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reate an aortosubclavian shunt, which reversed theetrograde flow in the vertebral artery. Flow remainedntegrade, even with exertion of the left arm. This is therst report of this kind of biological bypass in a patientith subclavian steal syndrome and multi-vessel coro-ary artery disease.

eferences

. Reivich M, Holling HE, Roberts B, Toole JF. Reversal of bloodflow through the vertebral artery and its effect on cerebralcirculation. New Eng J Med 1961;265:878–85.

. Brown AH. Coronary steal by internal mammary graft withsubclavian stenosis. J Thorac Cardiovasc Surg 1977;73:690 –3.

. Takach TJ, Reul GJ, Cooley DA, et al. Myocardial thievery: thecoronary-subclavian steal syndrome. Ann Thorac Surg 2006;81:386–91.

. FitzGibbon GM, Keon WJ. Coronary subclavian steal: a re-current case with notes on detecting the threat potential. AnnThorac Surg 1995;60:1810–2.

nusual Cause of Hoarseness ofoice: Giant Pulmonary Arteryneurysm

imal Raj, FRCR, Deepa Gopalan,usan Stewart, FRCP, andohn Dunning, FRCS(CTh), FRACS

epartments of Radiology, Pathology, and Cardiac Surgery,apworth Hospital NHS Trust, Cambridge, United Kingdom

e present an unusual case of hoarseness of the voiceecondary to giant pulmonary artery aneurysm withpecial emphasis on imaging findings and also to illus-rate preoperative and postoperative features on multi-etector computed tomography.

(Ann Thorac Surg 2011;91:285–7)© 2011 by The Society of Thoracic Surgeons

oarseness of the voice caused by damage of therecurrent laryngeal nerve as a result of cardiovas-

ular causes is known as Ortner’s or cardio-vocal syn-rome. It is a rare clinical entity with only a few pub-

ished case reports.

58-year-old woman was referred to our institution withoarseness of the voice and progressive dyspnea for 1ear. There was no history of weight loss or hemoptysis.he patient was an ex-smoker with past medical historyf hypertension, chronic obstructive airways disease, andtroke. Seventeen years prior, the patient had undergoneepair of a membranous ventricular septal defect, pulmo-ary valvotomy, and removal of fibrous obstructive bandcross the right ventricular outflow tract. She had subse-

ccepted for publication June 7, 2010.

ddress correspondence to Dr Raj, Papworth Hospital NHS Trust,

apworth Everard, Cambridge, CB23 3RE United Kingdom; e-mail:eepagopalan@btopenworld.com. (

2011 by The Society of Thoracic Surgeonsublished by Elsevier Inc

uently been well and was discharged from cardiacurgical follow-up.

Clinical examination was unremarkable except for theoarse voice. Basic laboratory tests were normal; these

ncluded full blood count and electrolytes. An electrocar-iogram showed sinus rhythm with a right-bundleranch block. A chest roentgenogram showed mild car-iomegaly with enlarged proximal pulmonary arteriesnd obscuration of the left hilum (Fig 1).The electrocardiographic-gated, contrast enhancedulti-detector-row computed tomography of the chest

evealed (Figs 2A, 2B) aneurysmal dilatation of the mainulmonary artery (PA) measuring 7 cm. Proximal mainight and left PA were also dilated at 4.1 cm and 3.2 cm,espectively. The right ventricle (RV) was mildly dilatednd hypertrophied with bowing of interventricular sep-um toward the left ventricle throughout the cardiacycle. Coronary arteries were normal. Cine images re-ealed mild RV global hypokinesis.On transthoracic echocardiography, the pulmonary

alve was not well seen but it was found to be moderatelytenosed with a peak gradient of 33 mm Hg, with mod-rate pulmonary regurgitation. The RV was mildly di-ated with mild impairment of the systolic function. Theeft ventricle was normal in size with mild systolicmpairment.

In view of the patient’s progressive symptoms and RVysfunction, she underwent cardiac surgery, whichhowed mono-valvular pulmonary valve with aneurys-al dilatation of the PA trunk and proximal right and left

A. The pulmonary valve was replaced with a 25-mmagna Ease valve. The PA trunk was excised with the left

A to pericardial reflection and the right PA to the originf the right upper lobe PA. A 28-mm Hemoshield graftMAQUET Cardiovascular LLC, Wayne, NJ) was used foreconstruction of the trunk, right PA, and left PA, with

ig 1. Frontal chest roentgenogram with a large opacity in the aor-opulmonary window, in keeping with dilated pulmonary artery

star).

0003-4975/$36.00doi:10.1016/j.athoracsur.2010.06.046

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nd-to-end suturing of the aorta over the right PA (FigsA, 3B).Macroscopic appearance of the resected specimens

evealed an unruptured PA aneurysm, with the mainrunk measuring 6 cm and the right PA measuring 4 cm.

icroscopic histopathologic examination showed no ev-dence of tumour, hemorrhage, dissection, or thrombus.here was no intimal atheroma or signs of inflammation.he PA wall measured 15 mm in thickness, with someisruption of elastic lamellae and patchy collagen re-lacement (Fig 4).At the time of writing this article, which was 5 months

ostoperatively, the patient had made an uneventfulecovery with resolution of dyspnea and improvement ofhe hoarse voice.

omment

nilateral vocal cord palsy causing hoarseness of theoice may result from involvement of recurrent laryngealerve (RLN) anywhere along its course from the brain-tem to its distal margins. The left RLN is more oftennvolved than right due to its longer course and extensionnto mediastinum. Compression of left RLN in its medi-stinal course secondary to cardiovascular disease isermed as Ortner’s or cardiovocal syndrome [1, 2].

ig 2. (A) Transaxial and (B) and sagittaleformats of electrocardiographic-gated multi-etector-row computed tomographic scan dem-nstrates a giant pulmonary artery aneurysmnvolving the main pulmonary artery (MPA),eft pulmonary artery (LPA), and the rightulmonary artery (RPA) branches. Ascendingorta (AA) is normal in caliber. (RV � rightentricle.)

ig 3. Volume-rendered reconstructions of (A)reoperative multi-detector-row computed to-ographic scan elegantly shows the main

ulmonary artery (MPA) aneurysm. (B) Post-perative image with the prosthetic pulmo-ary valve (arrow) and pulmonary artery re-onstruction with graft. (AA � ascendingorta; LPA � left pulmonary artery; RPA �ight pulmonary artery.)

There have been few published reports on this syn-rome secondary to enlarged left atrium, aortic aneu-ysm and persistent ductus arteriosus [1–3]. When firstescribed by Ortner, it was though to be secondary toompression of the left RLN by an enlarged left atrium [4,]. This however has since been disputed and this is nowhought to be secondary to compression of the left RLNetween the aorta and the PA [1]. There is relative lack ofublished reports highlighting isolated PA aneurysm as aause of cardiovocal syndrome.

Common causes of PA aneurysm include pulmonaryypertension, congenital heart disease, infection, neo-lasms, connective tissue disease, and vasculitis [6]. On

ts own PA aneurysm is asymptomatic and presentations usually secondary to complications such as thrombusormation, secondary emboli, dissection/ rupture or ex-rinsic compression of adjacent structures [6]. As theseases are uncommon, the natural history is ill defined,nd management remains controversial. The critical sizef a pulmonary aneurysm associated with high risk ofupture remains uncertain. Therefore, timing of surgicalntervention should be determined by other factors suchs change in right ventricular size and function due toulmonary regurgitation or pulmonary stenosis and not

he size of the aneurysm.Due to its wider use and availability multi-detector-

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ow computed tomography has emerged as the first linemaging modality in this scenario. Due to its high spatialesolution and three-dimensional reconstruction capabil-ties it is vital in diagnosis and surgical planning. Multi-etector-row computed tomography of the chest is alsoelpful in excluding other mediastinal causes of RLNalsy, such as neoplasm’s and aortic aneurysm. Onceetected, follow-up imaging can be performed by cardio-ascular magnetic resonance imaging as it will allowccurate assessment of right heart function and the statusf pulmonary valves.The reversibility of hoarseness after treatment of the

rimary cause in Ortner’s syndrome is limited [1, 4]. Asn this case, previous reports have suggested that it iseversible but dependent on the degree and durationf RLN injury. This again reinforces the importancef appropriate and timely management of theseatients.In conclusion, hoarseness of the voice secondary to

solated giant pulmonary artery aneurysm is a rare clin-cal entity. Due to its rarity, it can be easily missed if ones not aware of this entity. Imaging plays a vital role inimely diagnosis, management, surgical planning, andollow-up. Prompt treatment is vital for complete recov-ry of voice.

eferences

. Chen RF, Lin CT, Lu CH. Ortner’s syndromec—a rare causeof unilateral vocal cord paralysis: a case report. KaohsiungJ Med Sci 2009;25:203–6.

. Fennessy BG, Sheahan P, McShane D. Cardiovascularhoarseness: an unusual presentation to otolaryngologists. JLaryngol Otol 2008;122:327–8.

. Kokotsakis J, Misthos P, Athanassiou T, Skouteli E, Ronto-gianni D, Lioulias A. Acute Ortner’s syndrome arising fromductus arteriosus aneurysm. Tex Heart Inst J 2008;35:216–7.

. Chan P, Lee CP, Ko JT, Hung JS. Cardiovocal (Ortner’s)

ig 4. Section of main pulmonary trunk showing disruption of thelastic lamellae and some replacement by collagen. (Hematoxylinnd eosin, medium power; original magnification �200.)

syndrome left recurrent laryngeal nerve palsy associated withcardiovascular disease. Eur J Med 1992;1:492–5.

Ms

2011 by The Society of Thoracic Surgeonsublished by Elsevier Inc

. Mulpuru SK, Vasavada BC, Punukollu GK, Patel AG. Cardio-vocal syndrome: a systematic review. Heart Lung Circ 2008;17:1–4.

. Ling PK. Pulmonary artery aneurysm associated with se-vere degenerative aortic stenosis. Singapore Med J 2009;50:e350 –2.

ositron Emission Tomography/omputed Tomography for theiagnosis of Endocarditis inatients With Pulmonic Stentedalve/Pulmonic Stent

dit Yedidya, MD, Gideon Y. Stein, MD,ordehay Vaturi, MD, Leonard Blieden, MD,aana Bernstine, MD, Silvio D. Pitlik, MD, andhmuel Fuchs, MD

epartment of Internal Medicine “B,” Cardiology Department,epartment of Nuclear Medicine, and Department of Internaledicine “C,” Beilinson Hospital, Rabin Medical Center,

etah-Tikva; and The Sackler School of Medicine, Tel Avivniversity, Tel Aviv, Israel

ercutaneous pulmonic valve and pulmonic stent implan-ation have become a well-established treatment for recur-ent pulmonic stenosis or insufficiency in patients withepaired congenital heart disease. Late endocarditis is sel-om reported, but its diagnosis might be challenging due to

he limited visualization of the stented valve or stent byransesophageal echocardiography. We present 2 youngatients who were hospitalized for suspected endocarditisnd in whom the diagnosis was made with the aid of positronmission tomography/computed tomography scan.

(Ann Thorac Surg 2011;91:287–9)© 2011 by The Society of Thoracic Surgeons

he clinical experience with percutaneous pulmonaryvalve implantation in patients with right ventricle-to-

ulmonary artery conduit dysfunction after operative re-air of congenital heart disease has increased rapidly in last

ew years [1–4]. Stents in pulmonary arteries have beensed for a longer period of time and have become acceptedractice.Endocarditis complicating percutaneous pulmonary

alve implantation was reported to affect 3.2% of theatients within the first 5 months after the procedure [4].n early definitive diagnosis of this complication, how-ver, may be difficult due to lack of typical vascular andmmunologic phenomena [5, 6]. In addition, the presencef stented valve metal struts may cause echogenic arti-acts and nonvisualized spaces, reducing the accuracy ofransesophageal echocardiography (TEE) to clearly iden-ify valvular vegetation.

Recently, positron emission tomography (PET) with flu-

ccepted for publication June 7, 2010.

ddress correspondence to Dr Fuchs, Medicine B Department, Rabin

edical Center, 39 Jabotinski St, Petah-Tikva 49100, Israel; e-mail:

hmuelf@clalit.org.il.

0003-4975/$36.00doi:10.1016/j.athoracsur.2010.06.056