2
828 BRIEF REPORTS icant decrease in the size of the thrombus. A diagnosis of cerebral embolism was made and anticoagulant therapy was continued. The patient$ condition progressively deteriorated and she died 2 weeks later. In the 2 patients described, the findings were typical of thrombi; however, in contrast to previous studies,2p3 the LV wall motion was normal. The occurrence of systemic emboli was confirmed in case 1 and appeared highly likely in case 2. Both patients had a marked de- crease in the size of the LV thrombus after the embolic events on follow-up echocardiographic studies. Al- though the relative role of thrombus mobility could not be adequately defined, it appears reasonable to assume that normal ventricular systolic function was a con- tributing factor in causing emboli. The mechanism of development of thrombi in the presence of normal ventricular wall motion is unclear, but it is notable that both patients had an underlying malignant disease that was associated with an increased incidence of thrombosis.4 In addition, in case 1 there was marked eosinophilia, which in the setting of idiopathic hypereosinophic syndrome has been associated with intracardiac thrombi and embolism.5 Prior studies have suggested that 2-dimensional echocardiographic studies are of limited value in the assessment of patients with systemic embolic without clinical evidence of underlying heart disease.6 Our ob- servations in these 2 patients suggest that 2-dimensional echocardiography may be of value even if underlying heart disease is not suspected. This may be particularly true in patients with an underlying malignancy. The combination of LV thrombi and normal wall motion may increase the likelihood of subsequent embolic events. Acknowledgment: We gratefully acknowledge the assis- tance of Harriet Yankowitz in the preparation of this manuscript. 1. 2. 3. 4. 8. 6. References Haughland JM, Asinger RW, Mike11 FL, Elsperger J, Hodges Y. Embolic potential of left ventricular thrombi detected by two-dimensional echocar- diogaphy. Circulation 1984;70:586-598. Asinger RW, Mikell FL, Sharna 6, Hodges, M. Observations on detecting left ventricular thrombus with two-dimensional echocardiography: emphasis or avoidance of false positive diagnosis. Am J Cardiol 1981;47:145-156. Reeder GS, Tajik AJ, Seward JB. Left ventricular mural thrombus: two di- mensional echocardiographic diagnosis. Mayo Clin Proc 1981;58:82-88. Holland JF, Frei E. The hemostatic process and neoplastic disease. In: Cancer Medicine 2nd ed. Philadelphia: Lea & Febiger, 1982: 1328-1338. Goltdlener J-S, Barry MJ, Schooley RT, Harley JB, Roberts WL. Favll AS. Two-dimensional edhocardiograptiic assessnient of idiopathic hypereosi- noohilic svndrome. Circulation 1983:67:572-578. G&enland P, Knopman D, tilkell FL. Asinger RW, Anderson D, Good D. Echocardiography in diagnostic assessment of Stroke. Ann Intern Med 1981;95:51-53. Benign Intracardiac Thyroid Mass Causing Right Ventricular Outflow Tract Obstruction RICHARD J. SHEMIN, MD JAMES D. MARSH, MD FREDERICK J. SCHOEN, MD, PhD The presence of thyroid tissue within the heart is rare. Most reports have described intracardiac metastases from thyroid carcinoma. Herein we describe for the first time a benign intracardiac thyroid mass that was suc- cessfully excised. A 5%year-old woman with past systemic hypertension was noted to have a systolic ejection murmur at age 52 years. By age 58 years the intensity of the murmur had increased to grade 4/6 and was present along the left sternal border. It radiated to the upper sternal area, and an associated pal- pable thrill was present. The second heart sound was single. The patient had noted recently a slight decrease in exercise tolerance. Chest radiograph revealed a normal-sized heart, clear lungs and a prominent main pulmonary artery. The electrocardiogram revealed borderline right ventricular hypertrophy. On admission to the hospital, a 2-dimensional echocardiogram demonstrated a 2.5 X 1.5 cm, ovoid right ventricular (RV) outflow tract mass attached to the RVside of the ventricular septum, proximal to the pulmonary valve From the Departments of Cardiothoracic Surgery, Cardiology and Pa- thology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02 115. Manuscript received March 11, 1985; revised manuscript received May 8, 1985, accepted May 9, 1985. with possible involvement of the cusps. During the cardiac cycle, the mass moved with a ball valve-like motion. The heart was normal in size, configuration and chamber size (Fig, 1). The patient underwent surgical exploration with use of cardiopulmonary bypass. The pulmonary artery was opened, revealing the ovoid mass herniating through the pulmonary valve (Fig. 1). The valve cusps were normal. By retracting the valve cusps, the mass was visualized, origi- nating just below the pulmonary valve and extending down along the ventricular septum with a broad base. The mass FIGURE 1. Left, frame from 2dimensional echocardiographic study showing a round mass in the right ventricular outflow track (seen as an echo-dense round mass near center of this frame). Upper right, intra- operative photograph of the mass (arrow) being delivered into the surgical field through the pulmonary valve. Lower right, the excised mass with a muscular margin from the attachment to the ventricular septum.

Benign intracardial thyroid mass causing right ventricular outflow tract obstruction

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828 BRIEF REPORTS

icant decrease in the size of the thrombus. A diagnosis of cerebral embolism was made and anticoagulant therapy was continued. The patient$ condition progressively deteriorated and she died 2 weeks later.

In the 2 patients described, the findings were typical of thrombi; however, in contrast to previous studies,2p3 the LV wall motion was normal. The occurrence of systemic emboli was confirmed in case 1 and appeared highly likely in case 2. Both patients had a marked de- crease in the size of the LV thrombus after the embolic events on follow-up echocardiographic studies. Al- though the relative role of thrombus mobility could not be adequately defined, it appears reasonable to assume that normal ventricular systolic function was a con- tributing factor in causing emboli.

The mechanism of development of thrombi in the presence of normal ventricular wall motion is unclear, but it is notable that both patients had an underlying malignant disease that was associated with an increased incidence of thrombosis.4 In addition, in case 1 there was marked eosinophilia, which in the setting of idiopathic hypereosinophic syndrome has been associated with intracardiac thrombi and embolism.5

Prior studies have suggested that 2-dimensional echocardiographic studies are of limited value in the

assessment of patients with systemic embolic without clinical evidence of underlying heart disease.6 Our ob- servations in these 2 patients suggest that 2-dimensional echocardiography may be of value even if underlying heart disease is not suspected. This may be particularly true in patients with an underlying malignancy. The combination of LV thrombi and normal wall motion may increase the likelihood of subsequent embolic events.

Acknowledgment: We gratefully acknowledge the assis- tance of Harriet Yankowitz in the preparation of this manuscript.

1.

2.

3.

4.

8.

6.

References Haughland JM, Asinger RW, Mike11 FL, Elsperger J, Hodges Y. Embolic potential of left ventricular thrombi detected by two-dimensional echocar- diogaphy. Circulation 1984;70:586-598. Asinger RW, Mikell FL, Sharna 6, Hodges, M. Observations on detecting left ventricular thrombus with two-dimensional echocardiography: emphasis or avoidance of false positive diagnosis. Am J Cardiol 1981;47:145-156. Reeder GS, Tajik AJ, Seward JB. Left ventricular mural thrombus: two di- mensional echocardiographic diagnosis. Mayo Clin Proc 1981;58:82-88. Holland JF, Frei E. The hemostatic process and neoplastic disease. In: Cancer Medicine 2nd ed. Philadelphia: Lea & Febiger, 1982: 1328-1338. Goltdlener J-S, Barry MJ, Schooley RT, Harley JB, Roberts WL. Favll AS. Two-dimensional edhocardiograptiic assessnient of idiopathic hypereosi- noohilic svndrome. Circulation 1983:67:572-578. G&enland P, Knopman D, tilkell FL. Asinger RW, Anderson D, Good D. Echocardiography in diagnostic assessment of Stroke. Ann Intern Med 1981;95:51-53.

Benign Intracardiac Thyroid Mass Causing Right Ventricular Outflow

Tract Obstruction

RICHARD J. SHEMIN, MD JAMES D. MARSH, MD

FREDERICK J. SCHOEN, MD, PhD

The presence of thyroid tissue within the heart is rare. Most reports have described intracardiac metastases from thyroid carcinoma. Herein we describe for the first time a benign intracardiac thyroid mass that was suc- cessfully excised.

A 5%year-old woman with past systemic hypertension was noted to have a systolic ejection murmur at age 52 years. By age 58 years the intensity of the murmur had increased to grade 4/6 and was present along the left sternal border. It radiated to the upper sternal area, and an associated pal- pable thrill was present. The second heart sound was single. The patient had noted recently a slight decrease in exercise tolerance. Chest radiograph revealed a normal-sized heart, clear lungs and a prominent main pulmonary artery. The electrocardiogram revealed borderline right ventricular hypertrophy. On admission to the hospital, a 2-dimensional echocardiogram demonstrated a 2.5 X 1.5 cm, ovoid right ventricular (RV) outflow tract mass attached to the RVside of the ventricular septum, proximal to the pulmonary valve

From the Departments of Cardiothoracic Surgery, Cardiology and Pa- thology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02 115. Manuscript received March 11, 1985; revised manuscript received May 8, 1985, accepted May 9, 1985.

with possible involvement of the cusps. During the cardiac cycle, the mass moved with a ball valve-like motion. The heart was normal in size, configuration and chamber size (Fig, 1). The patient underwent surgical exploration with use of cardiopulmonary bypass. The pulmonary artery was opened, revealing the ovoid mass herniating through the pulmonary valve (Fig. 1). The valve cusps were normal. By retracting the valve cusps, the mass was visualized, origi- nating just below the pulmonary valve and extending down along the ventricular septum with a broad base. The mass

FIGURE 1. Left, frame from 2dimensional echocardiographic study showing a round mass in the right ventricular outflow track (seen as an echo-dense round mass near center of this frame). Upper right, intra- operative photograph of the mass (arrow) being delivered into the surgical field through the pulmonary valve. Lower right, the excised mass with a muscular margin from the attachment to the ventricular septum.

November 1,1985 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 56

FIGURE 2. A, gross and histologic appearance of surgically resected cardiac thyroid mass. Left, external surface; right, cut surface. The appearance of the sectioned surface strongly resembles that of the normal thyroid gland. 6, photomicrograph showing myocardium (M) at left, adjacent to large colloid-containing follicles resembling thyroid (T). C, photomicrograph showing large follicles and the peripherally scalloped colloid (arrowheads) characteristic of hyperplastic thyroid. Hematoxylin-eosin stain; X 325, reduced 35%.

was excised with a margin of normal muscle on the ventric- ular septum (Fig. 1). The patient recovered uneventfully. The excised mass was “rubbery” and measured 2 x 2 x 1 cm (Fig. 2). The external surface of this mass had a dense fibrous capsule. Microscopically, the mass was composed of thyroid tissue that had variations in follicular size, focal hemor- rhage, fibrosis, and calcific and cholesterol deposits consis- tent with adenomatous hyperplasia. It was not neoplastic and it was consistent with an intracardiac ectopic rest.

Thyroid function tests revealed a Td of 8.6 mg% (normal, 5 to I1 mg% ), a thyroid binding globulin index of 0.95 (nor- mal, 0.85 to 1.10) and a thyroid stimulating hormone of 2.5 t.tU/ml (normal, less than 5 uUfm1). A 12sI scan revealed a normal thyroid gland in the neck and no evidence of other ectopic foci.

This is the first recorded case of a benign thyroid rest of the RV outflow tract found during life. A previous case was found at autopsy in a 51-year-old woman with a systolic murmur.r The patient died of cerebral an- gioblastoma; at autopsy she was found to have a 4 X 5 X 6 cm mass originating from the RV aspect of the ventricular septum, just below the pulmonary valve and the mass obstructed the RV outflow tract. It too was composed of benign thyroid tissue. She had a normal thyroid gland.

With the exception of our patient and the one re- ported by Rogers and Kesten,l all studies of intracardiac thyroid tissue have reported metastases. A solitary thyroid metastasis to the heart has not been reported. Both cases of benign ectopic thyroid rests originated from the right side of the ventricular septum. During the patients’ middle age, they grew to a significant de- gree to cause RV outflow tract obstruction and a clinical systolic ejection murmur. Both patients had a normal thyroid gland in the neck. The patient described in this report had normal thyroid function. The RV outflow tract is often a site for symptomatic cardiac metastatic tumors and thyroid carcinoma frequently metastasizes to the heart. Although the potential for malignant transformation of intracardiac ectopic thyroid would seem to exist, primary thyroid cancer of the heart has not been reported.2 Thus, the presence of thyroid tissue in the heart does not portend a poor prognosis; complete resection is indicated and the condition is curable.

References

1. Rogers WM, Kesten HD. A thyroid mass in the ventricular septum obstructing the right ventricular outflow tract and producing a murmur. J Cardiovasc Surg 1963;4:175-180.

2. McAllister HA, Fenoglio JJ. Atlas of tumor pathology; fascicle 15; tumors of the cardiovascular system. Washington, D.C.: Armed Forces institute of Pathology, 1978:68-70.

onsurgical Treatment of the Vena Cava Syndrome

JAMES H. MONTGOMERY, MD VINCENT J. D’SOUZA, MD

RAYMOND 9. DYER, MD AUGUSTIN G. FORMANEK, MD

SUDHAKAR H. PRABHU, MD

From the Department of Radiology, Bowman Gray School of Medicine of Wake Forest University, 300 South Hawthorne Road, Winston-Salem, North Carolina 27103, and the Department of Cardiology, Long Island College Hospital, Brooklyn, New York. Manuscript received March 6, 1985; revised manuscript received April 18, 1985, accepted April 23, 1985.

Transvenous pacemaker electrodes and any other central venous catheter may cause superior vena cava (SVC) thrombosis. When more than 1 pacemaker electrode is present, contact between the electrodes accentuates the thrombotic tendency and may cause local injury and stenosis of the vessel. We present a patient in whom 2 pacemaker electrodes caused stenosis and thrombosis of the SVC, and the obstruction was subsequently successfully treated with streptokinase and transluminal angioplasty.

A 71-year-old woman had a permanent transvenous pacemaker implanted through the right cephalic vein in 1968 because of complete atrioventricular block. In April 1981, a second wire was inserted, using the left cephalic vein because