- Email: [email protected]
Septic pulmonary emboli secondary to an infected right atrial thrombus
178
Brief
Communications
American
cardiovascular medicine. 2nd ed. Philadelphia: W.B. Saunders Company, 19841399. Goodwin JF. The frontiers of cardiomyopathy. Br Heart J 1982;48:1. Benotti JR, Grossman W, Cohn PF. Clinical profile of restrictive cardiomyopathy. Circulation 1980,61:1206. Siegel RJ, Shah PK, Fishbein MC. Idiopathic restrictive cardiomyopathy. Circulation 1984;70:165. Shabetai R, Grossman W. Profiles in constrictive pericarditis, restrictive cardiomyopathy, and cardiac tamponade. In: Grossman W, editor. Cardiac catheterization and angiography. 2nd ed. Philadelphia: Lea & Febiger, 1980:358. 6. Cassling RS, Lortz JB, Olson DR, Hubbard TF, McManus BM. Fatal vasculitis (periarteritis nodosa) of the coronary arteries: Angiographic ambiguities and absence of aneurysms at autopsy. J Am Co11 Cardiol 1985;6:707.
Septic pulmonary emboli secondary infected right atrial thrombus
to an
Diana Lam, M.D., Bianka Emilson, and Elliot Rapaport, M.D., San Francisco, Calif. Right atria1 thrombi occur lessfrequently than clots in the left atrium. We wish to report a patient who, in the clinical setting of suspectedright heart endocarditis, was found echocardiographically to have a large right atria1 mass. This massproved to be a thrombus at surgery. A 37-year-old male intravenous heroin abuserpresented From the Cardiology Division of the Medical Service, San Francisco General Hospital Medical Center. Reprint requests: Elliot Rapaport, M.D., 5Gl Cardiology Division, San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110.
July 1987 Heart Journal
with a 3-day history of fever, chills, and pleuritic chest pain. Blood cultures were positive for Staphylococcus aureus. He received a l-day’s dose of nafcillin before leaving the hospital against medical advice. He returned 2 weekslater appearing cachectic, frankly toxic, and febrile to 38.4’ C. He was in respiratory distress and had developed hemoptysis. A chest film revealed multiple nodular densities in the lung fields, many with central cavitation, suggestive of septic emboli. Of note, careful examination of his extremities revealed no evidence of thrombophlebitis. A two-dimensional echocardiographic study revealed a brightly echogenicright atria1 (RA) mass that appearedattached at its baseto the lateral atria1 wall. The masswasprimarily situated posteriorly in the RA, at the origin of the inferior vena cava (IVC) (Fig. 1). During atria1 systole, it maderolling excursionstoward, but never through, the tricuspid valve (Fig. 2). The IVC waspatent when examined subcostally. All cardiac valves appeared normal and without evidence of vegetation. The initial echocardiographicimpressionwaseither that of a vegetation unattached to the tricuspid valve or a thrombus. Recurrent fevers despite antimicrobial therapy prompted surgical removal of the RA mass,which was suspectedto be the source of ongoingsepsis.At surgery the large 6 x 5 cm pedunculated mass(Fig. 3) wasfound attached to the RA at the junction of the IVC. The tricuspid valve was found to be uninvolved and appeared grossly normal. Pathologically, a few coloniesof gram-positive cocci were found within the sectionedorganized thrombus. Microbiologic cultures, however, failed to yield any organisms. An RA thrombus may be primary in origin or may be from a peripheral venous source.Primary RA thrombi are seen in low-output states, cardiomyopathy, cardiac arrhythmias, and in states associatedwith an enlarged right atrium.’ RA thrombus has also been described as a complication following right heart catheterization (in-
Fig. 1. Apical four-chamber view showing the echogenic thrombus (arrow) in the right atrium unattached to the tricuspid valve. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.
Volume Number
114 1, Part 1
Brief
Communications
179
Fig. 2. Parasternal short-axis view showingthe thrombus (arrow) attached to the lateral right atria1 wall, rolling toward but never through the tricuspid valve. Ao = aorta; TrV = tricuspid valve.
Fig.
3. Pathologic specimenof the thrombus resected from the patient’s right posterolateral atria1 wall.
dwelling pulmonary arterial catheters,* central venous alimentationp and transvenous pacemaker4).Echocardiographically, primary RA thrombi are usually relatively immobile and are attached to the atria1 wa11.5RA clots arising from peripheral venous sources,on the other hand, are generally elongated, freely mobile, and have no attachments.5~6 Two-dimensional echocardiographic evidence of these transiently trapped thromboemboli in the right atrium or right ventricle is being increasingly recognized.? The early antemortem detection of right heart thrombi in the clinical setting of pulmonary embolism has led to prompt successfulsurgical intervention in somereported casesand thereby avoidance of a potentially devasting outcome.5.1Finally, the differential diagnosis of an RA mass also includes tumors, most commonly myxomas. Echocardiographically, myxomas are usually globular or spherical masses,with well-delineated borders, and an internal speckledappearancedue to their tissue composition. They are generally mobile and are usually attached to the interatrial septum.8 Pyrexia, positive blood cultures, and pulmonary emboli
in the setting of intravenous drug abusewould suggestthe diagnosisof right-sided endocarditis in our patient? The absenceof grossevidence of right-sided valvular endocarditis in this patient may have been due to eradication of a small vegetation by antibiotic therapy, embolization of vegetations to the lung, or to valvulitis that was present but was subclinical. However, the clean valve at surgery mitigates against any of these postulates. It seemsmore reasonableto assumethat the infected RA thrombus was the sole source of the septic pulmonary emboli. The echocardiographicfinding of a large, infected, primary RA thrombus is rare. Its early detection importantly guided medical managementin the reported patient. We gratefully acknowledge phen Burns and the technical Becali.
the secretarial assistance of Steassistance of Marianne Franceschi-
REFERENCES
1. Panidis IP, Kotler MN, echocardiographic features
1984;107:745-758.
Mintz GS, Ross J. Clinical and of right atria1 masses. AM HEART J
180
Brief
Communications
American
2. Rowley KM, Clubb KS, Smith JW, Cabin HS. Right-sided infective endocarditis as a consequence of flow-directed pulmonary-artery catheterization. N Engl J Med 1984;31:1152-1156. 3. Pliam ME, Mogough EC, Nixon GW, Ruttenberg HD. Right atria1 ball valve thrombus: A complication of central venous aliment&ion in an infant. Diagnosis and successful surgical management of a case. J Thorac Cardiovasc Surg 1979;7&579. 4. Chan W, Ikram H. Echocardiographic demonstration of tricuspid valvulitis and right atria1 thrombus complicating an infected artificial pacemaker. A case report. Angiology 1978;29:559. 5. Felner JM, Churchwell AL, Douglas MA. Right atria1 thromboemboli: Clinical, echocardiographic and pathophysiologic manifestations. J Am Co11 Cardiol 1984;4:1041-1051. 6. Rosenweig MS, Nanda NC. Two-dimensional echocardiographic detection of circulating right atria1 thrombi. AM HEART J 1982;103:435-436. 7. Saner HE, Asinger RW, Daniel JA, Elsperger KJ: Twodimensional echocardiographic detection of right-sided cardiac intracavity thromboembolus with pulmonary embolism. J Am Co11 Cardiol 1984;4:1294-1301. 8. Come PC, Kurland GS, Vine HS. Two-dimensional echocardiography in differentially right atria1 and tricuspid valve mass lesions. Am J Cardiol 1979;44:1207-1212. 9. Robbins MJ, Soeiro R, Frishman WH, Strom JA. Right-sided valvular endocarditis: Etiology, diagnosis and an approach to therapy. AM HEART J 1986;111:128-135.
Termination of ventricular tachycardia transcutaneous cardiac pacing S. Serge Barold, M.B., B.S., F.R.A.C.P., Michael D. Falkoff, M.D., Ling S. Ong, M.D., Robert A. Heinle, M.D. Rochester, N. Y.
by
and
Transcutaneous external cardiac pacing was originally described in 1952 by Zoll,’ but poor patient tolerance led to its abandonment a few years later with the introduction
of transvenousendocardial pacing. However, transcutaneous cardiac pacing has regained popularity since 1983, when Falk et al.* demonstrated the feasibility of noninvasive pacing with large high impedance electrodes and a pulse generator delivering stimulation with a long pulse width of 20 to 40 msec. Several reports3-6have since confirmed the efficacy of transcutaneous pacing and its good patient tolerance for the treatment of bradycardia. Zoll et al3 recently reported their extensive experience with transcutaneous cardiac pacing involving five centers and indicated that they had unsuccessfullyattempted to terminate supraventricular tachycardia in six patients and ventricular tachycardia in two patients. In contrast, we successfullyterminated ventricular tachycardia by trans-
From the Division of Cardiology, Department of Medicine, Hospital, and the University of Rochester School of Medicine
The Genesee and Dentist-
ry. Reprint Hospital,
requests: Dr. S. Serge Barold, Division of Cardiology, 224 Alexander St., Rochester, NY 14607.
The Genesee
July 1987 Heart Journal
cutaneous cardiac pacing in a patient with recurrent. well-tolerated sustained ventricular tachycardia, and our observations constitute the basis of this brief report. A 69-year-old man was admitted to The Genesee Hospital for the treatment of recurrent sustained ventricular tachycardia. The patient suffered an anteroseptal myocardial infarction in 1980 and underwent coronary bypass surgery in early 1985 for severe three-vessel coronary artery disease. He remained well for about 7 months and then developed recurrent sustained ventricular tachycardia at a rate of 170/min while on no antiarrhythmic therapy. He was transferred to The Genesee Hospital because the ventricular tachycardia was refractory to conventional antiarrhythmic drugs used either singly or in combination. An invasive (transvenous) electrophysiologic study was performed when the patient was on procainamide at a level of 8 pg/ml. During a basic ventricular drive of lOO/min, the delivery of two premature ventricular stimuli induced sustained ventricular tachycardia, with a configuration identical to the spontaneous episodes, but at a rate of 150/min. Ventricular tachycardia was easily converted to sinus rhythm by burst ventricular pacing at 200/min. Amiodarone was started, and procainamide was continued. Several days later, procainamide was discontinued because ventricular tachycardia recurred when the level was 13 kg/ml. Quinidine gluconate and later tocainide were added to amiodarone therapy. For about 3 weeks the patient experienced numerous episodes of sustained ventricular tachycardia at a rate of 140 to 160/min, inconsistently terminated by intravenous lidocaine, and numerous cardioversions were performed. Many attacks of ventricular tachycardia were converted to sinus rhythm with a synchronized shock of 1 or 5 J delivered without sedation or anesthesia. Occasionally shocks of 20 J Or more were required, and these were always delivered with sedation. On two occasions a 50 J synchronized shock caused acceleration of ventricular tachycardia and degeneration into ventricular fibrillation, requiring immediate defibrillation. The attacks of ventricular tachycardia remained frequent even 4 weeks after starting amiodarone therapy, but the rate gradually slowed to about 100 to 105/min. Over a period of 4 days, five attacks of sustained ventricular tachycardia at a rate of 100 to 105/min were easily and quickly terminated by transcutaneous cardiac pacing with a Zoll-ZMI external pacemaker (ZMI Corporation, Cambridge, Mass.). The threshold for cardiac pacing was 80 mA (pulse width 40 msec). Initially we tried competitive asynchronous pacing (by removing the monitoring electrodes) at a rate of SO/min and at 90 mA output. This was discontinued in about 15 seconds to avoid prolonged chest discomfort. Subsequently, a short burst of five stimuli at 90 mA and the maximum rate setting (180/min) of the pacemaker successfully terminated the ventricular tachycardia (Fig. 1). Over the next 4 days, another four attacks of ventricular tachycardia at a rate of 100 to 105/min occurred and they were also successfully terminated by the delivery of five to eight transcutaneous stimuli at the maximum rate setting of the pacemaker and an output of
Brief
Communications
American
cardiovascular medicine. 2nd ed. Philadelphia: W.B. Saunders Company, 19841399. Goodwin JF. The frontiers of cardiomyopathy. Br Heart J 1982;48:1. Benotti JR, Grossman W, Cohn PF. Clinical profile of restrictive cardiomyopathy. Circulation 1980,61:1206. Siegel RJ, Shah PK, Fishbein MC. Idiopathic restrictive cardiomyopathy. Circulation 1984;70:165. Shabetai R, Grossman W. Profiles in constrictive pericarditis, restrictive cardiomyopathy, and cardiac tamponade. In: Grossman W, editor. Cardiac catheterization and angiography. 2nd ed. Philadelphia: Lea & Febiger, 1980:358. 6. Cassling RS, Lortz JB, Olson DR, Hubbard TF, McManus BM. Fatal vasculitis (periarteritis nodosa) of the coronary arteries: Angiographic ambiguities and absence of aneurysms at autopsy. J Am Co11 Cardiol 1985;6:707.
Septic pulmonary emboli secondary infected right atrial thrombus
to an
Diana Lam, M.D., Bianka Emilson, and Elliot Rapaport, M.D., San Francisco, Calif. Right atria1 thrombi occur lessfrequently than clots in the left atrium. We wish to report a patient who, in the clinical setting of suspectedright heart endocarditis, was found echocardiographically to have a large right atria1 mass. This massproved to be a thrombus at surgery. A 37-year-old male intravenous heroin abuserpresented From the Cardiology Division of the Medical Service, San Francisco General Hospital Medical Center. Reprint requests: Elliot Rapaport, M.D., 5Gl Cardiology Division, San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110.
July 1987 Heart Journal
with a 3-day history of fever, chills, and pleuritic chest pain. Blood cultures were positive for Staphylococcus aureus. He received a l-day’s dose of nafcillin before leaving the hospital against medical advice. He returned 2 weekslater appearing cachectic, frankly toxic, and febrile to 38.4’ C. He was in respiratory distress and had developed hemoptysis. A chest film revealed multiple nodular densities in the lung fields, many with central cavitation, suggestive of septic emboli. Of note, careful examination of his extremities revealed no evidence of thrombophlebitis. A two-dimensional echocardiographic study revealed a brightly echogenicright atria1 (RA) mass that appearedattached at its baseto the lateral atria1 wall. The masswasprimarily situated posteriorly in the RA, at the origin of the inferior vena cava (IVC) (Fig. 1). During atria1 systole, it maderolling excursionstoward, but never through, the tricuspid valve (Fig. 2). The IVC waspatent when examined subcostally. All cardiac valves appeared normal and without evidence of vegetation. The initial echocardiographicimpressionwaseither that of a vegetation unattached to the tricuspid valve or a thrombus. Recurrent fevers despite antimicrobial therapy prompted surgical removal of the RA mass,which was suspectedto be the source of ongoingsepsis.At surgery the large 6 x 5 cm pedunculated mass(Fig. 3) wasfound attached to the RA at the junction of the IVC. The tricuspid valve was found to be uninvolved and appeared grossly normal. Pathologically, a few coloniesof gram-positive cocci were found within the sectionedorganized thrombus. Microbiologic cultures, however, failed to yield any organisms. An RA thrombus may be primary in origin or may be from a peripheral venous source.Primary RA thrombi are seen in low-output states, cardiomyopathy, cardiac arrhythmias, and in states associatedwith an enlarged right atrium.’ RA thrombus has also been described as a complication following right heart catheterization (in-
Fig. 1. Apical four-chamber view showing the echogenic thrombus (arrow) in the right atrium unattached to the tricuspid valve. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.
Volume Number
114 1, Part 1
Brief
Communications
179
Fig. 2. Parasternal short-axis view showingthe thrombus (arrow) attached to the lateral right atria1 wall, rolling toward but never through the tricuspid valve. Ao = aorta; TrV = tricuspid valve.
Fig.
3. Pathologic specimenof the thrombus resected from the patient’s right posterolateral atria1 wall.
dwelling pulmonary arterial catheters,* central venous alimentationp and transvenous pacemaker4).Echocardiographically, primary RA thrombi are usually relatively immobile and are attached to the atria1 wa11.5RA clots arising from peripheral venous sources,on the other hand, are generally elongated, freely mobile, and have no attachments.5~6 Two-dimensional echocardiographic evidence of these transiently trapped thromboemboli in the right atrium or right ventricle is being increasingly recognized.? The early antemortem detection of right heart thrombi in the clinical setting of pulmonary embolism has led to prompt successfulsurgical intervention in somereported casesand thereby avoidance of a potentially devasting outcome.5.1Finally, the differential diagnosis of an RA mass also includes tumors, most commonly myxomas. Echocardiographically, myxomas are usually globular or spherical masses,with well-delineated borders, and an internal speckledappearancedue to their tissue composition. They are generally mobile and are usually attached to the interatrial septum.8 Pyrexia, positive blood cultures, and pulmonary emboli
in the setting of intravenous drug abusewould suggestthe diagnosisof right-sided endocarditis in our patient? The absenceof grossevidence of right-sided valvular endocarditis in this patient may have been due to eradication of a small vegetation by antibiotic therapy, embolization of vegetations to the lung, or to valvulitis that was present but was subclinical. However, the clean valve at surgery mitigates against any of these postulates. It seemsmore reasonableto assumethat the infected RA thrombus was the sole source of the septic pulmonary emboli. The echocardiographicfinding of a large, infected, primary RA thrombus is rare. Its early detection importantly guided medical managementin the reported patient. We gratefully acknowledge phen Burns and the technical Becali.
the secretarial assistance of Steassistance of Marianne Franceschi-
REFERENCES
1. Panidis IP, Kotler MN, echocardiographic features
1984;107:745-758.
Mintz GS, Ross J. Clinical and of right atria1 masses. AM HEART J
180
Brief
Communications
American
2. Rowley KM, Clubb KS, Smith JW, Cabin HS. Right-sided infective endocarditis as a consequence of flow-directed pulmonary-artery catheterization. N Engl J Med 1984;31:1152-1156. 3. Pliam ME, Mogough EC, Nixon GW, Ruttenberg HD. Right atria1 ball valve thrombus: A complication of central venous aliment&ion in an infant. Diagnosis and successful surgical management of a case. J Thorac Cardiovasc Surg 1979;7&579. 4. Chan W, Ikram H. Echocardiographic demonstration of tricuspid valvulitis and right atria1 thrombus complicating an infected artificial pacemaker. A case report. Angiology 1978;29:559. 5. Felner JM, Churchwell AL, Douglas MA. Right atria1 thromboemboli: Clinical, echocardiographic and pathophysiologic manifestations. J Am Co11 Cardiol 1984;4:1041-1051. 6. Rosenweig MS, Nanda NC. Two-dimensional echocardiographic detection of circulating right atria1 thrombi. AM HEART J 1982;103:435-436. 7. Saner HE, Asinger RW, Daniel JA, Elsperger KJ: Twodimensional echocardiographic detection of right-sided cardiac intracavity thromboembolus with pulmonary embolism. J Am Co11 Cardiol 1984;4:1294-1301. 8. Come PC, Kurland GS, Vine HS. Two-dimensional echocardiography in differentially right atria1 and tricuspid valve mass lesions. Am J Cardiol 1979;44:1207-1212. 9. Robbins MJ, Soeiro R, Frishman WH, Strom JA. Right-sided valvular endocarditis: Etiology, diagnosis and an approach to therapy. AM HEART J 1986;111:128-135.
Termination of ventricular tachycardia transcutaneous cardiac pacing S. Serge Barold, M.B., B.S., F.R.A.C.P., Michael D. Falkoff, M.D., Ling S. Ong, M.D., Robert A. Heinle, M.D. Rochester, N. Y.
by
and
Transcutaneous external cardiac pacing was originally described in 1952 by Zoll,’ but poor patient tolerance led to its abandonment a few years later with the introduction
of transvenousendocardial pacing. However, transcutaneous cardiac pacing has regained popularity since 1983, when Falk et al.* demonstrated the feasibility of noninvasive pacing with large high impedance electrodes and a pulse generator delivering stimulation with a long pulse width of 20 to 40 msec. Several reports3-6have since confirmed the efficacy of transcutaneous pacing and its good patient tolerance for the treatment of bradycardia. Zoll et al3 recently reported their extensive experience with transcutaneous cardiac pacing involving five centers and indicated that they had unsuccessfullyattempted to terminate supraventricular tachycardia in six patients and ventricular tachycardia in two patients. In contrast, we successfullyterminated ventricular tachycardia by trans-
From the Division of Cardiology, Department of Medicine, Hospital, and the University of Rochester School of Medicine
The Genesee and Dentist-
ry. Reprint Hospital,
requests: Dr. S. Serge Barold, Division of Cardiology, 224 Alexander St., Rochester, NY 14607.
The Genesee
July 1987 Heart Journal
cutaneous cardiac pacing in a patient with recurrent. well-tolerated sustained ventricular tachycardia, and our observations constitute the basis of this brief report. A 69-year-old man was admitted to The Genesee Hospital for the treatment of recurrent sustained ventricular tachycardia. The patient suffered an anteroseptal myocardial infarction in 1980 and underwent coronary bypass surgery in early 1985 for severe three-vessel coronary artery disease. He remained well for about 7 months and then developed recurrent sustained ventricular tachycardia at a rate of 170/min while on no antiarrhythmic therapy. He was transferred to The Genesee Hospital because the ventricular tachycardia was refractory to conventional antiarrhythmic drugs used either singly or in combination. An invasive (transvenous) electrophysiologic study was performed when the patient was on procainamide at a level of 8 pg/ml. During a basic ventricular drive of lOO/min, the delivery of two premature ventricular stimuli induced sustained ventricular tachycardia, with a configuration identical to the spontaneous episodes, but at a rate of 150/min. Ventricular tachycardia was easily converted to sinus rhythm by burst ventricular pacing at 200/min. Amiodarone was started, and procainamide was continued. Several days later, procainamide was discontinued because ventricular tachycardia recurred when the level was 13 kg/ml. Quinidine gluconate and later tocainide were added to amiodarone therapy. For about 3 weeks the patient experienced numerous episodes of sustained ventricular tachycardia at a rate of 140 to 160/min, inconsistently terminated by intravenous lidocaine, and numerous cardioversions were performed. Many attacks of ventricular tachycardia were converted to sinus rhythm with a synchronized shock of 1 or 5 J delivered without sedation or anesthesia. Occasionally shocks of 20 J Or more were required, and these were always delivered with sedation. On two occasions a 50 J synchronized shock caused acceleration of ventricular tachycardia and degeneration into ventricular fibrillation, requiring immediate defibrillation. The attacks of ventricular tachycardia remained frequent even 4 weeks after starting amiodarone therapy, but the rate gradually slowed to about 100 to 105/min. Over a period of 4 days, five attacks of sustained ventricular tachycardia at a rate of 100 to 105/min were easily and quickly terminated by transcutaneous cardiac pacing with a Zoll-ZMI external pacemaker (ZMI Corporation, Cambridge, Mass.). The threshold for cardiac pacing was 80 mA (pulse width 40 msec). Initially we tried competitive asynchronous pacing (by removing the monitoring electrodes) at a rate of SO/min and at 90 mA output. This was discontinued in about 15 seconds to avoid prolonged chest discomfort. Subsequently, a short burst of five stimuli at 90 mA and the maximum rate setting (180/min) of the pacemaker successfully terminated the ventricular tachycardia (Fig. 1). Over the next 4 days, another four attacks of ventricular tachycardia at a rate of 100 to 105/min occurred and they were also successfully terminated by the delivery of five to eight transcutaneous stimuli at the maximum rate setting of the pacemaker and an output of