1788 Alum and Silverman

1 I-second pause (Fig. 1). After the sinus pause, a marked decrease in waveform amplitude was noted bilaterally on the EEG followed by low-amplitude generalized fast activ- ity, which corresponded clinically to tonic-clonic seizure activity. Thirty seconds after the onset of the seizure and the return of the heart rate to baseline, there was cessation of seizure activity clinically and on EEG. A permanent VVI pacemaker was implanted the following day without com- plications. Telemetry monitoring after insertion of a pace- maker revealed no further episodes of bradycardia. The patient has had no further episodes of syncope or seizure activity during 14 months of follow-up.

Although loss of consciousness as a result of inadequate cardiac output is a common symptom associated with car- diac arrhythmias, frank seizure activity is a rare occur- rence.z-s This is the first report in which a seizure precip- itated by a period of asystole was documented by standard, simultaneous EEG and ECG recordings. As illustrated by this case, a marked reduction in EEG amplitude after the period of asystole is characteristic of cerebral ischemia and is the likely precipitant of the seizure. Without the use of simultaneous EEG and ECG monitoring, a correct diagno- sis could not have been made. Thus all adults with a new- onset seizure disorder, in whom routine EEG is nondiag- nostic, should have a careful cardiac and neurologic eval- uation, This is particularly relevant in elderly persons who may have unsuspected conduction system disease. The use of simultaneous EEG and ECG recordings or ambulatory EEG and ECG monitoring may provide useful diagnostic information and allow the physician to institute appropri- ate therapy.

REFERENCES

1.

2.

3.

4.

5.

Manolis AS, Linzer M, Salem D, Estes III NAM. Syncope: current diagnostic evaluation and management. Ann Intern Med 1990;112:850-63. Ziegler DK. Syncope and seizure. In: Rowland LP, ed. Mer- ritt’s textbook of neurology. Philadelphia: Lea & Febiger, 1989:14-21. Horn CA, Beckman RH, Dick II M, Lacina SJ. The congenital long QT syndrome. Am J Dis Child 1986;140:659-61. La<CW, Ziegler DK. Syncope problem solved by continuous ambulatorv simultaneous EEG/ECG recordine. Neuroloev 1981;31:11b4.

Y”

Beauregard LM, Fabiszewski R, Black CH, Lightfoot B, Schraeder PL, Toly T, Waxman HL. Combined ambulatory electroencephalographic and electrocardiographic recording for evaluation of syncope. Am J Cardiol 1991;68:1067-72.

Apical left ventricular lipoma presenting as syncope

Mohsin Alam, MD, and Norman Silverman, MD Detroit, Mich.

From tile Henry Ford Heart and Vascular Institute, Henry Ford Hospital.

Reprint requests: Mohsin Alam, MD, Echo-Doppler Laboratory, K-14, Henry Ford Hospital, 2799 W. Grand Blvd., Detroit MI 48202.

A.v HEANT J 1993;125:1788-1790

Copyright ’ 1993 by Mosby-Year Book, Inc. 0002.8703/93/$1.00 + .I0 4/4/45682

June 1993 American Hear1 Journal

lntracavitary tumors arising from either the right or left ventricle are usually benign and include myxoma, fibroma, papilloma, hemangioma and, in children, rhabdomyoma. Rarely, a malignant sarcoma encroaches on the right ven- tricular cavity. These tumors are most often diagnosed by two-dimensional echocardiography. Syncope can be a rare manifestation of ventricular tumors.‘-” Since lipoma is usually intramural or epicardial in location, it rarely obstructs blood flow. We present a patient with apical left ventricular lipoma who had recurrent syncope. The syn- cope was probably a result of intermittent obstruction of the left ventricular outflow tract by this elongated tumor duringsystole. To the best, of our knowledge, this is the first report of left ventricular lipoma in the apex of the left ven- tricle resulting in outflow obstruction.

A 67-year-old white man. who was in good health previ- ously, had a a-week history of recurrent syncope. The pa- tient first had an episode of syncope while stretching his neck back while he was on a ladder; he awoke to find him- self on the floor, sustaining a compression fracture of the seventh thoracic vertebra. Subsequently the patient would become dizzy if he sat up and would get relief by laying flat. Physical examination revealed blood pressure of 120 to 130 systolic to 70 to 80 mm Hg diastolic in supine, sitting, and standing positions. Pulse was 74 beats/min and regular. Cardiovascular examination was otherwise completely nor- mal with no gallops or murmurs. An electrocardiogram showed normal sinus rhythm and was otherwise normal. Telemetry and %4-hour Holter ECG monitoring were unremarkable for arrhythmia. The patient had a second episode of syncope in the hospital, which was witnessed. The patient was found slumped in a wheel chair while waiting for an echocardiogram and was unresponsive. He had a very faint pulse without tachycardia or bradycardia and was very diaphoretic. As soon as the patient was placed on a stretcher, before possible cardiopulmonary resuscita- tion, he awakened without sequelae. He was found to have a bounding pulse and normal blood pressure at this point. ECG revealed sinus tachycardia with a rate of 102 beats/ min. Transthoracic echocardiography demonstrated an apical left ventricular mass, which protruded into the left ventricle chamber near the outflow tract during systole (Fig. 1). There were no changes in tumor morphology, mo- tion pattern, or left ventricular Doppler inflow or outflow velocities in the supine or left lateral position. A transe- sophageal study performed to better delineate the site of attachment of the ventricular mass confirmed the findings of the transthoracic study (Fig. 2). Cardiac catheterization performed primarily to evaluate the coronary arteries be- fore surgical removal of the mass revealed insignificant ar- teriosclerotic lesions. A pulmonary artery injection with levophase angiography revealed an apical left, ventricular filling defect. Because of the patient’s symptoms, he was referred for surgery. At surgery the mass was excised by an incision in the left atrium and through the mitral valve. The mass, located in the left ventricular apex, was excised (Fig. 3) and found to be a lipoma by gross and microscopic ex- amination. The patient has been followed for 7 months and has had no recurrence of syncope. Coumadin has been pre- scribed for a 6-month period as prophylaxis against throm-

Volume 125, Number 6 American Heart Journal Alam and Silverman 1789

Fig. 1. Transthoracic two-dimensional echocardiogram from apical window. Note tumor (arrows) extending from apex of left ventricle with tip encroaching on left ventricular outflow tract. A, Aorta; LV, left ventricle; T, tumor.

Fig. 2. Transesophageal two-dimensional echocardiogram in biplane two-chamber view of the heart. Note elongated tumor (arrows) in left ventricle chamber. LA, Left atrium; LV, left ventricle; T, tumor.

bus formation at the site of attachment of the tumor in the left ventricle.

Syncope is not an unusual presenting feature of right and, less commonly, left atria1 myxoma.5r 6 Rarely syncope may be related to intravenous extension of metastatic tu- mors obstructing the mitral or tricuspid orifices.7s * To the best of our knowledge, there are only two case reports of left ventricular tumors located in the left ventricular outflow tract that resulted in symptoms of syncope or presynco- pe.3, lo We are not aware of a tumor located in the apex of

the left ventricle accounting for syncope. We believe that our patient had intermittent obstruction of the left ven- tricular outflow tract by the tip of the tumor, resulting in episodes of syncope and near syncope. This is supported by the fact that since surgery, the patient has had no symp- toms. Inasmuch as the symptoms were posture related, it is possible that changes in preload may also have contrib- uted to tumor obstructing the outflow tract. However, all echocardiographic studies were performed in a supine or left lateral position and not in a sitting or standing posture.

1790 Madu et al. June 1993

American Heart Journal

Fig. 3. Gross anatomic specimen of tumor (lipoma) excised from left ventricle.

We believe this is the first case report of a lipoma of the left ventricle detected by two-dimensional echocardiography resulting in syncope. Lipomatous hypertrophy of the atria1 septum and its free wall is not an unusual finding. These occur most frequently in elderly patients (>60 years of age) and less frequently (25 % ) in younger persons. Cardiac symptoms include atria1 and ventricular arrhythmias, or there may be no symptoms. Histologic findings consist of varying proportions of mature adipose tissue, fetal fat, en- trapped myocytes, blood vessels, and fibrous tissue.‘l Lipomas have been seen in the left ventricle (four patients) and two were asymptomatic.ll Right ventricular tumors have also been incriminated in the pathogenesis of syncope in that they can obstructing the right ventricular outflow tract.3l4 Tumors may involve the sinus nodeI or the base of the ventricular septum and the conducting system,3 re- sulting in bradyarrhythmia and/or tachyarrhythmia and/or syncope. Ventricular tachycardia may result from ventric- ular tumors, and this has also been implicated in the pathogenesis of syncope.2 In conclusion, an intracavitary lipoma of the left ventricle is presented that can be diag- nosed by two-dimensional echocardiography and may be implicated in the pathophysiology of syncopal episodes. Surgical removal of the tumor is curative and is warranted in symptomatic patients.

REFERENCES

1. Burke A, Johns JP, Virmani R. Hemangiomas of the heart. A clinicopathologic study of ten cases. Am J Cardiovasc Path01 1990;3:283-90.

2. Sheldon R, Isaac D. Metastatic melanoma to the heart presenting with ventricular tachycardia. Chest 1991;99: 1296-8.

3. Grieg LE. Downev W. Tatoulis J. Hunt D. Benien congenital I - I -

intracardiac thyroid and polycystic tumor causing right ven- tricular outflow tract obstruction and conduction disturbance. J Am Co11 Cardiol 1987;9:225-7.

4. Labib SB, Schick EC, Isner JM. Obstruction of right ventric- ular outflow tract caused by intracavitary metastatic disease: analysis of 14 cases. J Am Co11 Cardiol 1992;19:1664-8.

5. Puff M, Taff ML, Spitz WU, Eckert WG. Syncope and sudden

death caused by mitral valve myxomas. Am J Forensic Med Pathol 1986;7:84-6.

6. Peterson DI. Syncope due to right atria1 myxoma. Bull Clin Neurosci 1984;49:63-6.

7. Fogel RI, Balady GJ, Klein MD, Rajaii-Khorasani A. Meta- static renal cell carcinoma. An unusual cause of syncope. Chest 1990;98:481-2.

8. Lee PK, David TE, Sloggett C, Ross JR. Intravenous leiomy- omatosis with intracardiac extension: an unusual cause of car- diac syncope. Can Med Assoc ,J 1990;142:1257-9.

9. Rosenzweig A, Harrigan P, Popvic AD. Left ventricular myx- oma simulating aortic stenosis. AM HEART J 1989;117:962-3.

10. Bernstein M, Gerein A, Peretz DK. A case of left ventricular outflow trace tumor causing obstruction. J Thorac Cardiovasc Surg 1970;60:166-73.

11. McAllister Jr HA, Fenoglio JJ. Tumors of the cardiovascular system. Atlas of tumor pathology, Second Series, Fascicle 15. Washington, DC: Armed Forces Institute of Pathology, 20306. 6000.

12. Dolan G, Jones AP, Reilly JT. Immunoblastic lymphoma pre- senting with syncope due to sinoatrial node disease. Postgrad Med J 1990:66:395-7.

Primary intimal sarcoma of the pulmonary trunk simulating pulmonary embolism

Ernest C. Madu, MD,” David C. Taylor, BS,b Dennis S. Durzinsky, MD,” and Theodore D. Fraker, Jr., MD” Toledo, Ohio

From the Departments of aMedicine, “Pathology, and cSurgery, The Med- ical College of Ohio.

Reprint requests: Theodore D. Fraker, Jr., MD, Department of Medicine, Medical College of Ohio, 3000 Arlington Ave., P.O. Box 10008, Toledo, OH 43699.

AM HEART J 1993;125:1790-1792 Copyright 3 1993 by Mosby-Year Book, Inc. 0002-8703/93/$1.00 + .lO 4/4/45668