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Ann Thorac Surg 1995;59:538-541
© 1995 The Society of Thoracic Surgeons

Current Review

Cardiac Papillary Fibroelastoma

David M. Shahian, MD, Sherif B. Labib, MD, Greg Chang, MD

Departments of Thoracic and Cardiovascular Surgery, Cardiovascular Medicine, and Anatomic Pathology, Lahey Clinic, Burlington, Massachusetts


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Case Report
 Comment
 References
 
Papillary fibroelastomas are rare cardiac tumors, but they are the most common primary tumor of the heart valves. These lesions occur on any of the valves or endothelial surfaces of the heart and may be detected by echocardiography, cardiac catheterization, during open heart operation for other conditions, or at autopsy. Because of their potential for cerebral and coronary embolization, even small papillary fibroelastomas should be excised.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Case Report
 Comment
 References
 
Cardiac papillary fibroelastomas are rare and until the last decade had been identified primarily at autopsy or as incidental findings during cardiac operations. With the advent of transthoracic and transesophageal echocardiography, diagnosis of this lesion in living patients has been possible [1–14], and an aggressive treatment approach has evolved to prevent catastrophic cerebral or coronary embolization.

We review the prevalence, clinical presentation, diagnosis, pathology and pathogenesis, and treatment of this lesion, beginning with a case report from our institution.


   Case Report
Top
 Footnotes
 Abstract
 Introduction
 Case Report
Comment
 References
 
This 72-year-old man had been in good health. His past medical history was unremarkable except for hypertension and repair of an abdominal aortic aneurysm. He presented with sudden-onset left facial and left hand weakness on December 15, 1992. There had been no prior neurologic problems except for dizziness treated with meclizine hydrochloride (Antivert; Roerig Division, Pfizer Inc, New York, NY) in July 1992. Physical examination revealed no carotid bruits. There was a marked left facial droop with decreased pinprick sensation in the left face. The left grip was weak. Babinski's sign was negative. A cranial computed tomographic scan showed no infarct or hemorrhage. Carotid ultrasound showed no abnormalities. The patient was admitted for observation, and his left facial and hand weakness resolved over the next 48 hours. A transesophageal echocardiogram showed a small, mobile echodensity attached to the aortic valve by a short, thin stalk, which was thought to be a tiny fibroelastoma (Fig 1Go). No other source of the emboli was identified. Because the relationship of the lesion to the patient's symptoms was uncertain, the patient was treated with heparin (Wyeth-Ayerst Laboratories, Philadelphia, PA) and was subsequently discharged on warfarin sodium (Coumadin; Du Pont Pharmaceuticals, Wilmington, DE) therapy.



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  		Fig 1. . Tiny echodensity attached by a thin stalk to the tip of the aortic valve leaflet (arrow). (Ao = aorta; AV = aortic valve; LA = left atrium.)

 
The patient was readmitted to the hospital 2 week later with aphasia. His prothrombin time had been well controlled and at admission was therapeutic at 17.3 seconds. A cranial computed tomographic scan demonstrated intracranial hemorrhage in the left parietal area; warfarin sodium administration was discontinued, and vitamin K therapy was instituted to reverse its effects. Repeat transesophageal echocardiography showed no change in the size of the aortic valve lesion. Although the possibility of anticoagulant-related hemorrhage was considered, the prothrombin time had always been in the low therapeutic range. We believe that a second embolus developed despite warfarin sodium therapy, with subsequent bleeding into the brain. The patient made a full neurologic recovery and was discharged without anticoagulation therapy, with plans to remove the cardiac lesion as soon as the intracerebral process had stabilized.

To prepare for cardiac operation, the patient underwent a thallium stress test, which was negative for angina or ischemia. Because of the friable nature of the tumor, we elected not to perform selective left and right coronary catheterization [8].

The patient was readmitted to the hospital 5 weeks later and underwent exploration of the aortic valve during cardiopulmonary bypass. A 3-mm lesion was attached by an extremely thin stalk to the leading edge of the noncoronary cusp of the aortic valve. The lesion was excised with no damage to the valve leaflet and the aorta was closed. Histopathologic examination of the lesion confirmed the diagnosis of papillary fibroelastoma (Fig 2Go). The patient had an uncomplicated postoperative convalescence and was discharged. There have been no further neurologic events at 1-year follow-up.



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  		Fig 2. . Photomicrograph of resected papillary fibroelastoma. The lesion has a short stalk from which filiform projections arise. The core is elastotic with elastic granules. Fibrous deposition also is seen in the stalk and the center of the projections. The lesion is lined by hyperplastic endothelium.

 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
References
 
Prevalence
Papillary fibroelastomas are rare, representing less than 10% of all primary cardiac tumors [15] studied at autopsy or after resection. Several studies attest to the rarity of this lesion. Abu Nassar and Parker [16] collected 39 cases in the world literature before 1971. As of 1977, the Armed Forces Institute of Pathology had collected 42 cases [15], 36 of which arose from the valves. By 1991, a compilation of 56 cardiac valve tumors from the Walter Reed Army Medical Center, Brooke Army Medical Center, and the Armed Forces Institute of Pathology included 41 papillary fibroelastomas, the most common pathologic type [1]. At present, there are just over 100 reported cases in the literature [1–46].

Location
Although these lesions have been identified throughout the heart, approximately 90% occur on the valves [1, 15]. The lesions have been reported on all three leaflets of the aortic valve [2, 8, 13, 14, 17–22, 39, 40], the intima of the right coronary sinus and ostium in a patient with coexistent atherosclerotic coronary disease [23], the left ventricle including the septum and the outflow tract [11, 14, 22, 24, 25, 32], the anterior or posterior mitral valve leaflets [2, 6, 9, 10, 12, 21, 22], the mitral valve chordae [3, 22], the mitral valve papillary muscles [13, 16], the right ventricular endocardium near the papillary muscle origins [26, 27], the tricuspid valve [5, 9, 14, 24, 34], the left ventricular septum and the outflow tract [14, 22], the right atrial endocardium [28, 33], and the pulmonic valve [14, 20, 21]. Single and multiple [13, 22, 36, 45] lesions have been identified ranging in size from 0.1 to 4 cm [7, 22, 25]. Most are less than 1 cm in diameter [14, 16], and more than 90% are solitary [1, 15].

Clinical Presentation and Diagnosis
Although patients with this lesion have ranged in age from a neonate to a 92-year-old [15, 16, 25, 29, 30, 38], most patients are adults more than 50 years of age [1, 15]. Papillary fibroelastomas may occur as the only cardiac pathology, but they also have been described in association with congenital [27], valvular [13, 14], and atherosclerotic coronary artery disease [23].

Physical findings are conspicuously absent with these tumors, although 1 patient with a tricuspid valve lesion diagnosed by echocardiography had, in retrospect, a tumor ``plop'' noted on auscultation [5].

Before the availability of transthoracic and transesophageal echocardiography, papillary fibroelastomas were usually incidental autopsy [16, 21, 30] or cardiac surgical findings [27]. These tumors also have been detected during echocardiography or catheterization for cardiac valvular or coronary disease [5, 13, 14] or when investigating the source of an arterial embolus [4, 7].

The potential for fibroelastomas to cause serious complications has been increasingly apparent. Few asymptomatic fibroelastomas have been reported in the modern era [2]. However, the percentage of symptomatic fibroelastomas cannot be ascertained accurately because the pool of silent fibroelastomas is unknown.

Fibroelastomas of the left side of the heart have been associated more frequently with serious symptoms. Common presentations include angina or sudden death [2, 8, 16–21] or neurologic symptoms, such as transient ischemic attacks and cerebrovascular accidents [3, 4, 6, 7, 10–12, 16]. In the case of coronary ischemic syndromes, etiologic mechanisms have included prolapse of pedunculated left or right coronary cusp tumors into their respective coronary ostia [8, 17, 20] or direct embolization of tumor material from the cusp lesion to the coronary artery [17, 18]. Cerebrovascular symptoms have been described frequently [3, 4, 6, 7, 10–12, 16], and many of these patients have had multiple episodes [10, 12], in 1 case seven [11]. Tumor embolization may be responsible for some of these cerebrovascular events, but several authors also have suggested that these tumors provide a nidus for a platelet fibrin clot that subsequently embolizes [4, 6, 12].

Lee and associates [22] described a patient with multiple lesions of the left heart and an endocarditis-like illness. He underwent exploration for presumed vegetations that actually were papillary fibroelastomas.

Right-sided heart valve lesions have been reported less frequently than left-sided heart lesions, and the association with specific clinical findings has been less well defined for these pulmonary, tricuspid, right atrial, and right ventricular tumors [5, 9, 14, 21, 24, 27–29]. One congenital case of tricuspid valve fibroelastoma caused intermittent right ventricular outflow tract obstruction with cyanotic spells [29], and one elderly adult patient was described with pulmonary embolism and a tricuspid valve fibroelastoma [14], although the causative relationship was not described.

Pathology and Pathogenesis
Papillary fibroelastomas are usually small (<1 cm), single, stalked lesions that may be located on any of the heart valves or endocardial surfaces. They are classically described as having the appearance of a sea anemone. In the Armed Forces Institute of Pathology series [15], when these tumors involved the mitral or tricuspid valves they were more commonly located in the midportion of the atrial side. On the semilunar valves, they occurred anywhere on the leaflet, and with near equal frequency on the two sides.

The pathology has been well described [15, 24]. Multiple papillary fronds arise from a central stalk or pedicle. The papillae have a collagen core, contiguous with the connective tissue of the stalk and the endocardium, surrounded by a dense layer of elastic fibers. Around the central core is a peripheral zone of loose connective tissue containing mucopolysaccharide, which may be contiguous with the subintimal layer of endothelium [24]. Finally, there is a layer of hyperplastic endothelial cells contiguous with the valvular endothelium. The overall structure of the fronds resembles that of chordae tendineae [15].

Some papillary fibroelastomas are congenital, including the one described by Raeburn [30] in a 9-month-old child and a tricuspid valve tumor obstructing the right ventricular outflow tract described by Anderson and associates [29]. However, most lesions are probably acquired. Lee and associates [22] and Levinsky and associates [36] reported patients who had undergone septal myomectomy and in whom multiple papillary fibroelastomas subsequently developed that were not present at the initial operation. Cha and colleagues [13] also described a patient with papillary muscle and aortic valve fibroelastomas that were not present at the time of open mitral commissurotomy 10 years previously.

In acquired cases, there are several theories of pathogenesis, leading to a variety of previous descriptions including papillary myxoma, fibroma, hyaline fibroma, myxofibroma, hemangioelastofibroma, fibroelastic hamartoma, endothelial papillary excrescence, giant Lambl excrescence, fibroangiomyxoma, and hemangiofibroma [12, 15, 16, 24]. Some authors regard them as giant Lambl excrescences formed by layers of organizing fibrin deposition [13, 21, 28, 31]. In support of this theory, McFadden and Lacy [4] and Fowles and associates [12] reported fibrin thrombi attached to fibroelastomas. However, this is not a universal finding, and Fishbein and colleagues [24] did not find evidence of fibrin within or attached to such tumors in a detailed histologic examination. Noting the common association between papillary fibroelastomas and other cardiac lesions (valvular, pulmonary, or hypertensive heart disease), these authors speculated that turbulent blood flow and mechanical trauma may stimulate endothelial cell hyperplasia, rather than these lesions being of neoplastic origin.

McAllister and Fenoglio [15] noted that the location, prevalence, and structure of fibroelastomas are quite different from that of Lambl's excrescence. They regard fibroelastomas as true benign neoplasms [15].

Treatment
Since Lichtenstein and colleagues [27] described an incidental papillary fibroelastoma removed in 1976, numerous surgical excisions have been reported, either alone [2–4, 6–8, 10] or in conjunction with operation for other heart disease [13, 14]. These lesions, which usually have a stalk, have not been reported to recur. Accordingly, simple excision with or without leaflet repair [2–4, 6] is usually sufficient. Valve replacement may be necessary if the lesion is extensive, the resection distorts the valve anatomy, or in the presence of preexisting disease [10, 12, 13, 22]. Our case was treated with simple excision from the free edge of the aortic valve noncoronary cusp.

More problematic than the surgical technique, which requires cardiopulmonary bypass but which has been associated with low morbidity and mortality, is the decision whether or not to perform operation. Lesions detected during evaluation of unexplained myocardial or cerebral ischemic symptoms should certainly be removed, because there is strong circumstantial evidence of a causative relationship. However, what of those lesions that are totally asymptomatic and discovered incidentally? It is possible that there is a large pool of undetected and asymptomatic cases, and that those cases seen during evaluation of various cardiac or cerebral symptoms represent only the small proportion of patients who become symptomatic. Such reasoning would favor observation of incidental lesions. However, as echocardiography has become both more accurate and widely used, there has not been a proportionate increase in reports of asymptomatic, incidental fibroelastomas.

A small fibroelastoma cannot be neglected, because size does not correlate with the development of serious symptoms. Our patient had a 3-mm lesion and suffered two cerebral events, one of which was almost certainly caused by this lesion. Furthermore, there may be no premonitory symptoms or warning signs before a serious event, such as a stroke, myocardial infarction, or sudden cardiac death. Finally, from a technical standpoint, these lesions frequently have stalks and are easily removed with low perioperative morbidity and mortality.

We agree with those authors who recommend surgical removal of papillary fibroelastomas [1, 4, 6, 10], in the absence of major surgical contraindications. Given the thrombotic potential of such lesions, preoperative anticoagulation therapy is prudent [4, 6]. However, as demonstrated in our case, this precaution does not eliminate the risk of thromboemboli. Obviously, these recommendations would be modified if a large echocardiographic series revealed that silent papillary fibroelastomas were common, and that such lesions could remain asymptomatic.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Case Report
 Comment
 References
 
Address reprint requests to Dr Shahian, Department of Thoracic and Cardiovascular Surgery, Lahey Clinic Medical Center, 41 Mall Rd, Burlington, MA 01805.


   References
Top
 Footnotes
 Abstract
 Introduction
 Case Report
 Comment
 References
 

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ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
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