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Case Studies

Effective ADAPT Thrombectomy in a Patient with Acute
Stroke due to Cardiac Papillary Elastofibroma: Histological
Thrombus Confirmation
Francesco Biraschi, MD,* Francesco Diana, MD,† Francesco Alesini, MD,‡
Giulio Guidetti, MD,* and Simone Peschillo, MD, PhD*

A 75-year-old man with hypertension and atrial fibrillation was admitted to our
emergency room with right-sided hemiplegia and complete aphasia (National Institutes of Health Stroke Scale [NIHSS] score = 18). A noncontrast computed
tomography scan showed a slight hypodensity in the left insular region and a
bright hyperdense sign in the M1 tract of the left middle cerebral artery (MCA).
Angio-CT confirmed an occlusion of the M1 tract of the MCA. Magnetic resonance diffusion-weighted imaging/perfusion-weighted imaging was obtained and
revealed a mismatch in the left parietal cortical region. Complete revascularization
was achieved by thromboaspiration with the A Direct ASPIRATION first PASS
TECHNIQUE (ADAPT) technique. Histological examination of the embolic material revealed its nonthrombotic nature: cardiac embolic papillary elastofibroma
(PEF). At discharge, good recovery of right-side hemiplegia was observed. This
case report is the second in literature in which a histological confirmed cardiac
embolic PEF is reported as a cause of embolic stroke. PEF is a rare but potentially treatable cause of embolic stroke. Understanding the nature of the embolic
material would help in choosing the best revascularization approach. Key Words:
Stroke—mechanical thrombectomy—papillary elastofibroma—cardiac embolism—MR
perfusion—ADAPT—thrombus.
© 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.

Case Presentation
From the *Department of Neurology and Psychiatry, Endovascular
Neurosurgery/Interventional Neuroradiology, Sapienza University
of Rome, Rome, Italy; †Department of Radiology, Sapienza University of Rome, Rome, Italy; and ‡Department of Oncological,
Radiological and Anatomopathological Sciences, Sapienza University of Rome, Rome, Italy.
Received June 23, 2016; revision received July 12, 2016; accepted
July 17, 2016.
Address correspondence to Francesco Biraschi, MD, Department
of Neurology and Psychiatry, Endovascular Neurosurgery/
Interventional Neuroradiology, Sapienza University of Rome,
Policlinico Umberto I, Viale del Policlinico 155, Rome 00100, Italy.
E-mail: f.biraschi@gmail.com.
1052-3057/$ - see front matter
© 2016 National Stroke Association. Published by Elsevier Inc. All
rights reserved.
http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.07.026

A 75-year-old man with hypertension and atrial fibrillation was admitted to our emergency room with rightsided hemiplegia and complete aphasia (National Institutes
of Health Stroke Scale [NIHSS] score = 18). The patient
was found on the ground by the relatives early in the
morning. The patient was last seen well on the night before
he was admitted to the hospital. The patient was under
a well conducted anticoagulation therapy with apixaban.
At the emergency room, the noncontrast computed tomography scan (Fig 1, A) showed a slight hypodensity
in the left insular region and a bright hyperdense sign
on the M1 tract of the left middle cerebral artery (MCA)
(Fig 1, B). Angio-CT confirmed an occlusion of the M1
tract in the left MCA. No intravenous (IV) recombinant

Journal of Stroke and Cerebrovascular Diseases, Vol. ■■, No. ■■ (■■), 2016: pp ■■–■■

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F. BIRASCHI ET AL.

Figure 1. Noncontrast computed tomography demonstrates a slight
hypodensity in the left insular region (A) and a very bright hyperdense
sign in the left middle cerebral artery (B). Angio-CT confirmed an occlusion of the left middle cerebral artery (C).

tissue plasminogen activator was performed due to the
unknown onset time of symptoms. To evaluate the opportunity for a mechanical revascularization, a magnetic
resonance imaging scan was obtained. Diffusion-weighted
imaging sequences showed a hyperintensity in the left
insular region while the mean transit time was increased in the left parietal cortical region, suggesting a
mismatch in that region. No fluid-attenuated inversion
recovery changes were observed (Fig 2). In the angiosuite,
M1 occlusion was confirmed by the presence of collaterals
coming from the left anterior cerebral artery and from
temporal branches of the left MCA (Fig 3, A). Complete
revascularization was achieved by thromboaspiration
(NeuronMax, ACE64, 3MAX; Penumbra, Alameda, CA)
(Fig 3, B) in 15 minutes from groin puncture with a thrombolysis in cerebral infarction score of 3. The material
removed after the aspiration is shown in Figure 4. Macroscopic evaluation revealed a 1-cm white-pink hard

Figure 2. Magnetic resonance study with axial T2 fluid-attenuated inversion recovery (A), diffusion-weighted images (B), and mean transit time
(C) showing a mismatch in the left posterior parietal region.

Figure 3. Conventional angiography. Anteroposterior and lateral views
of the left internal carotid artery injection before (A) and after (B) treatment.

tissue-like material. On histological examination, the
hematoxylin/eosin stained slide showed a solid amorphous eosinophilic tissue, in which there were some
calcium depositions, intermingled with some peripheral
blood cells, such as red cells and monocytes. At the edge
of the lesion, there were some pseudopapillary (fingerlike) projections on the surface of which CD34 immunostain
showed the presence of some endothelial cells and the
Weigert–van Gieson histochemical stain revealed some
elastic fibers. No epithelial cells were found (immunohistochemistry for cytokeratin AE1/AE3 was negative).

Figure 4. (A) Macroscopic view of the embolic material aspirated. (B)
Histological examination: left: pseudopapillary fronds with calcific axis that
are considered to be the plate of the papillary fibroelastoma from which
the thrombus has been detached; middle: at the edge of papillary fronds
there were some elastic fibers retine (arrow—Veigert Van Gieson stain, 10×);
right: pseudopapillary (fingerlike) projections lined by some endothelial cells
(CD34 immunostain, 10×).

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ADAPT THROMBECTOMY IN A PATIENT WITH ACUTE STROKE

This complex of morphological, histochemical, and
immunohistochemical data referred to a thrombus characterized by papillary fronds lined by the endothelium
and elastic fibers that are considered to be the plate of
the ultrasound referred papillary fibroelastoma from which
the thrombus has been detached.

Discussion
To our knowledge, this is the second case in literature with histological confirmation of an embolic papillary
elastofibroma (PEF) causing an ischemic stroke treated
with mechanical thrombectomy.1 Histologically confirmed tumor fragments have been isolated from the
embolic material from coronary, pulmonary, and peripheral arteries, but not from cerebral embolism.2 Five cases
are reported in literature in which PEF is supposed to
be the stroke etiology treated with both IV3,4 and intraarterial recombinant tissue plasminogen activator,5,6 and
2 of these cases are associated with mechanical disruption,6,7
but none of the 5 cases has the histological confirmation of the embolic material. In these cases, an indirect
diagnosis of the embolic nature of the thombus was made
by histological analysis after cardiac PEF removal. It is
long debated about the nature of the embolic material
in these patients. Embolization may occur from the fragile
papillary fronds of the tumor itself or from a thrombus
formed within the tumor context. Our histological examination suggests that the nature of the emboli was a
wide calcified mass surrounded by fibrin with a papillary base of implant. Thus, we can affirm with certainty
that the embolization material was represented by a calcified mass that has come off the PEF and occluded the
M1 segment of the left MCA. The very calcific nature of
the thrombi was the reason why oral anticoagulant therapy
was not useful in preventing cardioembolism. The nature
of the embolic material has a relevant impact on therapeutic strategies to achieve recanalization. When
embolization is from the thrombotic material surrounding the mass, treatment with IV alteplase could be useful3,4;
on the other hand, when the embolizing material is a fragment from the tumor, fibrinolytic therapy is probably not
useful. In these cases, mechanical recanalization could be
the best effective treatment option for PEF embolism.7 In
our case, thromboaspiration has been proven to be feasible and efficient in restoring flow after a complete M1
occlusion. In our opinion thromboaspiration should be
the first-line choice compared to other mechanical techniques when hard-calcified tissue fragments characterize
the embolic material. Theoretically, indeed, it seems to

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be difficult to pass through a hard tissue-like material
coming from the tumor mass or a calcification, open a
stent-retriever, and remove the thrombus. Currently, there
are no tests that could predict the nature, either thrombotic or tumoral, of the embolic materials in patients with
PEF. In our case, noncontrast computed tomography provided helpful information showing a very bright
hyperdense sign in the MCA (156 Hounsfield units [HU])
that suggested the very calcific nature of the thrombus,
then confirmed by histological examination. A recent systematic review, which correlates the imaging and
histopathology of thrombi in acute ischemic stroke with
etiology and outcome, highlights how patients with favorable angiographic outcome had a significantly higher
mean clot HU than those with a poor angiographic
outcome.8 These results suggest how understanding the
nature of the embolic material dramatically would help
in achieving recanalization. Thus, we suggest a routine
histological examination of all clots removed during thrombectomy procedures to obtain a correlation between
neuroimages, histological analysis, and patient outcome.

References
1. Tejada J, Galiana A, Balboa Ó, et al. Mechanical
endovascular procedure for the treatment of acute ischemic
stroke caused by total detachment of a papillary
fibroelastoma. J Neurointerv Surg 2014;6:e37.
2. Gowda RM, Khan IA, Nair CK, et al. Cardiac papillary
fibroelastoma: a comprehensive analysis of 725 cases. Am
Heart J 2003;146:404-410.
3. Matijevic V, Poljakovic Z, Ilic I, et al. Cardiac papillary
fibroelastoma: source of cerebral embolism treated with
intravenous thrombolysis. J Stroke Cerebrovasc Dis
2011;20:485-487.
4. Corrado G, Panisi P, Checcarelli N, et al. An unusual cause
of ischemic stroke with successful thrombolysis. J Stroke
Cerebrovasc Dis 2013;22:e691-e692.
5. Palazzuoli A, Bruni F, Pasqui A, et al. Cardiac papillary
fibroelastoma: an unusual source of cerebral embolism
solved with local fibrinolysis. Neurol Sci 2002;22:469-472.
6. Ljevak J, Mišmaš A, Bazina A, et al. An infrequent type
of stroke with an unusual cause and successful therapy:
basilar artery occlusion caused by a cardiac papillary
fibroelastoma recanalized 12 hours after onset. Intern Med
2013;52:277-279.
7. Santos AF, Pinto J, Raos V, et al. Stroke and cardiac
elastofibroma: mechanical thrombectomy after thrombolytic
therapy. J Stroke Cerebrovasc Dis 2014;23:1262-1264.
8. Brinjikji W, Duffy S, Burrows A, et al. Correlation imaging
and histopathology of thrombi in acute ischemic stroke
with etiology and outcome: a systematic review. J
Neurointerv Surg 2016;doi:10.1136/neurintsurg-2016-012391;
[Epub 10 May 2016].