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Transient left ventricular dyskinesia as a consequence of myocardial stunning
1378
Brief Communications
Fig. 1. Serial ECG recordings 3 weeks before hospital el). and 2 weeks after admission (right panel), showing o&dial infarction. day ventricular dyskinesia was still present according to echocardiography. The subsequent clinical course was uneventful, and on serial ECGs we observed, within 2 weeks, complete disappearance of the Q waves, with reappearance of normal R waves and persistent negative T waves from precordial leads Vr to Ve (Fig. 1). Myocardial kinetics and contractility appeared normal according to echocardiography and radionuclide angiography. Six weeks after the acute episode occurred, a new catheterization showed a normal left ventricular ejection fraction, with full regression of the features of apical aneurysm (Fig. 2) and the absence of restenosis at the site of angioplasty. We thus propose that this patient had a dramatic acute ischemia, which
American
November 1992 Hewl Journal
admission (left panel). at admission (middle panthe transient QRS changes that simulate acute my-
stunned the myocardium without infarction and an early dyskinesia. However, full recovery occurred within 6 weeks after left anterior descending coronary artery angioplasty and treatment with angiotensin converting enzyme inhibitor. The patient underwent a submaximal exercise stress test; results were negative and he was discharged from the hospital with prescriptions for the same p-blocker, aspirin, and angiotensin converting enzyme inhibitor. In this case study, the absence of cardiac enzyme release, as well as the homogenous myocardial captation of fluoro2-deoxyglucose as visualized on positron emission tomography, allowed us to establish that the myocardium was stunned but not infarcted. However, the occurrence of an
volwne 124 Number 5
Brief Communications
1379
Fig. 2. Regional ventricular contractility at time of admission (A and B and E, left) and 6 weeks after angioplasty of the left anterior descending coronary artery and treatment with angiotensin-converting enzyme inhibitor (B and C and E, right), showing complete disappearance of left ventricular dyskinesia, with return of left ventricular regional motion to normal.
early “functional aneurysm” has been well documented, as well as its complete regression after myocardial revascularization and treatment with angiotensin converting enzyme inhibitor, which may enhance the recovery of function in stunned myocardium.ll In stunned myocardium, the cell’s energy metabolism is reduced, and consequently dyskinesia and regional ventricular dilatation may occur as they do in infarcted areas. This early functional aneurysm is mainly due to structural deformitieslz and differs from chronic aneurysm in its lack of fibrosis. Thus conceivably, such an aneurysm may be reversible when normal metabolic conditions are restored. This assumption is well illustrated by our case study, in which revascularization in combination with medical therapy allowed the recovery of
normal myocardium metabolism and favored full ventricular restructuring. Thus we suggest that in critically ischemic myocardium, even in the absence of infarction, an acute functional aneurysm may occur and may be fully reversible with the use of adequate therapy. REFERENCES
1. Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Weisfeldt ML. Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography. N Engl J Med I97~30&57-62. 2. Schuster EH, Bulkley BH. Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture. Circulation 1979;60:1532-8. 3. Hutchins GM, Bulkley BH. Infarct expansion versus exten-
1380
Brief Communications
American
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. converting enzyme in11. Przvklenk K. Kloner RA. Anaiotensin hibftors 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.
Mycobacterium
avium-intracellulare
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
Los Angeles
Katona,
MD,
School of Medicine,
16100 Ventura
Blvd.
Departn& No. 3, Encino,
November 1992 HearI Journal
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
Brief Communications
Fig. 1. Serial ECG recordings 3 weeks before hospital el). and 2 weeks after admission (right panel), showing o&dial infarction. day ventricular dyskinesia was still present according to echocardiography. The subsequent clinical course was uneventful, and on serial ECGs we observed, within 2 weeks, complete disappearance of the Q waves, with reappearance of normal R waves and persistent negative T waves from precordial leads Vr to Ve (Fig. 1). Myocardial kinetics and contractility appeared normal according to echocardiography and radionuclide angiography. Six weeks after the acute episode occurred, a new catheterization showed a normal left ventricular ejection fraction, with full regression of the features of apical aneurysm (Fig. 2) and the absence of restenosis at the site of angioplasty. We thus propose that this patient had a dramatic acute ischemia, which
American
November 1992 Hewl Journal
admission (left panel). at admission (middle panthe transient QRS changes that simulate acute my-
stunned the myocardium without infarction and an early dyskinesia. However, full recovery occurred within 6 weeks after left anterior descending coronary artery angioplasty and treatment with angiotensin converting enzyme inhibitor. The patient underwent a submaximal exercise stress test; results were negative and he was discharged from the hospital with prescriptions for the same p-blocker, aspirin, and angiotensin converting enzyme inhibitor. In this case study, the absence of cardiac enzyme release, as well as the homogenous myocardial captation of fluoro2-deoxyglucose as visualized on positron emission tomography, allowed us to establish that the myocardium was stunned but not infarcted. However, the occurrence of an
volwne 124 Number 5
Brief Communications
1379
Fig. 2. Regional ventricular contractility at time of admission (A and B and E, left) and 6 weeks after angioplasty of the left anterior descending coronary artery and treatment with angiotensin-converting enzyme inhibitor (B and C and E, right), showing complete disappearance of left ventricular dyskinesia, with return of left ventricular regional motion to normal.
early “functional aneurysm” has been well documented, as well as its complete regression after myocardial revascularization and treatment with angiotensin converting enzyme inhibitor, which may enhance the recovery of function in stunned myocardium.ll In stunned myocardium, the cell’s energy metabolism is reduced, and consequently dyskinesia and regional ventricular dilatation may occur as they do in infarcted areas. This early functional aneurysm is mainly due to structural deformitieslz and differs from chronic aneurysm in its lack of fibrosis. Thus conceivably, such an aneurysm may be reversible when normal metabolic conditions are restored. This assumption is well illustrated by our case study, in which revascularization in combination with medical therapy allowed the recovery of
normal myocardium metabolism and favored full ventricular restructuring. Thus we suggest that in critically ischemic myocardium, even in the absence of infarction, an acute functional aneurysm may occur and may be fully reversible with the use of adequate therapy. REFERENCES
1. Eaton LW, Weiss JL, Bulkley BH, Garrison JB, Weisfeldt ML. Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography. N Engl J Med I97~30&57-62. 2. Schuster EH, Bulkley BH. Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture. Circulation 1979;60:1532-8. 3. Hutchins GM, Bulkley BH. Infarct expansion versus exten-
1380
Brief Communications
American
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. converting enzyme in11. Przvklenk K. Kloner RA. Anaiotensin hibftors 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.
Mycobacterium
avium-intracellulare
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
Los Angeles
Katona,
MD,
School of Medicine,
16100 Ventura
Blvd.
Departn& No. 3, Encino,
November 1992 HearI Journal
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