Transient right atrial thrombus during acute myocardial infarction: Diagnosis by echocardiography

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BRIEF REPORTS

At least 2 explanations may be offered for this sequence . One, the coronary arteriograms failed to demonstrate a narrowing which in fact was present . Although it is well known that narrowing may be underestimated by angiography,s ,6 in this case the films were of high quality and in multiple projections, including hemiaxial views . Second, the arteries indeed were free of significant narrowing 4 months before necropsy . Based on the angiographic appearance of the obstructing lesion in our case, it is reasonable to believe that thrombus plays a major role in the genesis of spontaneous AMI in some patients subsequently shown to have angiographically normal coronary arteries . The reason for clot formation is not clear . It appears reasonable to believe that the atherosclerotic lesion at the site of the previous angiographic obstruction was initiated by organization of the observed thrombus .

References 1 . Raizner AE, Chahine RA . Myocardial infarction with normal coronary arteries . In : Hurst JW, ed . Update I, The Heart. New York : McGraw-Hill, 1979:147166.

FIGURE 2 . Photomicrograph of a cross-section of the proximal left anterior descending coronary artery 4 months after the AMI . (Hematoxytin and eosin stain : magnification X30, reduced 4% .) demonstrated either in that coronary artery or in any other . Second, necropsy 4 months after the "normal" arteriogram revealed a significant atherosclerotic lesion at the site of the occlusion demonstrated by angiogram at the time of the AMI (Fig . 2) .

Transient Right Atrial Thrombus During Acute Myocardial Infarction : Diagnosis by Echocardiography Patricia C . Come, MD

Echocardiographic diagnosis of right-sided cardiac thrombi is unusual . In the patient described herein, a large right atrial thrombus was detected after inferior myocardial infarction and was likely responsible for both systemic (paradoxical) and pulmonary emboli . A previously healthy 62-year-old man had an acute inferior wall transmural myocardial infarction, complicated by first-degree heart block . Cardiac catheterization revealed akinesia of the left ventricular inferior wall and slight apical dyskinesia . The right coronary artery was totally occluded, and it failed to open after 250,000 units of intracoronary

From the Charles A . Dana Research Institute and the Harvard-Thorndlke Laboratory of the Beth Israel Hospital, Department of Medicine, Beth Israel Hospital, and Harvard Medical School, Boston, Massachusetts . Manuscript received December 3, 1982 ; revised manuscript received December 21, 1982, accepted December 22, 1982 .

2 . Oliva PB, Brecki ridge JC. Acute myocardial infarction with normal or near a 1977 ;40 :1000-1007 . normal coronary arteries . Am J 3 . Arnett EN, Roberts WC . Acute myocardial infarction and angiographically normal coronary arteries . An unproven combination . Circulation 1976 ;53: 395-400. 4 . Henderson RR, Honing CE, Razavi M, Rose GG . Resolution of an obstructive coronary lesion as demonstrated by selective anglography in a patient with transmural myocardial infarction . Am J Cardlol 1973;31 :785-788 . 5 . Arnett EN, Isner JM, Redwood DR, Kent KM, Baker WP, Ackerstein H,

Roberts WC . Coronary artery narrowing in coronary heart disease : comparison of cineangiographic and necropsy findings . Ann Intern Med 1979 ; 91 :350-356 . 6 . Hutchins GM, Bulkley BH, Rldoltl RL . Correlation of coronary arteriograms and left ventriculograms with postmortem studies . Circulation 1977 ;56 : 32-37 .

streptokinase . During catheterization, complete heart block developed and a temporay transvenous pacemaker was inserted into the right ventricle ; it was removed 18 hours later . The hospital course was complicated by pain (thought to represent pericarditis), short runs (5 to 6 heats in duration) of atrial fibrillation, and transient left facial weakness and numbness . A computerized tomographic scan of the head revealed no hemorrhage, and intravenous heparin was, therefore, begun . Echocardiography at that time (Day 10) revealed a large left ventricle with a hypokinetic ventricular septum and apex. No thrombus was visualized within the left side of the heart. A large mass of echoes was apparent within the right atrium attached to the lower lateral right atrial wall by a narrow stalk, which allowed it to prolapse through the tricuspid valve orifice into the right ventricle during diastole . In ventricular systole, in the apical and subxiphoid 4chamber views, the right atrial mass appeared to push into the atrial septum at the presumed level of the foramen ovate, and in several frames a small part of the mass appeared to enter the left atrium by way of the atrial septum . Lung scan performed later that day demonstrated decreased perfusion, but normal ventilation in the superior segment of the right lower lobe and so bsegmental defects elsewhere . By the next day, 2-dimensional echocardiography documented disappearance of the right atrial mass . A repeat lung scan documented the new appearance of decreased perfusion in the left upper and lower lobes compatible with significant recurrent pulmonary emboli . The patient was discharged re-



BRIEF REPORTS

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FIGURE 1. Two-dimensional echocardiograms performed with a Hoffrel mechanical sector scanner . Apical 4-chamber views in systole (left panel) and diastole (right panel) demonstrate the large thrombus (T) attached to the lower lateral wall of the right atrium (RA). LV = left ventricle ; RV = right ventricle ; TV = tricuspid valve .

ceiving warfaria and digitalis on the 19th hospital day . Out-patient echocardiography 5 months after the myocardial infarction demonstrated no recurrence of the right atrial mass .

thrombus formation . The short runs of atrial fibrillation in this patient, lasting only 5 to 6 beats at maximum, were likely of too short a duration to produce sufficient stasis for clot formation . The presence of such an unusual complication of both acute myocardial infarction and right-sided cardiac catheterization raises the possibility that streptokinase administration may in some way have permitted thrombus formation . Experience with this patient raises the question of whether patients should be anticoagulated after streptokinase administration, irrespective of achievement of clot lysis .

Extravascular Obstruction of the Superior Vena Cava by Hematoma After Open-Heart Surgery and Diagnosis by Scintigraphy

can cause acute thrombotic obstruction of the SVC . 2,3 Etiologic distinction is important since the management of extravascular compression is surgical and that of thrombotic obstruction is usually medical . In the latter situation, manipulation of the catheter before the application of thrombotic dissolution therapy could contribute to an adverse outcome :' We recently observed SVC syndrome early after open-heart surgery in a patient in whom a balloon flotation catheter was in place . Roentgenographic and scintigraphic findings were important in making the etiologic diagnosis, and hence, in choosing the appropriate therapy .

To my knowledge, right atrial thrombi have not previously been documented by ultrasound in a patient with acute myocardial infarction . In my patient, it is likely that endothelial damage resulting from the right-sided cardiac catheterization or the subsequent placement and transient presence of a transvenous electrode for temporary pacing provided a nidus for

Mason H. Weiss, MD Timothy M . Bateman, MD Robert M . Kass, MD David E . Brown, CNMT Daniel S . Berman, MD Richard J . Gray, MD

Although the superior vena cana (SVC) syndrome has been well studied,' its acute occurrence complicating adult open-heart surgery has not been reported . In this setting, the possibility of SVC tamponade due to pericardial hemorrhage and ensuing clot formation must be considered . Postoperative monitoring with an indwelling pulmonary artery balloon flotation catheter From the Division of Cardiology, Department of Medicine, and the Department of Thoracic and Cardiovascular Surgery, Cedars-Sinai Medical Center, and the Department of Medicine, UCLA School of Medicine, Los Angeles, California . Manuscript received December 7, 1982 ; revised manuscript received December 24, 1982, accepted January 4, 1983 .

A 56-year-old woman underwent open-heart surgery because of dysfunction of a Harken prosthesis 12 years after mitral valve replacement . At surgery, dense adhesions from the previous operation were encountered . Replacement of the Harken prosthesis with a St . Jude value, however, was uneventful . Postoperatively, the patient had a low cardiac index with poor urinary output ; 24 hours after surgery, she had marked jugular venous distention without pulsations . Her face, arms, and upper torso had a peculiar bluish discoloration. Right atrial, pulmonary arterial, and pulmonary capillary wedge pressures were slightly elevated, and did not respond to volume challenge . Chest roentgenograms (Fig . 1) then showed that the right cardiac silhouette was particularly prominent . Technetium-99m equilibrium blood pool scintigraphy (Fig . 2) yielded an image, obtained 15 minutes after injection, of nearly absent radioactivity bordering the right heart base, including the region where the right atrium would normally be seen . An unusual and irregular concen-