ventricular tachycardias of different QRS morphologies, including the one identical to the clinical ventricular tachycardia. Dur- ing serial electropharmacologic testing, the inducibility of sustained ventricular tachycardia (VT) was not suppressed by procainamide, mexiletine, or flecainide, and she was treated with amiodarone. However, VT recurrence neces- sitated implantation of an automatic implantable cardio- verter-defibrillator. The presence of the inferobasal, apical septal, and distal anterolateral aneurysms was confirmed at surgery.

Idiopathic left ventricular aneurysms are rare. In many of the earlier reports, coronary angiography was not rou- tinely performed, congenital subvalvular aneurysms were misclassified, and serologic tests for Chagas’ disease were not obtained. Since 1971, there have been 10 reported cases of idiopathic left ventricular aneurysms.2-5 In all cases, the

1222 Brief Communications November 1990

American &art Journal

left ventricular aneurysms were single. All but one of these patients presented with recurrent sustained ventricular or atria1 tachyarrhythmias, and only two had moderate to severe heart failure. Aneurysmectomy was performed in three patients to treat arrhythmias, while another three had subendocardial resection for arrhythmia control. His- topathologic studies disclosed myocardial fibrosis without inflammation in three patients, myocarditis in one patient, and myocyte degeneration in another patient. Surgical re- section was not performed in our case because of multiple VT morphologies and aneurysms.

We believe this case represents multiple idiopathic left ventricular aneurysms. Normal coronary arteries seen on coronary arteriography as well as multiple locations of the aneurysms ruled out an ischemic etiology, and coronary embolism with subsequent lysis was felt to be very unlikely as intracardiac thrombi were never demonstrated by left ventricular angiography or two-dimensional echocardi- ography. Chagas’ disease is improbable, since several sero- logic studies for Chagas’ disease were negative in our patient. Although the patient had serologic evidence of syphilis, there was no history suggestive of primary or sec- ondary syphilis, and the patient had no stigmata of syph- ilis on physical examination and no echocardiographic or angiographic evidence of aortic root dilatation.

REFERENCES

1. Barratt Boyes BG, White HD, Agnew TM, Pemberton JR, Wild CJ. The results of sursical treatment of left ventricular aneurysms: an assessment of the risk factors affecting early and late mortality. J Thorac Cardiovasc Surg 1984;87:87-98.

2. Malay WC, Arrants JE, Sowell BF, Hendrix GH. Left ventric- ular aneurysm of uncertain etiology with recurrent ventricu- lar arrhythmias. N Engl J Med 1971;285:662-3.

3. Rimailho A, Cabrol C, Soyer R, Letac B, Bertrau P, Fouchard J, Guerin F. Surgical management of 4 cases of idiopathic left ventricular aneurysm. Arch Ma1 Coeur 1981;74:443-51.

4. Aizawa Y, Murata M, Satoh M, et al. Five cases of arrhyth- mogenic left ventricular aneurysm unrelated to coronary oc- clusion. Jpn Circ J 1986;50:45-55.

5. Sadoshima J, Taira Y, Shimokawa H, Koyanagi S, Takeshita A, Nakamura M. Two cases of dilated cardiomyopathy com- plicated by left ventricular aneurysm. Chest 1987;92:377-9.

Aortic pseudoaneurysm occurring after cardiac transplantation

David 0. Taylor, MD, Roger B. Rehr, MD, James A. Thompson, MD, George Vetrovec, MD, and James L. Tatum, MD. Richmond, Vu.

From the Departments of Radiology and Medicine. Medical College of Virginia.

Reprint requests: Dr. Roger B. Rehr, Cardiology Associates of West Read- ing, The Doctor’s Office Bldg., 301 South 7th Ave., W. Reading, PA 19611.

414123563

Fig. 1. Lateral chest radiograph reveals round density just anterior to ascending aorta (arrow).

Pseudoaneurysms are a rare, potentially fatal complication of vascular surgery. They have been reported following liver, pancreas, and kidney transplantation,’ but not to our knowledge following cardiac transplantation. This report describes two ascending aortic pseudoaneurysms that de- veloped after cardiac transplantation and illustrates the utility of magnetic resonance imaging (MRI) in the diag- nosis and evaluation of this entity.

Case No. 1. A 45-year-old white man underwent ortho- topic cardiac transplantation for end-stage ischemic cardi- omyopathy. His perioperative course was unremarkable, He was treated for a bacterial pneumonia 1 month after transplant and had episodes of acute rejection requiring pulsed steroids 2 months and 8 months following trans- plant. He never demonstrated evidence of endovascular infection nor did he have documented bacteremia. His post-transplant hypertension was well controlled. A lateral chest radiograph obtained during a routine follow-up visit revealed a round density in the anterior mediastinum an- terior to and abutting on the ascending aorta (Fig. 1). A computed tomographic scan (CT) of this area suggested the presence of a pseudoaneurysm near the level of the aortic anastomosis (Fig. 2). In an attempt to noninvasively obtain a better assessment of this abnormality, an ECG-gated MRI study of the chest was obtained using a Siemens