Cas clinique

DOI of or1University2University3Harbor-U

CorrespondEast Chestnuthotmail.com

Ann Vasc Surhttp://dx.doi.or� Annals of V�Edit�e par ELS

Thrombus muraux thoraciques : Une s�erieet une revue de la litt�erature

Marvin E. Morris,1 Edgar Luis Gali~nanes,2 W. Kirt Nichols,2 Charles B. Ross,1

Joe Chauvupun,3 Louisville, Kentucky, Columbia, Missouri, et Torrance, California, USA

Les thrombus muraux thoraciques (TMT) sont rares mais une source importante d’emboles dis-taux. Les options de traitement sont vari�ees, allant de la chirurgie ouverte, �a l’endovasculaire,et au traitement conservateur. Nous rapportons deux cas de TMT, un trait�e avec succ�es parstent de l’aorte thoracique pour embolisation visc�erale et p�eriph�erique, et l’autre trait�e demani�ere conservatrice pour embolisation digitale secondaire �a un TMT dans le tronc innomin�e.

Thoracic mural thrombi (TMT) are a rare but impor-

tant source of peripheral emboli. Treatment options

include systemic anticoagulation, surgical throm-

boendarterectomy, resection and replacement with

synthetic conduit, and exclusion with endovascular

stent grafts. We report two cases of TMT, one suc-

cessfully treated with endoluminal stent placement

of a descending thoracic aortic thrombus for persis-

tent infrageniculate embolization. The second

patient presented with hand ischemia from amobile

thrombus in the innominate artery andwas success-

fully treated by anticoagulation therapy.

CASE 1

A 44-year-old, Gravida 2 Para 1, woman with a history

significant for hypertension and menorrhagia requiring

high-dose estrogen therapy presented from an outside

hospital with acute chest and epigastric pain and numb-

ness of her right toes. She was in sinus rhythm. Her

iginal article: 10.1016/j.avsg.2011.05.030.

of Louisville, Louisville, KY, USA.

of Missouri, Columbia, MO, USA.

CLA Medical Center, Torrance, CA, USA.

ance : Marvin E. Morris, University of Louisville, 401Street, Louisville, KY 40059, USA, E-mail: dcmorris12@

g 2011; 25: 1140.e17-1140.e21g/10.1016/j.acvfr.2013.02.007ascular Surgery Inc.EVIER MASSON SAS

abdomen was soft and mildly tender without peritoneal

signs. Her pedal pulses were palpable bilaterally with

motor function intact. Computed Tomography (CT) of the

chest demonstrated an (Fig. 1A) aortic thrombus in the

ascending aorta and a (Fig. 1B) lesion in the mid-

descending thoracic aorta. CT of the abdomen and pelvis

revealed a small amount of free fluid within the pelvis and

focal areas along the small bowel, without evidence of

pneumatosis intestinalis. Findings from CT of the head

were negative. Transesophageal echocardiogram revealed

no evidence of cardiac thrombi. The patient was started on

a systemic heparin and transferred to our facility.

After twelve hours of intravenous unfractionated

heparin, her neurovascular examination changed, with

a loss of pedal pulses, worsening numbness, and decreased

motor function of the right lower extremity. Angiography

revealed emboli in the right tibioperoneal trunk and left

proximal anterior tibialis artery. We focused our efforts

on the descending thoracic lesion as the cause of her pro-

gressing lower extremity symptoms. We excluded the

descending thoracic thrombus with a (Fig. 1C) 116- �24-mm Talent graft. The location of the lesion allowed us

to minimize wire manipulation of the ascending lesion. In

a multidisciplinary decision involving our cardiothoracic

service, her thrombi in the ascending aorta were treated

with systemic anticoagulation. The increased morbidity

and mortality, a surgical intervention, and the anatomic

complexity of an endovascular approach dictated our

therapeutic algorithm. After stent deployment, the peri-

pheral emboli in her legs were treated with catheter-

directed thrombolysis for 24 hours.

Interval angiography demonstrated resolution of her

embolic lesions with good runoff bilaterally. Her pedal

pulses were again palpable. Systemic anticoagulation

with heparin was converted to warfarin with a target

1214.e17

Fig. 1. (A) Thrombus in the ascending aorta. (B) Thrombus in the mid-descending aorta. (C) Endovascular graft

covering the descending aorta.

1214.e18 Cas cliniques Annales de chirurgie vasculaire

international normalized ratio (INR) of 2-3. Her symp-

toms resolved and findings from hypercoagulability panel

were negative. A gynecologist was consulted for her

menorrhagia, and she was started on IM Depo-Provera.

She continued to do well and was discharged to home

on postoperative day 7 with close surveillance.

CASE 2

A 43-yeareold woman, who is a former 1.5-pack-per-day

smoker, with a history of diabetes mellitus, hypertension,

and menorrhagia was transferred with progressive ische-

mic pain and discoloration of the fingers of the right hand

over the course of 2 weeks. On presentation, she was in

sinus rhythm, with equal blood pressure in both upper

extremities and with palpable pulses in the ulnar and

radial arteries bilaterally. Cyanotic discoloration was

prominently noted in all five fingers of the right hand,

more pronounced in fingers 2-5. Ischemic changes in

these digits extended proximally to proximal inter-

phalangeal joint levels, with the fingers being cold and

painful to touch and movement (Fig. 2A). History was

negative for antecedent collagen vascular disorders, vas-

culitis, and thrombophilias. Home medications included

metformin, byetta, and a thiazide diuretic. Pertinent

laboratory findings included a platelet count of 499;

erythrocyte sedimentation rate was mildly elevated at 50.

A presumptive diagnosis of Reynaud syndrome was

entertained, and she was started on Methylprednisolone.

A transthoracic echocardiogram was negative for atrial

thrombus and cardiac valvular anomalies. CT angiogram

(CTA) revealed a large thrombus in the innominate artery

(Fig. 2B). Anticoagulation therapy was initiated with

unfractionated heparin infusion, and within 24 hours,

there was resolution of her hand cyanosis. Warfarin was

initiated with a target INR of 2.0-3.0. One year later, her

index finger was persistently cyanotic, but her remaining

digits were normal (Fig. 2C). Follow-up CTA revealed

resolution of her innominate artery thrombus (Fig. 2D).

She remains anticoagulated with warfarin with an INR

of 2-3.

DISCUSSION

TMT is an intriguing pathology with a dynamic the-

rapeutic armamentarium. TMT is increasingly

recognized as a source of peripheral emboli, either

to the viscera, cerebrovascular circulation, or most

commonly the lower extremities. TMT characterizes

an aortic thrombus in the ascending aorta or its

branches or the descending aorta, typically in young

people, in the absence of preexisting disease.1 Aortic

thrombus of the thoracic aorta most commonly

occurs in the transverse aortic arch with a pre-

dilection for the aortic isthmus and is often limited

to a focal lesion. This distinguishes all forms of

TMT from other atherosclerotic lesions, which are

traditionally found diffusely distributed throughout

the arterial system.2-6 Risk factors include younger

age, smoking, and a family history of athero-

sclerosis. The majority of reported cases have been

Fig. 2. (A) Cyanosis of the distal right hand. (B) Innominate artery thrombus. (C) Resolution of innominate artery

thrombus. (D) Resolution of cyanosis of distal right hand.

Vol. 25, No. 8, 2011 Cas cliniques 1214.e19

diagnosed after an embolic event. Currently

unknown, the pathophysiology is multifactorial;

theories include thrombophilias secondary to mali-

gnancy, and exogenous steroids use.1,2 Both our

patients had no definable thrombophilias, no ante-

cedent history of steroid use, and no evidence of

malignancy.

Mobile thrombi originating from the innominate

artery are extremely rare. Based on the limited am-

ount of literature, any recommendations on theman-

agement of innominate artery thrombus have to be

extrapolated from AMT. Innominate artery thrombi

clinically manifest as cerebrovascular events, digital

ischemia, arm fatigue, and angina.1,2 Anatomically,

tracheal interposition and atheromatous disease may

preclude diagnosis with transesophageal echocar-

diography (TEE). Gadolinium-enhanced magnetic

resonance angiogram (MRA) may provide complete

visualizations of the arch vessels, including the

innominate artery, in cases of normal TEEwith a high

clinical suspicion for right-sided embolic sources.

False-positive images due to circulatory turbulence

have been reported.1 CTA is now considered the

diagnostic modality of choice for operative planning.

In both of our cases, CTA was diagnostic and negated

the need for invasive angiography, which can be

catastrophic owing to the risk of thrombus migration

and embolization.7-9

1214.e20 Cas cliniques Annales de chirurgie vasculaire

Treatment algorithm is controversial; therefore,

there is no consensus for the appropriate therapeutic

regimen for TMT. Therapeutic options include

anticoagulation,2,10 thrombolysis,11 thromboaspira-

tion,12 open thromboendarterectomy, and exclusion

using endoluminal stent grafts. In general, a trial of

anticoagulation is pursued, with surgical repair or

endovascular intervention reserved for patients who

fail to respond. Persistence of a mass by TEE after

anticoagulation or highly mobile appearance of the

thrombus may lead to operative intervention. Sur-

gical options include thrombectomywith or without

resection of the atherosclerotic plaque, with repair of

the aorta using either Dacron or polytetrafluoroe-

thylene. In a contemporary series of nine cases of

TMT by Chakroun et al., 50% of patients had failure

of medical therapy, requiring surgical intervention;

Goueffic treated 38 patients with open surgical

techniques, with a mortality of 2.6%.1

Recurrence is a major issue with TMT, and long-

term anticoagulation is recommended. In the study

by Patra et al., recurrence was observed in 27% of

patients treated medically, typically in remote ana-

tomical locations. Recurrence after surgical repair

has been reported.3,4 Our initial patient was treated

with thoracic stent graft owing to progressive sym-

ptomatology and limb threat, and our second patient

received full anticoagulationwith an unfractionated

heparin bridge to warfarin. A subsequent CTA in 4

weeks showed complete resolution of her thrombus.

The discoloration of her hand took weeks to resolve,

but she is fully functionalwithout residual deficits or

further embolic events to date at 1-year follow-up.

The use of endovascular devices to treat sym-

ptomatic aortic pathology allows exclusion of the

plaque from the circulation while separating the

intima from rheological factors that may promote

platelet deposition and further embolization.13-18

Various case reports in the literature describe the use

of stent grafts as sole treatment or in conjunction

with other treatment options in the management of

thoracic mural thrombi. Our first case adds to the

body of literature supporting use of thoracic aortic

stent grafts to treat AMT.

Transluminal balloon angioplasty and stenting

has become the preferred method for management

of primary atherosclerotic lesions of the innominate

artery owing to a greater than 90% initial success

and limited morbidity. Long-term follow-up data

for treatment of atherosclerotic lesions are currently

not available.19-27 Although exclusion of mobile

thrombus in the innominate artery by stent grafting

is feasible by endoluminal techniques, experience is

limited. Because of the risk of embolization, open

exposure of the common carotid artery and clamping

with retrograde treatment of the innominate lesion,

complete with thorough flushing before closure,

would seem prudent. This technique has been

reported formanagement of standard atherosclerotic

lesions with favorable outcomes.15 For lesions

located at the origin of the innominate with invol-

vement of the ascending aorta, open thromboen-

darterectomy facilitated by circulatory arrest may be

required. Morbidity and mortality in these cases

can approximate 30%.1 Although data are anec-

dotal, as in our second case, a trial of anticoagulation

therapy seems practical, with more aggressive

interventions reserved for treatment failure.

Endovascular stenting for lesions in the ascend-

ing aorta has been reported in small series of

patients. Arch anatomy and configuration (whether

conical or tubular) in the cases of treatment of aneu-

rysmal pathology dictate treatment plan and suc-

cess. Important tenants of proper device placement

include the use of fixation with hooks, the appro-

priate oversizing, and caution not to compromise

aortic valve closure. A mismatch between the inner

and outer curvatures of the ascending aorta may

result in kinking of the stent graft.28 Temporary

cardiac arrest, rapid ventricular overpacing, and

partial atrial inflow occlusion to induce controlled

hypotension have been advocated to achieve suc-

cessful graft deployment.29-31 These anatomical

constraints limit aortic arch endovascular stenting to

high-risk surgical patients unfit for open repair.

In conclusion, TMT is a dynamic pathological

process with evolving therapeutic options. High cli-

nical suspicion is needed for diagnosis, and patient

care should be individualized with an emphasis

toward minimizing morbidity and mortality. The

use of aortic stent graft technology provides a mini-

mally invasive approach to treat this complex path-

ology. Innominate artery mobile thrombus (IAMT)

presents additional therapeutic dilemmas, with

anticoagulation representing a viable option for

management. Long-term anticoagulation therapy,

optimization of atherosclerotic risk factors, and

surveillance are essential because all available

treatment modalities may initially fail or be com-

plicated by late recurrence.

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