sion: two different complications of acute myocardial infarction. Am J Cardiol 197&41:1127-32. 4. Meizlish JL, Berger HJ, Plankey M, Errico D, Levy W, Zaret BL. Functional left ventricular aneurysm formation after acute anterior transmural myocardial infarction: incidence, natural history, and prognostic implications. N Engl J Med 1984;311:1001-6. 5. Bashour TT, Antonini C, Taylor D. Cardiac rupture before completed myocardial infarction. AM HEART J 1986;112:176-8. 6. Braunwald E, Kloner RA. The stunned myocardium: prolonged, postischemic ventricular dysfunction. Circulation 1982;66:1146-9.
7, Bashour TT, Kabbani S, Brenster HP, Wald SH, Hanna ES, Cheng TO. Transient Q waves and reversible cardiac failure during myocardial ischemia: electrical and mechanical stunning of the heart. AM HEART J 1983;106:780-3. 8. Brunken R, Tillisch J, Schwaiger M, Child JS, Marshall R, Mandelkern M, Phelps ME, Schelbert HR. Regional perfusion, glucose metabolism, and wall motion in patients with chronic electrocardiographic Q wave infarctions: evidence for persistence of viable tissue in some infarct regions by positron emission tomography. Circulation 198&73:951-63. 9. Bolli R, Pate1 BS, Hartley CJ, Thornby JI, Jeroudi MO, Roberts R. Nonuniform transmural recovery of contractile function in stunned myocardium. Am J Physiol 1989;257:H375H38.5. 10. Fine DG, Clements IP, Callahan MJ. Myocardial stunning in hypertrophic cardiomyopathy: recovery predicted by single photon emission computed tomographic thallium-201 scintigraphy. J Am Co11 Cardiol 1989:13:1415-18. 11. Przvklenk K. Kloner RA. Anaiotensin converting enzyme inhibftors improve contractile f&iction of stunned myocardium bydifferentmechanisonsofaction.A~H~~~~Jl991; 121:131930. 12, Hochman JS, Bulkley BH. Pathogenesis of left ventricular aneurysm: an experimental study in the rat model. Am J Cardiol 1982;50:83-8.
infection of an automatic implantable carclioverter defibrillator Peter Katona, MD, Isaac Wiener, Naresh Saxena, MD Los Angeles,
MD, and Calif.
Life-threatening ventricular arrhythmias have been successfully prevented with the use of automatic implantable cardioverter defibrillators (ICDs). These foreign bodies have many parts and are thus prone to occasional infection. We report here a case of an ICD infection with an unusual organism, Mycobacterium avium-intracellulare. A 31-year-old woman of Indonesian descent was in good health until 1 year before admission to the hospital, when she presented with ventricular fibrillation that required electrical defibrillation. Cardiac catheterization revealed significant left ventricular dysfunction and normal coronary arteries. Biopsy revealed nonspecific fibrosis, possibly From University of Medicine. Reprint requests: CA 91436 414140566
of California Peter
School of Medicine,
Departn& No. 3, Encino,
November 1992 HearI .kwnai
from cocaine use in the distant past. Electrophysiologic studies revealed no inducible arrhythmia. An ICD, with two epicardial patches and epicardial screw-in leads, was inserted via a left lateral thoracotomy. There were no postoperative complications. The ICD spontaneously discharged on two separate occasions during the following year while the patient was asleep. One year later, she noted the progressive onset of pain and swelling at the abdominal insertion site of the generator unit of the ICD. She had no erythema, fever, chills. nr sweats, and she had not had influenza or an upper respiratory tract infection recently. She denied any trauma to the area. There was no history of recent use of antibiotics, other medications, or recreational drugs. Her medical history was significant for genital herpes and inhalation of cocaine in the distant past. Vital signs were a body temperature, 99’ F; pulse, 84 beats/min; respirations, 18 breaths/min; and blood pressure, 110/70 mm Hg. She was an alert, oriented, cooperative woman who appeared to be her stated age and to be in no acute distress. Head and neck examination was unremarkable. Lungs showed minimal dullness and rales at the left base. Cardiac examination revealed a regular rhythm with a grade l/4 early systolic murmur at the apex. Abdomen was soft with normoactive bowel sounds and no orgiinomegaly; the generator site revealed a 5 x 7 cm hard rectangular mass in the left lower quadrant, which was very tender to palpation. There was significant surrounding edema but no erythema. Results of neurologic, back, and extremity examinations were normal. Initial laboratory tests including complete blood cell counts, chemistry panel, urinalysis, ECG, and chest x-ray studies were unremarkable. Erythrocyte sedimentation rate was 51 mm/hr. The area around the generator was aspirated, and 60 ml of purulent material was obtained. Gram stain showed many white blood cells but no organisms. The generator was removed on the next day. Results of gram stain and routine aerobic and anaerobic cultures were negative. Biopsy demonstrated noncaseating granuloma formation but no organisms. Further workup included computed tomographic and indium scans; skin t.ests for purified protein derivative, coccidioidomycosis, and Candida organisms; antinuclear antibody, serologic tests for Brucella organisms, coccidioidoidomycosis, and human immunodeficiency virus (HIV); T-cell subsets; and echocardiogram, all of which were essentially unremarkable. Results of all routine cultures including cultures of blood, urine, and aspirated material were negative. Four weeks after admission, cultures of peritoneal aspirate revealed the growth of a mycobacterium, which was later identified as Mycobacterium avium-intracellulaw. The patient was initially treated with isoniazid, rifampin, and ethambutol. Subsequent sensitivity tests showed the organism to be sensitive to ansamycin, ethambutol, and rifampin; and resistant to isoniazid, ethionamide, clofazimine, and ciprofloxacin. It was moderately sensitive to amikacin. The defibrillator leads were relocated to the other side of the abdomen 28 days after admission, and a new Ventak model 1550 ICD generator (Cardiac Pacemakers, Inc., St. Paul, Minn.) was reinserted 36 days after admission. The
Volume 124 Number 5
leads were not removed nor were they cultured at the time of surgery. The patient has now been followed up for over 2 years; she has been receiving isoniazid, rifampin, and ethambutol without any significant complications. We plan to continue antimicrobial therapy until the ICD is removed. The complex two-step process (abdominal incision and thoracotomy) that, is required for implantation of an ICD may lead to many problems. Complications may include atelectasis, effusions, and pneumothorax in the early postoperative period. Constrictive pericarditis, mechanical problems with patches and leads (e.g., crumpling of wires), and infections may occur later. ICD infection rates vary from 1 Y to 6 % according to various studies.lm3These infections may affect the pericardium, mediastinum, or the defibrillator pulse generator pocket. Predisposing factors for infection include diabetes, cachexia, the use of corticosteroids, malignancy, and reoperation to reposition the leads. Several reports of infection of ICDs have been published,l-:j but none have demonstrated infection with this organism. Alma& et a1.l described three cases of delayed infection (one each with no identified organism, Candida albicans, and Staphylococcus epidermidis). Kelly et aLz reported three acute cases (one as a result of Torulopsis glabrata and two that were caused by S. aweus). Goodman et al.:j reported seven infections (one with no identified organism, four with staphylococci, one with mixed anaerobes, and one with C. albicans). As might be expected, all of these 13 infections were caused by pyogenic organisms (10 with bacteria and 3 with yeast). The average interval between insertion of the ICD and infection was 8.5 months compared with 12 months in our study. Other atypical mycobacteria (M. fortuitum, M. chelonei, M. marianum, M. ulcerans) have been associated with various soft tissue infections. The latency period may be extremely long. Therapy usually consists of a combination of surgery and chemotherapy. M. avium-intracellulare is now seen most commonly in patients with HIV infection (our patient was HIV-negative) and responds very poorly to chemotherapy. The only other prosthetic device that was infected with M. allium-intracellulare, as reported in the literature, is a silicone breast implant.7 In almost all cases of ICD infection, a thoracotomy is required to remove all foreign material. Unfortunately, most infections that have been treated without patch removal have recurred.4 Rare isolated cases of successful treatment without thoracot,omy have been reported.5 Although the general recommendation in a setting such as this is removal of all foreign material, our patient was successfully treated without thoracotomy. This was probably due to the indolent nature of the organism. Addendum
The patient was well for 3 years after the initial diagnosis of infection. She was started on propranolol and had no ICD discharges on this medication. Follow-up echocardiography revealed a return of ventricular function to normal, though ECG continued to show abnormal ST-T segments. The patient requested discontinuation of antimicrobials. She subsequently presented with hemoptysis and was found to have bronchiectasis; cultures were positive for
avium-intracellulare. Recurrent wound infection of the ICD pocket developed. After reviewing the options and after results of electrophysiologic studies were found to be negative, the patient elected to have a thoracotomy with left lower lobectomy and removal of all ICD hardware. Cultures for mycobacteria are negative at 5 weeks. Mycobacterium
1. Almassi GH, Olinger GN, Troup PJ, Chapman PD, Goodman LR. Delayed infection of the imnlantable cardioverter-defibrillator: J Thorac Cardiovasc S&g 198&95:908-11. 2. Kelly PA, Wallace S, Tucker B, Hurvitz RJ, Ilvento J, Mirabe1 GS, Cannom DS. Postoperative infection with the automatic implantable cardioverter defibrillator: clinical presentation and use of the gallium scan in diagnosis. PACE Pacing Clin Electrophysiol l&3&11:1220-5. 3. Goodman LR, Almassi GH. Troun PJ. et al. Comnlications of automatic implantable cardioverter defibrillators: radiologic, CT, and echocardiographic evaluation. Radiology 1989; ,
Wanderly D, Maloney J, Edel T, McHenry M, McCarthy. Infections in implantable cardioverter defibrillator patients. PACE Pacing Clin Electrophysiol 1990;13:1360-4. 5. Taylor R, Cohen D, Widman L, Chilton R. Infection of an implantable cardioverter defibrillator: management without removal of the device in selected cases. PACE 1990;13:1352-5. 6. Furman S. Implantable cardioverter infection. PACE Pacing Clin Electrophysiol 1990;13:1351. I. Perry RR, Jaques DP, Lesar MS, d’Avis JC, Peterson HD. Mycobacterium avium infection in silicone injected breasts. Plast Reconstr Surg 1985;75:104-6. 4.
Successful repair of a pseudoaneurysm originating from a true left ventricular aneurysm John A. St. Cyr, MD, PhD, and David A. Fullerton, MD Denver,
Left ventricular aneurysm and pseudoaneurysm are two Ivery different pathologic entities, which are usually thought to be unrelated. Left ventricular aneurysm formation is consequent to myocardial infarction and histologically consists of all layers of the ventricular wal1.l It is commonly believed that true left ventricular aneurysms do not rupture.Z On the other hand, left ventricular pseudoaneurysm by definition results from ventricular disruption and lacks a true wall. For that reason, left ventricular pseudoaneurysm is prone to rupture.z Herein we report development of a left ventricular pseudoaneurysm from a chronic, mature, left ventricular aneurysm. The patient underwent successful surgical repair. A 75year-old man underwent cardiac catheterization for evaluation of angina. His medical history was significant for an anterior myocardial infarction, which occurred approximately 7 years before this cardiac catheterization. At From the Department of Surgery, University of Colorado Health Sciences Center,
Reprint requests: David A. Fullerton, MD, Department of Surgery, Campus Box C-310, University of Colorado Health Sciences Center. 4200 East 9th Ave., Denver, CO 80262.