Imaging Assessment of Intracardiac Foreign Bodies Joanna Kusmirek, M.D., Cristopher Meyer, M.D., Jeffrey Kanne, M.D., Mark Schiebler, M.D., Christopher François, M.D.

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IFB are rare, but pose potentially life-threatening complications. If detected early, they can be treated successfully using endovascular or open surgical techniques. Specific localization is necessary to avoid unnecessary and inappropriate therapeutic approach. Diagnosis of ICF may be easily suspected immediately after injury when there are clinical manifestations related to the heart, including cardiac tamponade or bleeding. This can be very challenging in the absence of trauma. The presenting symptoms are nonspecific and include pericarditis and pericardial effusion, pericardial tamponade, arrhythmia, thrombi, elevated troponin, fever/infection, shock and death. Therefore, extreme caution is required in certain sub-groups of the adult population, in which IFB may be found with increased frequency, including patients with history of vascular or thoracic interventions, patients with implanted cardiac or vascular devices, drug users. This diagnosis may also be made incidentally in asymptomatic patients, who potentially may become symptomatic in the future. Plain radiography provides the mainstay of imaging investigation. CT is helpful demonstrating the presence of radiolucent foreign bodies and determining the exact localization, especially prior to any planned intervention.

Sternal wire in RVOT

Migrated sternal wire BB in LV

SVC filter strout in PA

Retained mediastinal

drain IVC filter in RV

Retained sponges

AICD perforated heart

IV Mercury injection (suicide attempt)

PICC guidewire fragment in heart

A lead perforated RA

Retained Surgical Devices or Other Material Embolization to the Heart Form Distal Sites

…or Injury Related to Displaced Adjacent Extracardiac Devices

…Sometimes Resulting in Heart Injury Diagnosis of IFB can be challenging in the absence of suspected heart injury due to nonspecific symptomatology.

Cardiac imagers should be aware of typical imaging appearance and carefully search for foreign objects in the heart, especially in high risk adult populations, due to possible risk of life-threatening complications.

REFERENCES 1. Kavanagh PV, Mason AC, Müller NL, .Thoracic foreign bodies in adults. Clin Radiol. 1999 Jun;54(6):353-60. 2. Xang, X., Zhao, X., Du, D. and Xiang, X. (2012), Management of Metallic Foreign Bodies in the Heart. Journal of Cardiac Surgery, 27: 704–706. 3. Actis Dato GM, Arslanian A, Di Marzio P, Filosso PL, Ruffini E. Posttraumatic and iatrogenic foreign bodies in the heart: Report of fourteen cases and review of the

literature. J Thorac Cardiov Sur 2003;126:408–14. 4. Kim TJ, Goo JM, Moon MH, Im JG, Kim MY. Foreign bodies in the chest: how come they are seen in adults?, Korean J Radiol. 2001 Apr-Jun;2(2):87-96. 5. Levisman J, Shemin RJ, Robertson JM, Pelikan P, Karlsberg RP. Migrated Sternal Wire into the Right Ventricle: Case Report in Cardiothoracic Surgery J Card Surg

2010;25:161-162.

6. Jassar AS, Nicotera SP, Levin N, Vernick WJ, Szeto WY.Inferior vena cava filter migration to the right ventricle.J Card Surg. 2011 Mar;26(2):170-2. 7. Kumar SP, Mahtabifard A, Young JN. Fractured inferior vena cava filter strut presenting as a penetrating foreign body in the right ventricle: report of a case.J Card Surg.

2008 Jul-Aug;23(4):378-81. 8. Janjua M, Omran FM, Kastoon T, Alshami M, Abbas AE. Inferior vena cava filter migration: updated review and case presentation. J Invasive Cardiol. 2009 Nov;21(11):606-

10. 9. Izutani H, Lalude O, Gill IS, Biblo LA. Migration of an inferior vena cava filter to the right ventricle and literature review. Can J Cardiol. 2004 Feb;20(2):233-5.

Right IJ venous catheter crosses at the level of the caval atrial junction into the left atrium consistent with ASD. The catheter traverses the left ventricle and ascending aorta, innominate artery and extending to the origin of the right subclavian artery. The right atrium, right ventricle,

and main pulmonary artery are enlarged consistent with shunt vascularity. ASD sinus venosus was confirmed on CMR. Dysfunctional pacer Displaced pacer Misplaced pulmonary catheters

Misplaced or Fractured Intracardiac Devices…

Explant valve with a fractured fragment.

Joanna Kusmirek, M.D., Cristopher Meyer, M.D., Jeffrey Kanne, M.D., Mark Schiebler, M.D., Christopher François, M.D.

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Imaging Manifestations of Eosinophilic Heart Disease Although the etiology of EHD is not always apparent, important causes include hypersensitivity to a drug or substance, parasitic infections, or vasculitidis (such as Churg-Strauss syndrome). EHD occurs also in more than 50% of patients with idiopathic hypereosinophilic syndrome, which represents a spectrum of diseases, including Davies’ endomyocardial fibrosis and Loffler’s myocarditis. The spectrum of clinical presentation is wide including acute carditis (endocarditis, myocarditis, pericarditis), new onset heart failure with ventricular dilation or restrictive changes, electric disturbances (sinus tachycardia, conduction delays and ST-T wave abnormalities), acute coronary syndrome, and cardiogenic shock. Peripheral blood eosinophilia is not necessarily seen in all cases of EHD, and thus, the diagnosis is often not suspected clinically. The natural history of EHD is usually rapidly progressive untreatable congestive heart failure and death, which may be sudden. Clinical improvement is possible with early corticosteroid treatment; therefore early diagnosis is extremely important. Endomyocardial biopsy is a valuable tool to confirm the diagnosis if positive, but it is not a very sensitive technique because the infiltrates in EHD are often focal (estimated sensitivity 50%). CMR is a valuable diagnostic tool in suspected EHD as it can visualize pattern of inflammatory changes in the myocardium. Imaging may also be helpful in treatment monitoring.

Eosinophilic heart disease is a rare, potentially fatal disease, which is rarely recognized clinically and often first discovered at postmortem examination.

The gold diagnostic standard is endomyocardial biopsy, however it is invasive, time consuming and low sensitivity method.

Cardiac MR emerges as a valuable diagnostic tool establishing the diagnosis. It may be also useful in evaluation of prognosis and treatment response.

Churg-Strauss is a rare syndrome that includes asthma, eosinophilia, pulmonary infiltrates, upper airway inflammation and variable frequency of renal, neurological, cutaneous, and cardiac involvement • Eosinophilic, granulomatous infiltrates and vasculitis • Antineutrophil cytoplasmic antibodies present in 30-60% (pANCA >

cANCA) • Autoantibodies frequently present (anti-Jo-1, anti-synthetase, anti-

Mi-2, anti-SRP) Cardiac disease present in 15-60% and is most common cause of death Typical imaging findings Myocardium: Decreased left ventricular systolic function, segmental

hypokinesis in areas affected, edema present during acute inflammation, Myocardial delayed enhancement in majority of patients (up to 90%) subendocardial, mid myocardial or subepicardial

Pericardium: Pericardial effusion may be present

Churg-Strauss Syndrome Case Presentation 46 year old female with a history of asthma and multiple allergies, presented with palpitations, dyspnea, and orthopnea. Labs: leukocytosis with absolute eosinophil count of

560 (N:0-500). ECG: sinus rhythm, non-specific intraventricular

conduction delay, probable anterior infarct CXR: Cardiomegaly TEE: biventricular thrombus. Cath was normal. CMR showed findings most consistent with

eosinophilic endocarditis

Hypereosinophilic Syndrome

Hypereosinophilic Syndrome is defined as persistent (> 6 months) peripheral blood eosinophilia (≥ 1500 eosinophils/mm3) and lack of evidence for a known causes of eosinophilia (such as parasitic infection, allergy, or hematologic malignancy), with multiorgan infiltration with eosinophils: heart, lungs, liver, GI tract, kidneys, nervous system and possible damage.

Cardiac Disease • Combined right and left ventricular

involvement in ≈ 50% • Fibrous obliteration of ventricular

apices • Atrioventricular valve regurgitation • Pericardial effusion may be present

REFERENCES: 1. Pillar N, Halkin A, Aviram G. Hypereosinophilic syndrome with cardiac involvement: early diagnosis by cardiac magnetic resonance imaging. Can J Cardiol. 2012 Jul-

Aug;28(4):515. 2. Al Ali AM, Straatman LP, Allard MF Ignaszewski AP. Eosinophilic myocarditis: Case series and review of literature. Can J Cardiol 2006;22(14):1233-1237. 3. Miszalski-Jamka T, Szczeklik W, Sokolowska B, Karwat K, Jazwiec P, Musial J. Cardiac involvement in hypereosinophilic syndrome. Pol Arch Med Wewn 2013, 123(5),

253-254. 4. Allanore Y, Vignaux O, Arnaud L, Puéchal X, Pavy S, Duboc D, Legmann P, Kahan A. Effects of corticosteroids and immunosuppressors on idiopathic inflammatory

myopathy related myocarditis evaluated by magnetic resonance imaging. Ann Rheum Dis. 2006 Feb;65(2):249-52. 5. Kim EY, Chang SA, Lee YK, Choi JO, Choe YH. Early non-invasive diagnosis and treatment of acute eosinophilic myopericarditis by cardiac magnetic resonance. J

Korean Med Sci. 2011 Nov;26(11):1522-6. 6. Post MC, Boomsma MF, van Heesewijk JP, Grutters JC, Van der Heyden J. Cardiac magnetic resonance imaging showing complete resolution of subendocardial

involvement in Churg-Strauss syndrome. J Thorac Imaging. 2011 Aug;26(3):W81-2. 7. Kleinfeldt T, Nienaber CA, Kische S, Akin I, Turan RG, Körber T, Schneider H, Ince H. Cardiac manifestation of the hypereosinophilic syndrome: new insights. Clin Res

Cardiol. 2010 Jul;99(7):419-27. 8. Alter P, Maisch B. Endomyocardial fibrosis in Churg-Strauss syndrome assessed by cardiac magnetic resonance imaging. Int J Cardiol. 2006 Mar 22;108(1):112-3. 9. Puvaneswary M, Joshua F, Ratnarajah S. Idiopathic hypereosinophilic syndrome: magnetic resonance findings in endomyocardial fibrosis. Austral Radiol 2001; 45:524

–527.

10. Syed IS, Martinez MW, Feng DL, Glockner JF. Cardiac magnetic resonance imaging of eosinophilic endomyocardial disease. Int J Cardiol. 2008 Jun 6;126(3):e50-2. 11. Cheung SC, Chan CW Insights of prognostication of Davies disease: what could we learn from serial magnetic resonance imaging studies? Int J Cardiol. 2010 Jul

9;142(2):e32-4. 12. Salanitri GC. Endomyocardial fibrosis and intracardiac thrombus occurring in idiopathic hypereosinophilic syndrome. AJR Am J Roentgenol. 2005 May;184(5):1432-3. 13. Salemi VM, Rochitte CE, Shiozaki AA, Andrade JM, Parga JR, de Ávila LF, Benvenuti LA, Cestari IN, Picard MH, Kim RJ, Mady C. Late gadolinium enhancement magnetic

resonance imaging in the diagnosis and prognosis of endomyocardial fibrosis patients. Circ Cardiovasc Imaging. 2011 May;4(3):304-11. 14. Rezaizadeh H, Sanchez-Ross M, Kaluski E, Klapholz M, Haider B, Gerula C. Acute eosinophilic myocarditis: diagnosis and treatment. Acute Card Care. 2010. 15. Pillar N, Halkin A, Aviram G. Hypereosinophilic syndrome with cardiac involvement: early diagnosis by cardiac magnetic resonance imaging. Can J Cardiol. 2012 Jul-

Aug;28(4):515. 16. Ommen SR, Seward JB, Tajik AJ. Clinical and echocardiographic features of hypereosinophilic syndromes. Am J Cardiol 2000;86:110-3. 17. Aggarwal A, Bergin P, Jessup P, Kaye D. Hypersensitivity myocarditis presenting as cardiogenic shock. J Heart Lung Transplant 2001;20:1241-4. 18. Hiltya KC, Koonceb JA, Stonec RW, Ramos-Duranb L, Pyled LA, Batalisc NI, Hardie AD, Taylor MH. The Role of Cardiac MRI in the Diagnosis and Management of

Loeffler’s Endocarditis: A Case Report with Clinical and Pathologic Correlation., The Open Cardiovascular Imaging Journal, 2010, 2, 10-13 10. 19. Hajsadeghi S, Chitsazan M, Pouraliakbar HR, Sadeghipour A. From an isolated right ventricular thrombus to the diagnosis of the hypereosinophilic syndrome. Journal

of Cardiology Cases (2011) 3, e133—e136

Case Presentation 29 year old female with a history of asthma diagnosed at age of 21 years, presented with chest pain, dyspnea, nonproductive cough, rash in lower extremities, 9kg weight loss. Labs: elevated troponin of 6.6 (N:0.0-0.3),

leukocytosis with absolute eosinophil count of 5970 (N:0-500).

ECG: Q waves in III and AVF as well as abnormal R waves progression in V1-V4 suggestive of anteroseptal infarction.

TEE: findings as below, Cath was normal. CMR showed findings most consistent with Churg-Strauss syndrome.

TEE: Mildly dilated RV, moderately reduced systolic function. Mildly increased estimated peak RV systolic pressure, severely hypokinetic mid- to apical segments of the LV with reduced EF of 20%.; a moderate pericardial effusion.

CT: Diffuse bilateral patchy ground glass opacities, more severe at the upper lobes than the lower lobes. There are also associated nonspecific

nodular opacities at the bilateral lower lobes.

CT: Cardiomegaly, a small pericardial effusion, low attenuation clot in the left ventricle.

Loeffler Endocarditis (also known as simple pulmonary eosinophilia ) typically presents with transient radiographic infiltrates and elevated eosinophil count in peripheral blood. Usually the cause is not identified but a number of allergens have been linked to the syndrome, including parasites (ascaris, strongyloides, ankylostoma) and drugs (aspirin, penicillin). Typical imaging findings CXR, HRCT: transient non segmental air space opacification unilateral or bilateral, usually predominantly peripheral distribution. The most common cardiac manifestation is endocarditis. Acute eosinophilic infiltration of endocardium and myocardium results in thrombosis, inflammation, and fibrosis of intramural coronary arteries, mural thrombosis and endocardial fibrosis. Subsequently a restrictive type cardiomyopathy can develop.

Case Presentation 58 year old male with a history of asthma and hypertension, presents with substernal chest pain and dyspnea. POS: Fever, fatigue, productive cough Labs: leukocytosis of 15.9 with absolute eosinophil count

of 7980 (N:0-500). ECG: sinus tachycardia, LA and LV enlargement CXR: Cardiomegaly, bilateral pleural effusions, bilateral

patchy airspace opacities, more on the left

Pulmonary: affected in ≈ 40% Pleural effusions Transient hazy

opacities or consolidation Nodules ≤ 1cm with surrounding ground-glass attenuation

TEE: Estimated EF 25%, diffuse hypokinesis with akinetic apex, severe diastolic LV dysfunction. The apical third of LV and RV obliterated by masses that adhere to the endocardium and have appearance typically associated with thrombi. Small pericardial effusion.

CMR: SSFP images demonstrate dilated and hypokinetic left ventricle and moderate pericardial effusion. Perfusion images show diffuse subendcardial hypoperfusion and transmural hypoperfusion in the septum. Delayed postcontrast images show transmural infarct and no reflow in the septum.

SSFP long axis images demonstrate thrombi in the both ventricles, a small pericardial effusion and cardiomegaly. Diffuse subendocardial enhancement is present on the LGE images.

CT: Cardiomegaly. Small pericardial effusion. Moderate bilateral pleural effusions.

CMR: SSFP images demonstrate a small pericardial effusion and cardiomegaly with reduced EF. LGE images show

patchy late subendocardial enhancement.

Loeffler Endocarditis