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Table of Contents    
Year : 2013  |  Volume : 61  |  Issue : 1  |  Page : 80-82

Bronchogenic adenocarcinoma masquerading as recurrent embolic strokes and myocardial infarction due to nonbacterial thrombotic endocarditis

1 Department of Neurology, Indraprastha Apollo Hospital, New Delhi, India
2 Department of Radiology, Indraprastha Apollo Hospital, New Delhi, India

Date of Submission20-Nov-2012
Date of Decision22-Nov-2012
Date of Acceptance25-Nov-2012
Date of Web Publication4-Mar-2013

Correspondence Address:
Sushma Sharma
Department of Neurology, Indraprastha Apollo Hospital, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.108020

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How to cite this article:
Suri V, Sharma S, Jadhav N, Rastogi R. Bronchogenic adenocarcinoma masquerading as recurrent embolic strokes and myocardial infarction due to nonbacterial thrombotic endocarditis. Neurol India 2013;61:80-2

How to cite this URL:
Suri V, Sharma S, Jadhav N, Rastogi R. Bronchogenic adenocarcinoma masquerading as recurrent embolic strokes and myocardial infarction due to nonbacterial thrombotic endocarditis. Neurol India [serial online] 2013 [cited 2023 Dec 7];61:80-2. Available from:


A 56-year-old lady presented with abrupt onset blurring of vision and speech abnormalities. Examination revealed right homonymous hemianopia, posterior aphasia and right hemiparesis. Magnetic resonance imaging (MRI) brain revealed multiple acute infarcts in the left temporal, bilateral fronto-parietal and left thalamic regions. Two days later, the neurological status worsened with development of cerebellar signs. Repeat MRI brain revealed fresh bilateral cerebellar infarcts [Figure 1]a and b. MR-angiography and computed tomography angiography (CTA) revealed normal cerebral and neck vessels but for hypoplastic right vertebral artery [Figure 1]c and d. Twenty-four hour Holter monitoring was negative for significant arrhythmia. 2D echocardiogram revealed left ventricular (LV) apical hypokinesia and Troponin I was positive, being suggestive of myocardial infarction (MI). Prothrombotic and vasculitic workup were normal. There was thrombocytopenia (68,000/cmm). Prothrombin time, activated partial thromboplastin time and serum fibrinogen levels were normal. D-dimer was raised (5.40 μg/dl). Low molecular weight heparin and anti-ischemic therapy for MI were started. CT coronary angiography revealed bilateral pulmonary artery thrombi and vegetations on the superior surface of the left coronary cusp of the aortic valve with mild aortic regurgitation [Figure 2]a. Trans-esophageal echocardiogram confirmed the presence of 9 mm vegetation on the left coronary cusp of the aortic valve with mild aortic regurgitation, besides LV apical hypokinesia. Lower limbs arterial Doppler revealed left popliteal artery embolic occlusion. The patient remained afebrile and serial aerobic and fungal blood cultures were sterile. Contrast-CT chest and abdomen revealed splenic infarct, left renal infarct and left lung upper lobe posterior segment wedge-shaped density, thickened overlying pleura and enlarged pretracheal, subcarinal and supraclavicular subcentimetric lymph nodes, minimal pericardial effusion and right main pulmonary artery thrombus [Figure 2]b and c.
Figure 1: Axial FLAIR images of the brain demonstrating infarcts in the left and right temporo-occipital regions and bilateral cerebellar hemispheres (arrows), seen as hyperintense areas (a) and (b). These areas showed restricted diffusion on DWI sequences. Magnetic resonance angiography of the cerebral blood vessels (c) and neck vessels (d) Showed no significant abnormality except hypoplastic right vertebral artery

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Figure 2: Axial image of the computed tomography (CT) angiogram of the heart demonstrating iregular hypodense vegetations (arrow) in relation with the left cusp of the aortic valve (a). Transaxial CT images revealing irregular hypodense mass in the posterior segment of the upper lobe of the left lung (thick arrow), thickened overlying pleura and enlarged mediastinal lymph nodes (thin arrows) (b) and splenic and renal infarcts, (c) (arrows)

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A possibility of nonbacterial thrombotic endocarditis (NBTE) with recurrent cerebral and systemic embolism, with MI as the presenting manifestation of primary neoplastic lung lesion, was considered. Further evaluation with whole body positron emission tomography (PET) CT revealed FDG avidity of lung lesion and of the enlarged lymph nodes. Histopathology of transbronchial lymph node biopsy revealed bronchogenic adenocarcinoma. The patient was managed with low molecular weight heparin, platelet transfusion and cryoprecipitate, along with Erlotinib, for primary lung malignancy.

NBTE is characterized by deposition of small sterile friable fibrin-platelet noninflammatory vegetations on the heart valves, usually occurring in advanced malignancy (especially mucin-producing adenocarcinomas) and hypercoagulable states. [1],[2] Friabilty causes a higher tendency for embolism. Unlike infective endocarditis, valve destruction is not seen. [3] Pathogenesis involves local valvular damage mediated by elevated circulating cytokines and malignancy-associated hypercoagulable state. Preexisting valvular lesion, if present, significantly enhances this process. [4]

NBTE is rare, with incidence ranging from 1% to 1.6% (in different autopsy series), an underlying malignancy having been found in 32-80%. [4] First presentation of lung carcinoma as NBTE-related cardioembolic stroke is even rarer; in a recent large Indian study involving 607 patients of lung cancer, none of the patients was reported to have such presenting features. [5] Treatment includes anticoagulation with heparin and treating the underlying malignancy. Oral vitamin K antagonists and thrombolysis are not recommended, as the former is not efficacious (probably due to some non vitamin K-dependant pro-coagulants related to underlying neoplasm) [6] and the latter may enhance the risk of further embolism from friable vegetations. Surgical valvular repair is considered in those with potentially curable cancers who have severe valvular dysfunction or recurrent embolic events despite adequate anticoagulation. [1],[4],[7]

 » References Top

1.Aryana A, Esterbrooks DJ, Morris PC. Nonbacterial thrombotic endocarditis with recurrent embolic events as manifestation of ovarian neoplasm. J Gen Intern Med 2006;21:12-5.  Back to cited text no. 1
2.Devulapalli S, Pinto N, Gandothra C, Jayam-Trouth A, Kurukumbi M. A rare case of occipital stroke as a consequence of nonbacterial thrombotic endocarditis in ovarian clear cell carcinoma: A case report. Case Rep Neurol 2012;4:84-91.  Back to cited text no. 2
3.Smeglin A, Ansari M, Skali H, Oo TH, Maysky M. Marantic endocarditis and disseminated intravascular coagulation with systemic emboli in presentation of pancreatic cancer. J Clin Oncol 2008;26:1383-5.  Back to cited text no. 3
4.Ferlan G, Fiorella A, De Pasquale C, Tunzi F. Primary coronary embolism as an unusual manifestation of nonbacterial thrombotic endocarditis in a patient with gastric cancer. Cardiol Res Pract 2010;2010:319732.  Back to cited text no. 4
5.Dey A, Biswas D, Saha SK, Kundu S, Kundu S, Sengupta A. Comparison study of clinicoradiological profile of primary lung cancer cases: An Eastern India experience. Indian J Cancer 2012;49:89-95.  Back to cited text no. 5
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6.Bell WR, Starksen FF, Tong S, Porterfield JK. Trousseau's syndrome. Devastating coagulopathy in the absence of heparin. Am J Med 1985;79:423-30.  Back to cited text no. 6
7.Bathina JD, Daher IN, Durand JB, Yusuf SW. Acute myocardial infarction associated with non-bacterial thrombotic endocarditis. Tex Heart Inst J 2010;37:208-12.  Back to cited text no. 7


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