Left atrial myxoma

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CASE REPORTS

Left Atrial Myxoma Hemodynamic

and Phonocardiographic

ALI R. GHAHRAMANI, M.D. JOHN R. ARNOLD, M.D. FRANK J. HILDNER, M.D. LEONARD S. SOMMER, M.D. PHILIP SAMET, M.D. Miami, Florida

Two cases of left atrial myxoma are presented, with a review of clinical clues which may help in distinguishing this disease from mitral valve disease. Suggestive features in the apexcardiogram and internal and external phonocardiograms are discussed, together with related hemodynamic events indicated on the pulmonary capillary wedge, left atrial and left ventricular pressure tracings. The origins of various auscultatory features are analyzed in the light of specific hemodynamic events. Hemolytic anemia was present in one case, and ruptured chordae tendineae with scarring and myxomatous degeneration of the mitral leaflets in the other. Possible mechanisms for these lesions related to myxoma are discussed. The role of cardiac fluoroscopy, left ventricular cineangiog raphy and the levophase of pulmonary angiography in helping to delineate left atrial myxoma is also mentioned. Left

atrial

serious

From the Department of Internal Medicine, Division of Cardiology, Mount Sinai Hospital of Greater Miami, Miami Beach, Florida; Cardiovascular Laboratory, Jackson Memorial Hospital, Miami, Florida; and the University of Miami, School of Medicine, Miami, Florida. Requests for reprints should be addressed to Dr. Ali R. Ghahramani, Cardiovascular Laboratory, Jackson Memorial Hospital, 1700 N.W. 10th Avenue, Miami, Florida 33136. Manuscript re-

ceived July 6, 1970.

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Features

yet

myxoma curable

is a rare disorder

disorder.

The

diagnosis of this too often made for suspected mitral

is unfortunately

postmortem or, at best, during surgery stenosis. A number of excellent and detailed reviews of large series of patients with left atrial myxoma have been published [l-7]. Only recently, however, have reports appeared in the literature correlating the unique hemodynamic events and phonocardiographic features in patients with this disease [8-lo]. Our purpose is to define additional features which may assist in the diagnosis of left atrial myxoma, to report its association with ruptured chordae tendineae and to describe intracardiac phonocardiographic features which have not been recorded previously. CASE

REPORTS

Case 1. A sixty-six year old housewife was transferred to the Jackson Memorial Hospital on November 2, 1967, because of refractory heart failure. She had enjoyed good health until May 1967, when she began to experience intermittent episodes of exertional dyspnea. Between June and November of 1967 she was hospitalized on four occasions because of weakness, dyspnea, anorexia and weight loss.

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Figure 1. Case 1. Apexcardiogram with phonocardiogram illustrating a notch (NJ on the upstroke of the ejection wave due to ejection of the tumor from the left ventricle into the left atrium. This corresponds to the loud delayed first heart sound. As the tumor enters and comes to rest within the left ventricle it causes a small hump (X) on the early diastolic trough of the apexcardiogram which is followed by the tumor plop (T.P.) on the phonocardiogram. She noted intermittent anterior chest pain, cough and orthopnea. During her hospital admissions low grade pyrexia, transient right hemiparesis, periods of mental confusion and electrocardiographic changes suggestive of anterior wall ischemia were observed. She was treated with digitalis and diuretics for congestive heart failure. She was also given anticoagulant therapy for hemoptyses possibly caused by pulmonary emboli. There was no past history of rheumatic fever. On admission the patient was pale and weak, with moderate dyspnea at rest. Her pulse rate was lOO/ minute and regular; blood pressure was 110/70 mm Hg. Pertinent physical findings included distention of the neck veins at 45 degrees with prominent jugular V waves, moderate hepatomegaly and ankle edema. The apical impulse was located at the fifth intercostal space in the mid-clavicular line. A subtle but diffusely TABLE

I

Hemodynamic

Findings

Determination Pressure (mm Hg) Right atrial mean Right ventricle Main pulmonary artery Pulmonary capillary wedge A wave V wave Mean Left atrial V wave Mean Left ventricle dp/dt (mm Hg/sec) Aorta Left atrial-left ventricular mean diastolic gradient Cardiac output (L/min) Cardiac index (L/min/M*) Pulmonary vascular resistance (dynes/set-cm+)

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Case1

Case2

10 66/10 66124

5 53/4 55122

16 44 28

16 42 28

... ... 100/g 1,600 9af50 15 6.3 3.3 230

46 30 120/g 1,950 120/62

10 3.8 1.8 485

sustained right ventricular impulse was felt over the precordium. The first heart sound was very loud and was followed by a grade l/6 apical pansystolic murmur. The pulmonic closure sound was accentuated. There was an early diastolic sound and an inconstant short grade l/6 mid-diastolic rumble at the apex. A phonocardiogram showed a loud and delayed first heart sound with continuing vibrations throughout the isometric contraction period, a pansystolic murmur and an early diastolic sound. This sound occurred 0.11 second after the aortic closure and shortly after a hump shown on the apexcardiogram. Also, a notch was seen on the upstroke of the apexcardiogram coinciding with loud, components of the first heart sound (Figure 1). Laboratory studies revealed’ normochromic normocytic anemia with a hemoglobin level of 9.7 gm per cent, erythrocyte sedimentation rate of 71 mm, gamma globulin level of 2.2 gm per cent, reticulocyte count of 8 per cent and normal blood urea nitrogen and electrolyte levels. Serum lactic dehydrogenase (LDH) and serum glutamic oxaloacetic transaminase (SGOT) levels were elevated. Direct Coombs’ test was positive, and hemosiderin deposits were noted in the urine. Serum haptoglobin was decreased. Five blood cultures were negative. The electrocardiogram showed wide, notched P waves consistent with left atrial enlargement, low voltage and nonspecific ST-T wave abnormality probably due to the effects of digitalis therapy. Chest roentgenogram demonstrated left atri’al enlargement, cardiomegaly and interstitial pulmonary edema. A lung scan showed diffuse perfusion defects in the bases of both lungs. Cardiac catheterization demonstrated (Table I) a mean pulmonary capillary wedge pressure of 28 mm Hg (Figure 2). Pulmonary artery pressure was 801 24 mm Hg. The left ventricular end-diastolic pressure was normlai. Left ventricular pressure tracings showed a notch on the upstroke and another on the downstroke nearly coinciding with the C and notched V waves on the pulmonary wedge tracing. Pulmonary arteriogram

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disclosed a filling defect in the left atrium (Figure 3). No mitral valve deformity was noted. At open heart surgery, a pedunculated, irregularly shaped mass composed of a cluster of glistening, translucent nodules was found in the left atrium attached to the lower part of the atrial septum and moving freely up and down through the mitral valve. It weighed 35 gm and had a diameter of 4 cm. No evidence of mitral valve dysfunction or deformity was noted after resection of the tumor. Histologically, the neoplasm consisted of loosely arranged swollen cells with stellate, hyperchromic nuclei. There were sheets of hyalinized eosinophilic material and moderate edema. The patient had an uneventful postoperative course with resolution of the anemia and clearing of pulmonary congestion. During the two years of follow-up she has remained well while taking no cardiac medications. Repeat Coombs’ test and tests for intravascular hemolysis were negative. A sixty-seven year old white man was ad. Case 2. mitted to Mt. Sinai Hospital on June 24, 1969, with symptoms of progressive cardiac decompensation since March 1969. For the preceding twenty years he had experienced a burning sensation in the left side of the chest provoked by lifting heavy objects, sexual intercourse and emotional upheaval. He denied having any syncopal episodes or rheumatic fever. A heart murmur was heard in 1956 for the first time and a diagnosis of mitral valve disease was made in 1964. In May 1969 he had been admitted to another hospital and treated for congestive heart failure with digitalis and diuretics. Because of persistent symptoms of paroxysmal nocturnal dyspnea and exertional dyspnea, he was referred for further diagnostic studies and consideration of mitral valve surgery. On admission the heart rate was go/minute, and the blood pressure was 124/72 mm Hg. There was mild cyanosis of the lips and fingernails. The neck veins were not distended. The point of maximal cardiac impulse was located in the fifth left interspace at the anterior axillary line. There were no thrills or heaves. The first heart sound was greatly accentuated and prolonged. The second heart sound was physiologically split; the pulmonary component was louder than the aortic component. A striking and unusually loud third heart sound was heard all over the precordium. A pansystolic murmur, grade 3/6, was audible maximally at the apex. It radiated to the left axilla and did not vary with respiration. The biochemical profile was normal. The hematocrit was 38 per cent, and the hemoglobin level was 12.6 gm per cent. Peripheral blood smear revealed no abnormalities. Direct Coombs’ test and serologic tests were negative. Haptoglobin was 104 mg per cent, and the gamma globulin level was 2 gm. The reticulocyte count was 0.9 per cent. Urine hemosiderin was negative. Erythrocyte sedimentation rate was elevated at 52 mm. The electrocardiogram

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100 80 60 40 20



LEFT ATRIA1 MYXOMA

MITRAL STENOSIS

Figure 2. Case 1. Simultaneous left ventricular and pufmonary capillary pressure tracings comparing characteristic features of left atria/ myxoma with mitral stenosis during sinus rhythm. Left, left atria/ myxoma demonstrating a notch (N,) on the upstroke of the left ventricular tracing due to ejection of the tumor from the left ventricle into the left atrium reflected by a prominent C wave on the pulmonary capillary tracing. After an X descent, the tal/ peaked V wave is probably due to limitation of left atrial filling by the tumor mass within the atrium with or without mitral regurgitation. Notch (N,) on the downstroke of the left ventricular tracing corresponds to the notched V wave due to a tendency toward premature mitral valve opening (see text). The very rapid Y descent is due to movement of the tumor mass from the left atrium into the mitral orifice and left ventricle. Following the rapid Y descent the gradient throughout diastole is fairly constant with a relatively small end-diastolic A wave on the pulmonary capillary tracing. Right, in mitral stenosis there is no notch on the left ventricular upstroke. The V wave is less prominent than in myxoma. There is a gradual Y descent and tapering reduction of the gradient throughout diastole until it is exaggerated by the large presystolic A wave.

Figure 3. Case 1. Levophase of pulmonary angiogram showing a filling defect in the left atrium at or near the mitral orifice.

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\

Figure 5. Case 2. Posteroanterior roentgenogram showing the calcified tumor in the left atrium during systole and barium in the esophagus.

LEFTATRIA1 MYXOMA

Figure 4. Case 2. External phonocardiogram, carotid pulse and apexcardiogram show a delayed, loud and prolonged first heart sound, pansystolic murmur and a loud third heart sound (tumor sound).

Figure 6. Case 2. Posteroanterior roentgenogram showing the tumor in the left ventricle during diastole and barium in the esophagus.

MITRALSTENOSIS

Figure 7. Left, Case 2. Simultaneous left atrial and left ventricular pressure tracing with simultaneous internal phonocardiographic recording from the left ventricular outflow tract, illustrating high frequency vibrations through the isometric contraction period and a pansystolic murmur. Right, comparable data in a patient with mitral stenosis.

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showed a normal sinus rhythm with left atrial enlargement and biventricular hypertrophy. A phonocardiogram showed a loud and delayed first heart sound, a pansystolic murmur and a loud third heart sound occurring 0.12 second after the aortic closure (Figure 4). Chest roentgenogram revealed left atrial enlargement, moderate left ventricular enlargement, prominent pulmonary arteries, decreased pulmonary vascularity of the lower lobes and Kerley B lines. On image amplification chest fluoroscopy, a calcified mass was seen moving like a ping pong ball to the left ventricle during diastole and back to the left atrium during systmole (Figures 5 and 6). Hemodynamic findings are summarized in Table I. Simultaneous left atrial and left ventricular pressure recordings revealed a prominent C wave on the left atrial tracing corresponding to a notch on the upstroke of the left ventricular tracing. A less prominent notch was seen on the downslope of the left ventricular tracing. Left atrial pressure recording disclosed a small A wave, dominant V wave and steep Y descent (Figure 7). Intracardiac phonocardiography at the left ventricular outflow tract demonstrated high frequency vibrations throughout isometric contraction period and a pansystolic murmur (Figure 7). As the phonocatheter was advanced towards the left ventricular inflow tract, the systolic murmur became less obvious; instead high frequency vibrations registered beginning with the second heart sound, persisting through the early part of diastole and ending with the third heart sound (Fig rut-e 8). Left ventricular cineangiography revealed severe mitral regurgitation which delineated the atrial myxoma

Figure 9. Case 2. Right anterior oblique view of reft ventricular cineangiogram delineating the myxoma in the left atrium via the regurgitant jet.

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Figure 8. Case 2. Internal sound tracing from the left ventricular inflow tract showing the high frequency vibrations in early diastole ending with a loud tumor filling sound. The systolic murmur is less apparent.

with its ball valve action (Figures 9 and 10). At open heart surgery the calcified left atrial myxoma was attached by a long stalk to the septum just superior to the mitral valve. The myxoma moved from the left atrium to the left ventricle in diastole and vice versa in systole. There were several ruptured chordae tendineae of the posterior mitral leaflet. The anterior leaflet was thin and scarred. An area of scarring was also present in the left ventricular endocardium. These changes were apparently the result of trauma caused by the tumor. The myxoma was removed in its entirety, and the mitral valve was replaced with a large size Beall prosthesis. The tumor was rounded, measuring 4 cm in diameter with an attached stalk 2.5 cm in length by 1 cm in width. On cross section it showed areas of

Figure 10. Case 2. Right anterior oblique view of left ventricular cineangiogram, showing the myxoma in the left ventricle.

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calcification and cyst formation. The mitral leaflets showed myxomatous degeneration. Microscopic examination failed to disclose any evidence of bacterial endocarditis or rheumatic disease. COMMENTS The clinical similarity of left atrial myxoma to mitral stenosis is often stressed, since both lesions become manifest through mechanical obstruction of the mitral valve. On auscultation a loud first heart sound, a loud pulmonic closure and an early diastolic snapping sound followed by a diastolic rumble may be heard in both diseases. The roentgenographic signs of left atrial enlargement, right heart prominence and pulmonary congestion are also common. In addition, the electrocardiogram in both conditions may show P mitrale with changes of right ventricular hypertrophy. A number of nonspecific clues which may arouse suspicion of left atrial myxoma may be recognized at the bedside. Features which should raise the question of myxoma in a patient suspected of having mitral stenosis [l-11] include (1) absence of history of rheumatic fever; (2) recent or sudden onset of intermittent, progressive, positional dyspnea, clouding of consciousness or even syncope in the presence of sinus rhythm; often, relief of dyspnea on lying down and aggravation of dyspnea on sitting up, the reverse of usual dyspnea related to valvular disease; (3) lack of correlation between physical findings, timing of the opening snap, roentgenologic examination and severity of symptoms; (4) beat to beat or positional variation in auscultatory features, blood pressure, heart rate and symptoms related to mitral valve obstruction, with dramatic improvement by changes in posture; (5) embolic phenomena in the presence of sinus rhythm; (6) suspicion of bacterial endocarditis despite negative blood cultures; and (7) striking disparity in the degree of venous engorgement in the lung fields, ascribed to selective pulmonary vein obstruction [12]. Constitutional symptoms and anemia are frequently associated with myxoma of the heart. Multiple small emboli to muscles may occur [13] and may account for some of the constitutional symptoms and high SGOT levels. Our first patient (Case 1) presented with fever, hemolytic anemia, high erythrocyte sedimentation rate, elevated serum gamma globulin levels, positive Coombs’ test, hemosiderinuria and decreased serum haptoglobin, all of which disappeared after removal of the tumor. Fifteen of forty patients with left atrial myxoma described by Goodwin [l] had a hemo-

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globin value of less than 80 per cent. Vupio and Nikkila [14] studied the hemolytic nature of the anemia in a case of left atrial myxoma. They speculated that a high carbohydrate content of the tumor may result in the liberation into the circulation of a polysaccharide, similar to bacterial endotoxin, causirg hemolysis. Currey et al. [15] recently demonstrated the presence of circulating antibodies in the heart muscle of a patient with left atrial myxoma and disappearance of these antibodies following surgery. Whether in response to a polysaccharide or to circulating myocardial protein, an immune mechanism probably accounts for the constitutional features in the disease. An immune or autoimmune mechanism provides a more plausible basis for the hemolytic anemia than the former explanation of mechanical trauma to red blood cells resulting from turbulence produced by the tumor. It is rare for all of these features to be present in any one patient. This is illustrated in our patients who presented with refractory heart failure and exertional dyspnea of several months’ duration. Symptoms had been intermittent initially, presumably because the tumor produced less constant mitral obstruction when it was smaller. The physical signs of mitral valve disease varied from time to time. The mid-diastolic ruqble was short and inconstant, with no presystolic component despite the presence of sinus rhythm. At times only a systolic murmur could be heard at the apex. In addition, the early diastolic “pseudo opening snap” was heard 0.11 second (Case 1) and 0.12 second (Case 2) after aortic valve closure; this interval was inconsistent with tight mitral stenosis. Fut-thermore, the sound occurred during the early rapid filling period on the apexcardiogram (Figure 1) rather than at the 0 point, as would an opening snap. In Case 2, the early diastolic sound coincided with the F point as would a third heart sound. Moreover, there was beat to beat variation in the intensity of this sound, similar to cases reported in the literature [16,17]. The first and third heart sounds in Case 2 were so loud that several observers thought the patient might have a mitral valve prosthesis. Such a loud first heart sound is unusual in mitral insufficiency and should raise the possibility of atrial myxoma. An early diastolic sound simulating an opening snap has been reported in 50 per cent of the recorded cases of left atrial myxoma [l]. Cobbs [ill has designated this early diastolic sound in left atrial myxoma as the “tumor plop.” Although the

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term lacks scientific refinement, it well describes the sound which, in our cases, was more of a thud or gallop sound than the higher pitched snapping sound produced by opening of the thickened nonflexible valve in mitral stenosis. The term “tumor plop” also suggests the mechanism responsible for the sound. Rather than being a “tumor opening snap,” as it has been loosely referred to by previous investigators, it is actually an obstructive and filling phenomenon resulting from the tumor abruptly coming to rest within the ventricle. The simultaneous left ventricular and pulmonary capillary wedge tracings in Case 1 (Figure 2) and the left ventricular and left atrial pressure recordings in Case 2 (Figure 7) illustrate a number of features which have been described by Pitt et al. [8] in two cases of left atrial myxoma. The left atrial A wave is small compared to the usual large A wave in mitral stenosis during sinus rhythm. This may be due to less volume within the left atrium in late diastole with myxoma as contrasted with mitral stenosis since the tumor mass is primarily within the ventricle at that moment. In addition, the intermittent nature of the obstruction to left atrial emptying and the short duration of the disease may not result in the same degree of left atrial enlargement as is seen with long-standing mitral stenosis. A notch is consistently present on the left ventricular upstroke which coincides with the prominent C wave in left atrial or pulmonary wedge pressure. The same notch is seen on the apexcardiogram coinciding with the loud component of the first heart sound (Figure 1). The upstroke notch on the ventricular pressure curve and apexcardiogram is attributed to the movement of the tumor out of the ventricle into the left atrium during isometric contraction, causing a momentary decrease in ventricular volume reflected as a transient delay in ventricular pressure rise [8,9]. The prominent C wave is due then to the volume displacement of the tumor mass as it is propelled into the left atrium [18]. It has previously been suggested that the mechanism responsible for the loud first heart sound is the forceful ejection of the tumor from the left ventricle back into the left atrium, striking the mitral orifice or the atrial wall [7]. We propose, however, that the abrupt and extreme tensing of the valve leaflets with delayed mitral closure may also be responsible for the loud first heart sound. Mitral closure occurs simultaneously with expulsion of the tumor from the valve orifice when the left ventricular pressure has reached 20 to 40 mm

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Hg (Figure 7). Closure of the mitral valve will, therefore, occur with greater excursion and more forceful tensing of leaflets under a higher differ ential pressure, and more rapid rate of rise of left ventricular pressure (dp/dt) [19]. Acceleration and deceleration of the tumor and surrounding blood would generate sonic vibrations. These sonic vibrations as well as tensing of mitral apparatus probably contribute to the loudness and prolongation of the first heart sound [20]. The tall V wave and rapid Y descent in myxoma contrasts with a less impressive V wave and gradual Y descent in mitral stenosis. As described by Pitt et al. [8] the initial rapid fall in left atrial pressure (Y descent) in myxoma results largely from the tumor mass moving from the atrium into the ventricle rather than from blood leaving the atrium. In addition, a small notch is seen on the descending limb of the ventricular pressure curve and on the V wave of the pulmonary capillary wedge tracing just before the rapid Y descent. This may reflect a tendency towards premature opening of the normal mitral valve produced by the tall V wave and movement of the tumor mass. Another interesting feature on the apexcardiogram in Case 1 was an early diastolic notch falling on the zero point just preceding the tumor plop. Ongley et al. presented an apexcardiogram (Figure 68, [21]) in a patient with a ball-valve thrombus of the left atrium illustrating a similar but less impressive early diastolic impulse on the chest wall, which coincided with the “plop” of the ballvalve thrombus. Upon examination of our apexcardiograms in patients with documented mitral stenosis we found none showing chest wall deflection at the time of the opening snap. Accordingly, this early diastolic notch or impulse on the apexcardiogram may, in itself, distinguish the tumor plop from the opening snap. Its presence on the apexcardiogram supports our impression that the tumor plop is essentially a left ventricular event, depending on the tumor mass. We could find only two other recorded cases of left atrial myxoma in which the apexcardiograms showed a similar notch on the systolic upstroke [8,10]. Movement of a peduncuiated myxoma creates sonic vibrations. These sounds were recorded in one patient (Case 2) by intracardiac phonocardiography from the left ventricular inflow tract (Figure 8). They started with the second heart sound, coinciding with the onset of the tumor movement at the beginning of diastole from the left atrium towards the left ventricle. and continued through

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the early part of diastole up to the third heart sound when the tumor rested in the left ventricle. The presence of traumatic endocardial scars indicated further that the tumor did in fact strike the left ventricular wall. Sudden impedance of these vibrations by the left ventricular wall produced a loud third heart sound. Transseptal left heart catheterization and in particular left atrial injection of contrast media could in theory be potentially hazardous because of inadvertent puncture of the tumor, and tumor dislodgement breaking into fragments with systemic embolization. Mitral valve occlusion is another possibility. We therefore suggest only a transseptal left atrial needle puncture, without passage of a catheter into the left atrium. Observing the levophase of a pulmonary angiogram is a good method of visualizing an obstructive mass in the left atrium, whether due to myxoma or thrombus, as is also left ventricular angiography in a patient with mitral regurgitation. As in Case 1, however, the filling defect can be difficult to visualize (Fig-

ure 3). Left ventricular cineangiography, as in our Case 2 (Figure 9), will often allow visualization of the left atrial chamber by a “jet” of regurgitation

[221. Scarring and myxomatous degeneration of the mitral leaflets in the absence of apparent rheumatic heart disease or bacterial endocarditis, as well as organic mitral regurgitation due to ruptured chordae tendineae in association with left atrial myxoma (Case 2), have not been reported previously. We believe that the ruptured chordae tendineae, degeneration of the mitral leaflet and the area of scarring seen in the left ventricular endocardium in left atrial myxoma are due to stress and trauma of the calcified tumor moving forcibly through the mitral valve and striking the mitral valve apparatus as well as the left ventricular wall. ACKNOWLEDGMENT Dr. James Jude and Dr. Jack Greenberg cardiac surgery upon these patients.

performed

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Goodwin JF: Diagnosis of left atrial myxoma. Lancet 1: 644, 1963. Goodwin JF: Symposium on cardiac tumors. Amer J Cardiol 21: 307, 1968. Harvey WP: Clinical aspects of cardiac tumors. Amer J Cardiol 12: 334, 1968. Greenwood WF: Profile of atrial myxoma. Amer J Cardiol 21: 367,, 1968. Greenwood WF: Myxoma of the left atrium. Brit Heart J 22: 189, 1,960. Differing JT, Gardner RE, Roe BF: Intracardiac myxomas with report of two u,nusual cases and successful removal. Circulation 23: 929, 1961. Abbott QA, Warshawski FE, Cobbs BW, Jr: Primary tumors and pseudo-tumors of the heart. Ann Surg 155: 855, 1962. Pitt A, Bertram PH, Schaefer J, Criley JM: Myxoma of the left atrium. Hemodynamic and phonocardiographic consequences of sudden tumor movement. Circulation 36: 408, 1967. Penny JL, Gregory JJ, Ayers SM, Giannelli S, Rossi P: Calcified left atrial myxoma simulating mitral insufficiency: hemodynamic and phonocardiographic effects of tumor movement. Circulation 36: 417, 1967. Zitnik RS, Guilian ER, Burchell HB: Left atrial myxoma: phonocardiographic clues to diagnosis. Amer J Cardiol 23: 588, 1969. Hurst JW, Logue RB: The Heart, New York, McGrawHill Book Co., 1966, p 943. Hair TE, Jr, Orgain ES, Scaly WC, McIntosh HD: Myxoma of the left atrium. Observation on two cases with successful removal and review of di-

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