Calcified Left Ventricular Thrombus Causing Repeated Retinal Arterial Emboli

Calcified Left Ventricular Thrombus Causing Repeated Retinal Arterial Emboli

Calcified Left Ventricular Thrombus Causing Repeated Retinal Arterial Emboli· Clinical, Echocardiographic, and Pathologic Features ]atne8 G. Cullen, M...

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Calcified Left Ventricular Thrombus Causing Repeated Retinal Arterial Emboli· Clinical, Echocardiographic, and Pathologic Features ]atne8 G. Cullen, M.D.; Kathleen K01'CfJ8ka, R.D.M.S.; Gene Musser, M.D.;t Nelson B. Schiller, M.D.;t and

Rolph D. Clark, M.D.

1be clinical, ech~ and petholock features of • diflcrete caIdfled left ventricular tbrombas are presented in • you.. adult man with • tw~year history of transient visual Ield defects leading to eventnaI loss of vision in his left eye. M-mode and CI'OIBo sedional echocardlopapble studies snaested • .... ..... euendinl IICI'OlM the left ventricle. TIaese 6ndinp were confirmed at surgery when • c:ald6ed ..... pathoIoaJcaDy consistent with • c:ald6ed thrombns WIllI reDIOved. 'Ibe pertinent lltentnre on the echocudfolnphIe dlagnOl1s of left ventricular thrombi Is reviewed.

We

present the findings in a young, otherwise healthy adult with repeated retinal arterial embolization in whom a discrete calcified left ventricular thrombus was diagnosed by both M-mode and cross-sectional echocardiograms and was subsequently confirmed at surgery. Although mural thrombi are quite common in patients with coexisting left ventricular disease, no evidence of myocardial abnormality was present in this patient's history, electrocardiogram, or biplane left ventricular cineangiogram. The case illustrates that M-mode and cross-sectional echocardiograms are valuable tools in the evaluation of patients with unexplained embolic phenomena.

CASE REPoRT This 27-year-old lumber-trock driver came to his 10cal physician in 1975, complaining of transient vertigo and

·From the Division of Cardiology, Presbyterian Hospital of Pacific Medical Center San Francisco. tPresently with Division -;{ Cardiology, Madison General Hospital, Madison, Wis. tCardiovascular Division, Department of Medicine, University of California, San Francisco. IfsJJrlnt rsquut8: Dr. Clark, p~ HQ6PUDl. PO BO% 7999, San Frand8co 94120

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visual disturbances. Left central retinal arterial occlusion and left monocular blindness were detected, but the findings from physical examination were otherwise unremarkable . The patient was placed on therapy with sodium warfarin (Coumadin), but over the next two years he experienced approximately 20 episodes of transient defects in the visual field, despite therapeutic anticoagulation. In March 1978, after a severe episode of loss of the right upper visual field, he was referred to Pacific Medical Center. The patient denied a history of trauma to the chest, rheumatic fever, cardiac murmur, palpitations, petechiae, intravenous use of drugs, fever, loss of weight, hematuria, focal weakness, and sensory change. The findings from physical examination were normal, except for optic atrophy and left monocuIar blindness with a focal retinal arterial embolic lesion on the right, which had the appearance of calcium. The electrocardiogram demonstrated a pattern of Wolff-Parkinson-White preexeitation, but was otherwise normal; no arrhythmias were noted during cardiac monitoring. On the chest x-ray film, the cardiac size was normal, but a large irregular area of calcification was noted in the region of the left ventricle. M-mode echocardiographic studies on condensed scan demonstrated a relatively nonmobile, left ventricular echodense mass extending from the level of the chordae tendineae across the left ventricular cavity toward the apex, where the mass appeared contiguous with the interventricular septum (Fig 1 and 2) . In addition. presystolic anterior notching of the endocardium of the left ventricular p0sterior wall consistent with "type-A" Wolff-Parkinson-White preexcitation was seen near the mitral valve (Fig 1). The remainder of the echocardiogram was normal. Cross-sectional echocardiographic studies confirmed the presence of a left ventricular mass; the apical four-chamber view (Fig 3) and the parasternal long-axis view (Fig 4) demonstrated an irregular, relatively noumobile echo-dense structure occupying the entire left ventricular apex and extending approximately 5 em toward the base of the heart to approximately the level of the papillary muscles. The remainder of the cross-sectional study was normal, with a pattern of symmetric left ventricular contraction and no evidence of other intracardiac lesions. Biplane left ventricular cineangiographic studies showed a large, intracavitary calcified mass in the left ventricular apex contiguous with the interventricular septum . Left ventricular size and contractile pattern were normal, with no mitral regurgitation. Coronary arteriograms were also normal. At surgery 8 large calcified intracavitary mass was observed, involving the apex, the interventricular septum, the free left ventricular wall, and to a small extent the FIGURE 1. Condensed M-mode scan from aortic root (AO) toward left ventricular apex, Solid tm'OW indicates abnormal echocardiographic densities extending from just below mitral valve across left ventricular cavity to interventricular septum ( IVS ). Note normal motion of left ventricular posterior wall (LVPW) posterior to these echocardiographic densities. Open arrow indicates presystolic anterior motion of left ventricular posterior wall typical of Wolff-ParkinsonWhite syndrome (type A). LA, Left atrium.

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, FiGURE 2. Abnormal echocardiographic densities (Mass) appear contiguous with intervenbicular septum ( IVS ) within left venbicular cavity. Normal intervenbicular septum, and left venbicular posterior wall (LVPW) motion are evident.

papillary muscles. The mass was split in its center, with a raw surface of calcium exposed. The mass was completely excised without need for mitral valwlar replacement. Pathologic examination of the mass demonstrated acellular hyalinized material with calcification, most consistent with a calcified thrombus. No evidence of myxoma was found on careful review and repeated sectioning. In two years of follow-up, the patient has not experienced further embolic episodes. DISCUSSION

Left ventricular masses, although quite uncommon, are responsible for considerable morbidity and often are undetected until discovered at surgery or autopsy. Pathologically, such masses may be myxomas, primary or metastatic malignant neoplasms, benign tumors, or left ventricular thrombi. Although left ventricular myxomas are reported most commonly.v" we focus our attention on left ventricular thrombi and their echocardiographic diagnosis. Reports of left ventricular thrombi occurring as isolated discrete masses are rare. 1 U Most frequent are reports of mural thrombi found in association with left ventricular aneurysms or in areas of previous infarction. Echocardiograms have only recently been shown to

be useful in the diagnosis of left ventricular masses. Two cases of left ventricular myxoma diagnosed as a discrete mass by M-mode echocardiograms8,. and an intracavitary metastatic melanoma and an intramural left ventricular hemangioma diagnosed by cross-sectionaI eehoeardiogramsw occur in the literature. On the other hand. left ventricu1ar mural thrombus may pose a more difficult problem with respect to echocanliographic diagnosis, primarily because of its often apical location and small adherent nature. Horgan et alII suggested a left ventricular thrombus on M-mode echocardiograms on the basis of septa1 thinning and vague, "dust-like" abnormal echoes near the interventricu1ar septum in a patient with a prior anterior myocardial infarction; however, Ports et ~1 report that these Mmode echocardiographic findings are nonspecific and were suggestive in only two of eight patients with documented left ventricular thrombi. Cross-sectional echocardiograms in these eight patients, alI with previous myocardiaJ. infarction and documented left ventricular aneurysms, detected the four large, inhomogeneous left ventricular thrombi but did not identify the four cases of smaller, adherent mural thrombi; these latter cases were not reliably detected by either M-mode or twodimensional echocanliograms. Thus, the cross-sectional echocardiogram appeared to be a more sensitive tool than the conventional echocardiogram; however, even it was unable to detect a large number of left ventricular thrombi. Reeder and coDeaguesl l reported that two-dimensional echocanliograms correctly diagnosed ten of 13 patients as having left ventricular thrombi in whom surgical or pathologic confirmation was available. Cross-sectional echocardiograms offer several distinct advantages over conventional M-mode echocardiograms in the diagnosis of left ventricular masses. First, suspected intracardiac abnormalities can be more accurately distinguished from nonspecific or artifactual echoes, both because of the superior spatial orientation provided by the two-dimensional sector and because the cross-sectional echocardiogram a1Iows visualization of the left ventricle from several different windows (parasternal, apical, and subcostal) . A questionable abnormality in one view should always be visualized in the same anatomic location from another window before a mass is definitely diagnosed. In addition, cross-

Apex

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F'JctmE 3. Stop-frame image of apical four-chamber view . Mass (MA) is seen in left ventricular ( LV) apex. RV, Right ventricle; RA, right abium; and LA, left abium.

LEFT YEJlTRICUW THROMBUS CAUSING

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Post sectional echocardiograms are ahle to examine parts of the left ventricle that are inaccessible to accurate diagnosis by the M-mode technique. This advantage is particularly applicable to visualization of the left ventricular apex, a common site of thrombi, which is not reliably examined by conventional echocardiograms but is well visualized with the two-chamber and fourchamber apical views of the two-dimensional echocardiogram; however, with both echocardiographic techniques, accurate diagnosis of a left ventricular mass is critically dependent on proper gain settings on the receiver and on the acoustic mismatch between the mass and blood. The detection of a left ventricular thrombus by current echocardiographic instruments may require the higher acoustic impedance of an organized thrombus, as opposed to that of a recently formed clot. Our patient is unusual in several respects. Only one other article10 and recently several abstracts1 SoU have reported the echocardiographic diagnosis of a left ventricular thrombus occurring as a discrete mass, rather than as vague echocardiographic densities. Contrary to reported experience, the left ventricular thrombus in this patient was wen identified hy conventional M-mode echocardiograms. Clinically, the repeat retinal arterial emboli seen in this patient have not previously been described in association with left ventricular masses. The extensive calcification of the thrombi in this case is also quite unusual, as is the unexplained absence of coexisting myocardial disease which would predispose to such thrombus formation.

REFERENCES 1 Young RD, Hunter, WC. Primary myxoma of the left ventricle with embolic occlusion of the abdominal aorta and renal arteries. Arch Pathol Lab Med 1947; 43:86-91 2 Newman HA, CordeD AR, Prichard RW. Intracardiac myxoma: literature review and report of six cases, one successfully treated. Am Surg 1966; 32:219-30 3 Gerbode F, Kerth WJ, HiD JD. Surgical management of tumors of the heart. Surgery 1967; 61:94-100 4 Danta G, Williams DO. Multiple emboli from left ventricular myxoma. Br Heart J 1969; 31:799-802 5 Mandel MM, Strimel WHo Ventricular myxoma associated with cerebral embolism. JAMA 1970; 214:2154-56

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FICUllE 4. Stop-frame image through parasternal long axis of left ventricle. Mass (MA) is seen in left ventricular apeL Ant, Anterior; Inf, Inferior; S, septum; AO, aortic root; Sup, superior; PW, left ventricular posterior waD; MY, mitral valve; LA, left atrium; and Post, posterior.

6 Wilcox BR, Carter JM. Left ventricular myxoma: case of successful removal. Ann Surg 1971; 173:131-34 7 Collins HA, Collins IS. Clinical experience with cardiac myxoma. Ann Thorac Surg 1972; 13:450-57 8 Morgan D, Palazola J, Reed W, Bell H, Kindred L, et aL Left heart myxomas. Am J Cardioll977; 40:611-14 9 Meller J, Teichhelz L, Pichard A, Matta R, Litwak R, et al. Left ventricular myxoma: echocardiographic diagnosis and review of the literature. Am J Med 1977; 63:816-23 10 Levisman J, MacAlpin R, Abbasi A, Ellis N, Eber L. Echocardiographic diagnosis of a mobile, pedunculated tumor in the left ventricular cavity. Am J Cardiol 1975; 36:957-59 11 Ports TA, Cogan J, Schiller NB, Rapaport E. Echocardiography of left ventricular masses. Circulation 1978; 58:528-36 12 Horgan JH, O'M Shiel F, Goodman AC. Demonstration of left ventricular thrombus by conventional echocardiography, J Clin Ultrasound 1976; 4:287-88 13 Reeder GS, Tajik AJ, Seward JB. Detection of left ventricular thrombus with two dimensional echocardiography (abstract) . Circulation 1979; 6O(suppI2) :11-19 14 Mikell FL, Asinger RW, Sharma B, Francis G, Hodges M. Serial evaluation of LV thrombus by two dimensional echocardiography ( abstract) . Circulation 1979; 6O(suppI2) : 11-19 15 Gottdiener JS, Schooley RT, Maron BJ, Fauci AS. Cardiac abnormalities in the hypereosinophilic syndrome (abstract) . Circulation 1979; 6O(suppl 2):11-19

Midsystolic Closure of the Aortic Valve in Primary Pulmonary Hypertension• YoJainori L. Dol, M.D.; lUchard L. Bishop, M .D.; Tet81IroSugiura, M.D .; and David H. Spodlck, M.D., F.C.CY.

EchOC8l'diop1qlbk f!gmlnaflon In • patient with primary pulmonary hypertension demonstrated midsys-

°From the Cardiology Division, Department of Medicine, St. Vincent Hospital; and University of Massachusetts Med. ical School,Worcester, MA. Reprint reqU88ts: Dr. Dol, 3m DrofdorI. DeptlJ'tmenl of Medlcine, OBtk Medical College, 2-1 Daigaku-cho, Takataukl-city, Osa1cJJ, Japan 560

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