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Ann Thorac Surg 2005;79:2145-2147
© 2005 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, University of Düesseldorf, Düesseldorf, Germany
b Institute of Diagnostic Radiology, University of Düesseldorf, Düesseldorf, Germany
Accepted for publication December 10, 2003.
* Address reprint requests to Dr Borowski, Klinik für Thorax- und Kardiovaskularchirurgie der Universität Düsseldorf, Germany Moorenstrasse 5, 40225, Düesseldorf, Germany (E-mail: dr.borowski{at}t-online.de).
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Introduction |
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A 46-year-old woman was admitted to the stroke unit of our hospital for severe bilateral migraine headache, apathy, and decreased attentiveness. Six months before admission she had a single cerebral embolism event of an "undetermined cause," which she recovered from completely. Neurologic examination revealed left-sided neglect, and visual, auditory, and partially sensory deficiencies with apractic disturbances. Splinter hemorrhages in the patient’s nail beds and Osler’s nodes were observed on the upper extremities.
Laboratory studies revealed a hemoglobin value of 8.2 g/dL; a normal white blood count; a platelet count of 46 x 1,000/µL; a normal prothrombin; a normal partial thromboplastin time; a normal fibrinogen level; a normal antithrombin III; a normal factor XII; normal plasminogen; normal proteins C and S; a D-dimer of 1,515 µg/mL; a negative anticardiolipin antibody test; a negative prothrombin 20210; a negative factor V Leiden mutation; a negative liver function test; a lactate dehydrogenase of 427 U/L; normal albumin; normal ß-globulins and 
-globulins; and elevated 
1 and 2 globulins.
Multiple urine and blood cultures were negative. Cerebrospinal fluid showed no signs of infection. The chest roentgenogram and electrocardiogram were normal.
Computed tomography of the brain showed multiple strokes involving both cerebral cortices in different perfusion territories. Diffusion-weighted magnetic resonance imaging visualized restricted proton diffusions (supra- and infra-tentorial) in nearly all areas, indicating acute multiple cardiogenic embolism (Fig 1). Noninvasive magnetic resonance angiography showed a completely normal intracerebral vasculature. A transthoracic echocardiography revealed normal heart dimensions and function, mild aortic regurgitation, and no evidence of vegetations. At transesophageal echocardiography, vegetations smaller than 5 mm in diameter could be visualized attached to the left coronary and noncoronary aortic cusps (Fig 2).
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Due to the risk of hemorrhagic transformation of the large cerebral ischemic infarcts, especially with the presence of thrombocytopenia, we decided not to perform cardiac surgery, and medication with antibiotics and anticoagulation with heparin were administered. During the next 2 days the patient experienced further systemic embolization with left-sided hemiparesis, hemianopia, and a decreased level of consciousness. On computed tomography of the brain, cerebral edema with midline shift and ventricle narrowing were observed. Following the recommendations of the consulting neurologist and the neurosurgeon, the patient underwent open heart surgery with aortic valve replacement.
During surgery, the aortic valve cusps were found to be entirely normal, but were covered with pedunculated vegetations mainly on their free edges at the ventricular surface. In addition, similar vegetations were found attached to the inner wall of the ascending aorta. Histopathologic examination of the valve specimen revealed no signs of inflammatory reaction; the vegetations consisted mainly of fibrin core and platelet thrombi suggestive of marantic endocarditis.
The postoperative course was uneventful with the exception of thrombophlebitis, which developed in both legs despite anticoagulation. Five weeks later the gynecologic investigation revealed ovarian neoplasm of an advanced stage. Therefore, the patient underwent radical tumor surgery with hysterectomy and lymphadenectomy. Postoperatively, multiple cerebral and pulmonary emboli and in due course, recurrent pleural and pericardial effusions of carcinomatous origin occurred. The respiratory situation of the patient deteriorated. Therapy resistance also developed. Then the patient had pneumonia develop, and she died due to respiratory insufficiency 4 months after cardiac surgery.
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The pathophysiologic mechanisms of the NBTE are still not understood and are hypothetical. Monocyte or macrophage can interact with malignant cells, releasing and activating factors causing endothelial damage and thrombosis, as recently suggested [4]. A prothrombic or hypercoagulable state of a different range and expression seems to be an associated feature of this entity. In cancer, the signs and symptoms of the prothrombic state can range from asymptomatic abnormal coagulation tests to massive thromboembolism and disseminated intravascular coagulation, and clinical embolization can occur before detection of cancer [5, 6]. In patients with NBTE, the type of coagulation disorder seems to be dependent on the type of underlying neoplastic disease [5, 6], as in our patient. According to the investigations of Blann and Lip [6], ovarian cancer was associated with increased platelet activation and possibly abnormal blood vessel wall function in terms of reduced sensitivity to prostacyclin (a thrombotic mass in the aorta).
Today there are no established treatment strategies for thrombotic coagulopathy associated with cancer, but anticoagulation should be seriously considered [2]. Lee and associates [7] demonstrated that low molecular-weight heparin effectively reduces the risk of recurrent thromboembolism more effectively than oral anticoagulants in patients with cancer.
Other authors have reported that treatment with heparin alone [8] does not prevent further emboli, and cancer patients on oral anticoagulants still have an increased embolization risk [6]. These observations are consistent with ours; despite effective anticoagulation with heparin and later with Phenprocoumon (Hoffman-La Roche, Grenzach-Whylen, Germany), our patient postoperatively had disseminated thrombophlebitis and pulmonary emboli develop, and later on, systemic embolism again.
Another important issue in the decision making for cardiac surgery is distinguishing the infective endocarditis from the NBTE. The indispensable role of transesophageal echocardiography in the detection of NBTE has been emphasized, and failure to detect NBTE by transthoracic echocardiography has been well documented [9]. Characteristic features of NBTE-related vegetations have also been sufficiently described [9, 10]. As in our case, the characteristic feature was a single, small vegetation attached to the coaptation surfaces of the valve, which did not destruct the valve tissue; therefore, essentially it was not affecting its functionality or only very little of it [10]. Histopathologic and bacteriologic examinations of the removed valve tissue or attached thrombus, or both, can additionally support the diagnosis of NBTE (ie, no signs of acute inflammatory reaction, lack of bacteria in serial histologic sections and cultures, and presence of fibrin core in the thrombus) [10].
Recent studies [11] have also emphasized the role of modern neuroimaging techniques (eg, diffusion-weighted magnetic resonance imaging) as a helpful diagnostic tool in the differentiation of stroke patterns between NBTE and infective endocarditis. Patients with NBTE uniformly have one typical stroke pattern with multiple, widely distributed, small and large strokes, whereas patients with infective endocarditis exhibit all four described stroke patterns [11]. This is probably due to the fact that vegetations in NBTE have little cellular organization and therefore have a higher fragmentation potential.
In summary, NBTE should always be considered in patients with recurrent systemic embolization, with or without underlying neoplastic disease. When clinical signs of infection are missing, small vegetations on the aortic valve along the coaptation line without destruction of leaflets are present on transesophageal echocardiography, which are often not detected on transthoracic echocardiography, and when characteristic stroke pattern on diffusion-weighted magnetic resonance imaging with multiple strokes in several brain territories is observed, a suspicion of NBTE should be aroused. Once the diagnosis of NBTE is established, adequate anticoagulation based on diagnostic testing for coagulopathies should be initiated [5, 12], and the immediate search for an underlying malignancy disease should be started.
Cardiac surgery should be considered in patients with potentially curable cancer and avoided in those with advanced, noncurable malignancies, because the surgery may not prevent further embolization. In patients with potentially curable cancer and tumor-associated coagulopathy, surgery for cancer as a first therapeutic priority to eliminate the cause of the coagulation disorder should also be considered.
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This article has been cited by other articles:
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  A. Smeglin, M. Ansari, H. Skali, T. H. Oo, and M. Maysky Marantic Endocarditis and Disseminated Intravascular Coagulation With Systemic Emboli in Presentation of Pancreatic Cancer J. Clin. Oncol., March 10, 2008; 26(8): 1383 - 1385. [Full Text] [PDF]
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