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Fig. 3. A thoracic CT scan confirmed the presence of a round cystic cardiac mass without a precise def- inition of the localization and the anatomic relationship. C, Cyst.

According to blood tests, eosinophilia is present in 20 9, of cases.’ The serologic diagnosis can be obtained by sev- eral methods (e.g., radioallergosorbent test, indirect hema- glutination reaction, basophil degranulation test, and latex agglutination test). Indirect hemagglutination, the test that was used in our patient, has a sensitivity of 82 0;) and a specificity of 91’; ; these rates are similar to those of the radioallergosorbent test, better than those of the latex ag- glutination test, and worse than rates derived from the ba- sophil degranulation test.

Nowadays, the use of larvicidal agents during surgery and preoperative Albendazole therapy are considered use- ful to reduce the incidence of recurrence, which may reach 10 5. There is no agreement with respect to the most ad- equate duration of preoperative treatment period for albendazole, but it has been suggested that this therapy should be continued for 4 weeks before surgery. It is com- monly accepted that treatment of cardiac hydatid disease must be surgical in all cases2 because of the incidence of sudden death (20’0), rupture in the cardiac chambers (39 ?t8 ), or rupture into the pericardium (10% )l; however, to our knowledge, there are very few published cases of sur- gical removal of hydatid cysts located in the IVS.2 Only patients with recurrent or inoperable disease should be considered candidates for chemotherapy with albendazole; the recommended standard therapeutic regimen is four cycles of 30 days, each with a dose of 10 mg/kg per day and a rest period of 2 weeks between cycles, in an attempt to avoid toxicosis (18”;. of the patients have adverse effects),6 but the response to this treatment must be evaluated until at least 1 year after therapy is completed.

REFERENCES

1. O’Connor F, Tellez G, Montero C, Nuiiez L, Figuera D. Hidatidosis cardiaca: a prop6sito de 10 cases intervenidos quirhrgicamente. Rev Esp Cardiol 1988;41:97-102.

2. Ottino G, Villani M, De Paulis R, Trucco G, Viara J. Resto- ration of atrioventricular conduction after surgical removal of a hydatid cyst of the intraventricular septum. J Thorac Car- diovasc Surg 1987;93:144-7.

3. Oliver JM, Sotillo J, Dominguez F, et al. Two dimensional echocardiographic features of echinococcosis of the heart and great blood vessels. Circulation 1988;78:327-37.

4. Russo G, Tamburino C, Cuscuni J, et al. Cardiac hydatid cyst with clinical features resembling subaortic stenosis. AM HEART J 1989;117:1385-7.

5. Desnos M, Brochet E, Cristofini P, et al. Polivisceral echino- coccosis with cardiac involvement imaged by two dimensional echocardiography, computed tomography and nuclear mag- netic resonance imaging. Am J Cardiol 1987;59:383-5.

6. Davis A, Dixon H, Pawlowski Z. Multicentre clinical trials of benzimidazole-carbamates in human cystic echinococcosis (phase 2). Bull WHO 1989;67:503-8.

Dynamic left ventricular outflow tract obstruction 4 years after aortic valve replacement

Masataka Sata, MD, Shin-ichi Momomura, MD, Katsu Takenaka, MD, Teruhiko Aoyagi, MD, Toshiyuki Takahashi, MD, Takashi Serizawa, MD, and Tsuneaki Sugimoto, MD. Tokyo, Japan

Dynamic left ventricular outflow obstruction is character- istic of hypertrophic obstructive cardiomyopathy. In-

From the Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo.

Reprint requests: Masataka Sata, MD, Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, 7-3-l Hongo, Bunkyo- ku, Tokyo, 113, Japan.

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.-- Ire

Fig. 1. Simultaneous ascending aortic and left ventricular pressure records before (A) and after (B) valve replacement. A, A 90 mm Hg peak systolic pressure gradient was observed. B, Peak pressure gradient in- creased to 130 mm Hg during postextrasystolic contraction (arrow).

creased contractility, decreased preload, and decreased af- terload aggravate such an obstruction.’ In this report we describe a patient in whom marked left ventricular outflow tract obstruction developed after aortic valve replacement; the pathophysiology of the outflow obstruction and its as- sociation with aortic valve replacement is also discussed.

A 64-year-old woman, who was known to have had a pre- cordial murmur for several years, noted dyspnea during exercise in 1986; she was admitted to our hospital for the first time in April 1987. Results of an echocardiographic study showed a hypertrophic left ventricle, involving in particular the basal interventricular septum (18 mm), with no evidence of systolic anterior movement of the anterior mitral leaflet. Cardiac catheterization demonstrated a 90

mm Hg peak systolic pressure gradient between the left ventricle and the ascending aorta (Fig. 1, A). There was no pressure gradient in the left ventricle on a pullback tracing. Aortic valve replacement was performed on June 26,1987, at which time an adhesive and calcified aortic valve was excised and replaced with a 21 mm St. Jude Medical pros- thetic valve. After valve replacement the patient was entirely free of symptoms for 4 years until she began to complain of shortness of breath and palpitations during exercise in February 1991. Administration of digoxin, isos- orbide dinitrate, and furosemide caused worsening of the symptoms. She was readmitted to the hospital in May 1991 for an extensive medical workup. Results of an echocar- diographic study did not demonstrate any malfunction of

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-_ toward

MV

PW

- t ! f I

f xc I set

Fig. 2. A, M-mode echocardiogram shows systolic anterior movement of anterior mitral leaflet (arrow), and continuous Doppler tracings across left ventricular outflow tract show increased velocity of 4.9 m/set. B, After administration of metoprolol, systolic anterior movement of anterior mitral leaflet was reduced, and flow velocity across left ventricular outflow decreased to 2.6 m/set.

the artificial valve. The basal interventricular septum was as thick as before the valve replacement, but a marked sys- tolic anterior movement of the anterior mitral leaflet was observed. Continuous Doppler tracings across the left ven- tricular outflow tract revealed increased velocity of 4.9 m/set (Fig. 2, A), whereas the velocity across the artificial valve was 3.2 m/set. A second cardiac catheterization was performed. After catheterization of the left ventricle by the transseptal approach, the peak pressure gradient between the left ventricule and the ascending aorta was 30 mm Hg during normal sinus rhythm, whereas the pressure gradient increased to 130 mm Hg during a postextrasystolic con- traction (Fig. 1, Bf. Dynamic left ventricular outflow tract obstruction was strongly suspected. Digoxin and isosorbide dinitrate were discontinued, and the patient was treated with metoprolol (60 mg daily). Two weeks later the echocardiogram showed significant improvement in the patient’s outflow obstruction (Fig. 2, B) and the symptoms disappeared.

In this patient the hypertrophic interventricular septum probably caused narrowing of the left ventricular outflow tract even before valve replacement, but because of the in-

creased afterload as a result of aortic stenosis, the left ven- tricular outflow obstruction presumably remained subclin- ical. However, because afterload was markedly reduced af- ter aortic valve replacement and left ventricular contraction was increased, the left ventricular obstruction became overt and clinical symptoms developed. Administration of metoprolol, as well as the discontinuance of digitalis and vasodilating agents, improved the obstruction significantly. This fact strongly suggests that enhanced left ventricular contraction and decreased preload caused worsening of the left ventricular outflow obstruction. Several reports have demonstrated the coexistence of functional hypertrophic subaortic stenosis with aortic stenosis.2-6 Parker et al.2 re- ported a patient who died of left ventricular outflow obstruction after aortic valve replacement for aortic steno- sis. Left ventricular outflow obstruction is usually masked by coexisting with valvular aortic stenosis and may become overt only after the valve is replaced. It is virtually impos- sible to diagnose this uncommon complication of aortic stenosis before surgery. Therefore we must be aware of the development of functional subaortic stenosis when the pa- tient has signs and symptoms of aortic stenosis, including

1088 Brief Communications

exertional dyspnea and systolic murmur, even after aortic valve replacement.

REFERENCES

1.

2.

3.

4.

5.

6.

Wynne J, Braunwald E. The cardiomyopathies and myo- carditides. In: Braunwald E, ed. Heart disease. 3rd ed. Phila- delphia: WB Saunders Co, 19881427-8. Parker DP, Kaplan MA, Connolly JE. Coexistent aortic val- vular and functional hypertrophic subaortic stenosis. Am J Cardiol 1969;24:307-17. Morean JR. Idiouathic hvnertrouhic stenosis: variabilitv of obstruction. Milif Med 1972;137:238-40. Block PC, Powell WJ, Dinsmore RE, Goldblatt A. Coexistent fixed congenital and idiopathic hypertrophic subaortic steno- sis. Am J Cardiol 1973;31:523-6. Nanda NC, Gramiak R, Stah PM, Stewart S, DeWeese JA. Echocardiography in the diagnosis of idiopathic hypertrophic subaortic stenosis coexisting with aortic valve disease. Circu- lation 1974;50:752-7. Thompson R, Ahmed M, Pridie R, Yacoub M. Hypertrophic cardiomyopathy after aortic valve replacement. Am J Cardiol 1979;45:33-41.

Primary lymphoma of the right atrium with fatal neoplastic pulmonary embolism

Reinaldo B. Bestetti, MD, PhD, Fernando A. Soares, MD, PhD, Edson G. Soares, MD, PhD, and J. Samuel M. Oliveira, MD, PhD RibeirZio Preto, Brazil

The occurrence of a primary malignant lymphoma of the right atrium is extremely rare. Indeed, Somers and Lothe’ have found only two cases from among 6664 consecutive autopsies. The clinical pictures that were observed in a few patients, as reported in the literature, were congestive heart failure,l, 2 pericardial effusion with or without cardiac tamponade,’ acute pericarditis,3 angina-like chest pain4 and syncope.5 Recurrent massive pulmonary neoplastic embolism, as far as we know, has never been observed in patients with a primary malignant lymphoma of the right atrium.

A 55-year-old woman was transferred to our institution in poor physical condition because of general malaise, weakness, and inappetence that had lasted for 30 days. She had experienced syncope 20 days before. The physical ex-

amination showed pallor, cold extremities, respiratory dis- tress, a heart rate of 140 beats/min, and a systolic arterial pressure of 80 mm Hg. The resting ECG showed a right bundle branch block pattern. Chest x-ray films disclosed

From the Department of Pathology and Internal Medicine, Rib&lo Preto Medical School, S&o Paul0 University.

Reprint requests: d. Samuel M. Oliveira, MD, PhD, Faculty of Medicine, Department of Pathology, Ribeirlo Preto, 14049, SP Brazil.

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Fig. 1. Posteriorly opened right cardiac chambers exhib-

iting the neoplasia attached to the interatrial septum, pro- truding through the atrioventricular valve, and compress- ing the septal cusp (arrow). TU, Tumor; RA, right atrium: RV, right ventricle.

right pleural effusion. Two-dimensional echocardiography was not helpful because of some difficulties in obtaining a clear image. A subsequent needle pleural aspiration dis- closed the presence of hemorrhagic fluid. On the basis of these findings, the patient underwent pulmonary angiog- raphy, which revealed a filling defect in the artery that supplies the right inferior lung lobe. A diagnosis of pulmo- nary embolism was established. She was then treated with heparin plus dicumarol. A marked improvement in her clinical condition occurred, and she remained well for 12 days. She then experienced sudden cardiogenic shock from which she did not recover. At autopsy, the classical findings of congestive heart failure were observed. Heart weight was 410 gm. The gross aspect of the heart showed biventricular hypertrophy; the right ventricle was more hypertrophied. The coronary arteries were normal, as were the cardiac valves. A tumor-like mass inside the right atrium was firmly attached to the lower and posterior regions of the

interatrial septum. The mass invaded the septum with a base of 1.5 cm and then opened as a fungoid (grape-like) mass of 4 cm in diameter. Part of the tumor protruded through the tricuspid valve, which prevented full closure