In a 62-year-old man with permanent atrial fibrillation and recurrent stroke, a large right atrial thrombus attached to a permanent pacemaker lead was incidentally identified by transesophageal echocardiography. Surgical treatment, recommended because of the large dimensions of the mass, was refused by the patient, and thrombus was successfully dissolved by anticoagulant treatment. Pathogenesis of pacemaker lead thrombosis, clinical implications, diagnostic and therapeutic options are discussed

Damir Fabijanić

Ivica Vuković

Lovel Giunio

Marija Vujičić

Nebojša Knežević

Ratko Ermacora

Hrčak - Portal of scientific journals of Croatia

Coll. Antropol. 29 (2005) 1: 159–161UDC 616.125-005.6:616-073Case ReportRight Atrial Pacemaker Lead ThrombosisIncidentally Detected by TransesophagealEchocardiographyDamir Fabijani}, Lovel Giunio, Marija Vuji~i}, Ivica Vukovi}, Ratko Ermacora and Neboj{a Kne`evi}Department of Medicine, Division of Cardiology, University Hospital »Split«, Split, CroatiaA B S T R A C TIn a 62-year-old man with permanent atrial fibrillation and recurrent stroke, a large right atrial thrombus at-tached to a permanent pacemaker lead was incidentally identified by transesophageal echocardiography. Surgicaltreatment, recommended because of the large dimensions of the mass, was refused by the patient, and thrombus wassuccessfully dissolved by anticoagulant treatment. Pathogenesis of pacemaker lead thrombosis, clinical implications,diagnostic and therapeutic options are discussed.Key words: pacemaker, stroke; thrombosis; transesophageal echocardiographyIntroductionPacemaker lead induced venous thrombosis is awell-known phenomenon that occurs in approximately30–45% of patients after implantation of a permanenttransvenous pacemaker1. However, development of right-heart thrombosis in the presence of permanent pace-maker leads has been rarely described. We report a caseof a large right atrial thrombus attached to a pacemakerlead incidentally diagnosed by transesophageal echo-cardiography (TEE).Patient and MethodsA 62-year old man had an echocardiographic exami-nation done four weeks after the recurrence of an ische-mic stroke. He had been treated because of arterial hy-pertension, ischemic cardiomyopathy, and permanentatrial fibrillation. A single-chamber pacemaker (Med-tronic SPECTRAX S) with steroid eluting unipolartransvenous lead with silicone insulation was implan-ted, because of symptomatic bradyarrhythmia, thirteenyears ago. CT of the brain confirmed several smallerischemic cerebral insults in the left parietal, right occip-ital and temporal region. The patient was receiving as-pirin 100 mg daily, as well as antihypertensive therapy.Clinical and laboratory parameters (including coagula-tion parameters) were within normal limits. The elec-trocardiogram confirmed atrial fibrillation and normalfunction of the pacemaker in the VVI mode. Transtho-racic echocardiogram (Vivid 3, General Electric, Mil-waukee, WI, USA) with a 2.5 to 3.5 MHz ultrasoundtransducer demonstrated increased left atrial diameter(LA = 46 mm) as well as a reduced left ventricular sys-tolic function (LVEF = 45%). A mobile mass was seen inthe right atrium, but its echocardiographic evaluationwas difficult because of the patient’s obesity. TEE usinga 5-MHz multiplane imaging transducer, which wasperformed owing to poor transthoracic echocardiogra-phic images and inability to exclude an intracardiac em-bolic source showed a large thrombus (25  21 mm) at-tached to the atrial segment of the pacemaker lead(Figure 1). The thrombotic mass did not propagatethrough tricuspide orifice, and there were no sign ofacute or chronic right ventricular inflow or outflow ob-struction. A spontaneous echocontrast in the left atriumand left atrial appendage, as well as reduced emptyingflow velocity of left atrial appendage (0.22 m/s) was de-tected. The superior vena cava was free of thrombus. Noother intracardiac masses were found. TEE examina-tion with bubble contrast study (0.9% saline) and Val-salva maneuvre did not show intracardiac shunt on theatrial and/or ventricular level. Other intracardiac mas-ses, atrial or ventricular septal defect were not found.Three-dimensional ultrasonography with Doppler study159Received for publication August 24, 2004U:\coll-antropolo\coll-antro-1-2005\fabijanic.vp17. lipanj 2005 08:24:18Plate: 1 of 3Color profile: DisabledBlack  150 lpi at 45 degreesof the carotid arteries that is a reliable diagnostic me-thod in evaluating atherosclerotic lesions of carotid ar-teries 2, as well as a TEE imaging of the thoracic aortadid not show plaques that could be potential sources ofembolization. Lung scintigraphy by technetium 99 didnot reveal any perfusion defects.Because of the thrombus size and mobility surgicalremoval of thrombus was recommended to our patient,but was refused. Thrombolytic therapy was not admin-istered because of the recent stroke, and the patient wastreated with low-molecular weight heparin followed byper os anticoagulant therapy with target INR within therange of 2.5 to 3.5. Echocardiographic follow-up con-firmed gradual dissolution of the thrombus after 6weeks. After complete resolution of thrombus chronicanticoagulant therapy was continued according to Euro-pean Society of Cardiology (ESC) guidelines for perma-nent atrial fibrillation with recommended INR between2.0 and 3.0.DiscussionSerious thrombotic and embolic complications are re-ported to occur in 0.6–3.5 % of patients with permanenttransvenous pacing leads1. Right atrial pacemaker leadthrombosis has been less frequently described, present-ing either as an incidental echocardiographic finding3 orby symptoms of right-sided heart failure4, obstruction orembolization of pulmonary artery5.Several mechanisms have been postulated in thepathogenesis of pacemaker lead induced thrombosis6.The long-term residence of permanent pacemaker leadsmay act as a continous nidus for the formation of throm-bus. In cases of dual-chamber pacing multiple pace-maker wires increase the total surface area of foreignmaterial at risk for thrombus formation. Pacemakerleads may produce a foreign-body-type reaction withsubsequent inflammation and fibrosis along the courseof the wire, and this may lead to thrombus propagationalong the pacing lead. Furthermore, congestive heartfailure, hypercoagulable states such as antithrombinIII, protein C and S deficiencies, thrombocytosis, malig-nancies, and possibly pacemaker lead material itself,may predispose to thrombosis7–9. It has been shown thatpacemaker leads with different types of insulation havevarious thrombogenicity. Namely, thrombogenicity ofpolyurethane leads may be lower than that of siliconeleads9.Intracardiac, generally right atrial lead thrombosisis more dangerous and difficult to manage. The hemo-dynamic significance of the intracardiac clot depends onits size, ranging from one to several centimeters in di-ameter, and location10. Atrial arrhythmias can occur ifthe sinoatrial area is involved. Similar to atrial myxo-mas, intracardiac thrombus may cause functional tri-cuspid stenosis or insufficiency, and should be conside-red when refractory right ventricular failure is present4.Systemic embolization can be related with perma-nent pacing in several ways. Paradoxical embolus canresult in the presence of an established or transientintracardiac right-to-left shunt (i.e. latent foramenovale)11. Transvenous pacemaker leads may be placedunintentionally into the left ventricle via a patent fora-men ovale or through atrial septal defect, resulting inthromboembolic complications, primarily embolic stro-ke12,13. Finally, patients in a VVI pacing mode have ahigher incidence of paroxysmal and permanent atrial fi-brillation, which independently predisposes to embolicevents. Patients with VVI pacing mode have a signifi-cantly higher incidence of reduced left atrial appendagefunction than patients with atrioventricular sequential(VDD, DDD) pacing14–16.D. Fabijani} et al.: Pacemaker Lead Thrombosis, Coll. Antropol. 29 (2005) 1: 159–161160Fig. 1. Transesophageal echocardiographic image: large thrombus (thick arrow) attached to the atrial portion of thepacemaker lead (thin arrow). LA = left atrium; RA = right atrium; LV = left ventricle; RV = right ventricle.U:\coll-antropolo\coll-antro-1-2005\fabijanic.vp17. lipanj 2005 08:24:20Plate: 2 of 3Color profile: DisabledBlack  150 lpi at 45 degreesDespite accepted clinical guidelines for the strokeprevention in patients with atrial fibrillation, our pa-tient was treated only with aspirin 100 mg daily. Carls-son et al.17 have reported that only 28% of the patientswith permanent pacemaker and atrial fibrillation wereanticoagulated; only 10.8% of those who were not anti-coagulated had contraindications to the therapy. Theyconcluded that the majority of pacemaker patients withatrial fibrillation, for whom anticoagulation is indi-cated, failed to receive it. Those caring for these patientsare urged to ensure its much widely use.In spite of the considerable size of the thrombus ourpatient was asymptomatic, and thrombosis of the pace-maker lead was detected incidentally. The position ofthe pacemaker lead in the right ventricle was confirmedby TEE, and the existence of a right-to-left shunt wasexcluded by contrast echocardiography. Therefore, thepacemaker lead thrombus could not be related with theprevious ischemic strokes in our patient. Probable so-urces of recurrent stroke were thromboemboli due topermanent atrial fibrillation, as suggested by the re-duced emptying flow velocity of the left atrial append-age (0.22 m/s), the spontaneous echocontrast in leftatrium and left atrial appendage defined as a 3+ = mod-erate (dense swirling pattern during the entire cardiaccycle), according the criteria of Fatkin et al.18. Our pa-tient was treated with a low-molecular weight heparinand gradual dissolution of the thrombotic formation wasdocumented by echocardiography. Chronic anticoagu-lant therapy with warfarin was administered because ofthe increased risk of a repeated ischemic stroke.We recommend that all patients with permanentpacemakers who have an increased risk for lead throm-bosis, including those with congestive heart failure,hypercoagulable states, and immobilization, should beconsidered for systemic anticoagulation. However, be-cause a case of the pacemaker lead thrombosis withmassive pulmonary embolism within 12 hours after apermanent transvenous pacemaker implantation hasbeen reported19, anticoagulant therapy should be star-ted early.R E F E R E N C E S1. BARAKAT, K., N. M. ROBINSON, R. A. SPURRELL, Cardiology,93 (2000) 142. — 2. TETICKOVIC, E., M. GAJSEK-MARCHETTI, J.MATELA, V. FLIS, Coll. Antropol., 25 (2001) 511. — 3. SCHIFTER, R.D., M. L. KOZER, I. B. SAUL, C. V. R. REDDY, Angiology, 50 (1999) 855.— 4. WIERZBOWSKA, K., M. KRZEMINSKA-PAKULA, M. MARS-ZAL-MARCINIAK, J. DROZDZ, J. ZASSLONKA, J. D. KASPRZAK, Pa-cing. Clin. Electrophysiol., 24 (2001) 391. — 5. HUNG, M. J., C. H.WANG, L. T. KUO, W. J. CHERNG, Echocardiography, 17 (2000) 329. —6. DACOSTA, S. S., A. SCALABRINI NETO, R. COSTA, J. G. CALDAS,M. MARTINELLI FILHO, Pacing. Clin. Electrophysiol., 25 (2002) 1301.— 7. GODEC, D., M. BALIJA, Coll. Antropoll., 20 Suppl. (1996) 27. — 8.TISKARUDMAN, L., G. KRAJACIC-KARAS, J. DELAC, R. SABOL, F.J. RUDMAN, Coll. Antropoll., 18 Suppl. (1994) 15. — 9. PALATIANOS,G. M., M. K. DEWANJEE, G. PANOUTSOPOULOS, M. KAPADVANJ-WALA, S. NOVAK, G. N. SFAKIANAKIS, Pacing. Clin. Electrophysiol.,17 (1994) 141. — 10. NICOLOSI, G. L., P. A. CHARMET, D. ZANUT-TINI, Br. Heart. J., 43 (1980) 199. — 11. LOUTOLAHTY, M., M. SARA-STE, J. HARTIALA, Clin. Physiol., 15 (1995) 265. — 12. ALTUN, A., O.AKDEMIR, O. ERDOGAN, O. ASLAN, G. OZBAY, Angiology, 53 (2002)609. — 13. ARBANE, M., J. SCHLAPFER, N. AEBISHER, L. KAPPEN-BERGER, Europace, 1 (1999) 202. — 14. YOSHITOMI, H., K. TANABE,T. ASANUMA, H. SHIMIZU, M. KOBAYASHI, Y. MURAKAMI, K. SA-NO, Y. ISHIBASHI, T. SHIMADA, Echocardiography, 15 (1998) 473. —15. SIMANTIRAKIS, E. N., F. I. PARTENAKIS, S. I. CHRYSOSTOMA-KIS, E. G. ZURIDAKIS, N. E. IGOUMENIDIS, P. E. VARDAS, Heart, 77(1997) 428. — 16. LEE, T. M., S. F. SU, K. L. CHIEN, Y. J. LIN, W. J.CHEN, M. F. CHEN, C. S. LIAU, Y. T. LEE, Heart, 78 (1997) 262. — 17.CARLSSON, J., S. MIKETIC, G. DEES, S. HAUN, A. CUNEO, U. TEB-BE, Europace, 2 (2000) 115. — 18. FATKIN, D., R. P. KELLY, M. P. FE-NELEY, J. Am. Coll. Cardiol., 23 (1994) 961. — 19. KARAVIDAS, A., G.LAZAROS, E. MATSAKAS, N. KOUVOUSIS, C. SAMARA, E. CHRI-STOFORATOU, A. ZACHAROULIS, Echocardiography, 21 (2004) 429.D. Fabijani}Department of Internal Medicine – Kri`ine, University Hospital Split, [oltanska 2, 21000 Split, Croatiae-mail: damir.fabijanic@st.htnet.hrTROMB NA VODI^U ELEKTROSTIMULATORA SRCA U DESNOM ATRIJU – SLU^AJAN NALAZTRANSEZOFAGUSNOM EHOKARDIOGRAFIJOMS A @ E T A KU 62-godi{njeg mu{karca s permanentnom fibrilacijom atrija i ponavljaju}im mo`danim infarktom, transezofa-gusnom ehokardiografijom je u desnom atriju na elektrodi trajnog elektrostimulatora srca prikazan ve}i ugru{ak.Zbog veli~ine ugru{ka preporu~en je operativni zahvat kojeg je bolesnik odbio, pa je ugru{ak otopljen primjenomantikoagulansa. U radu se razmatra patogeneza ugru{ka na elektrodi elektrostimulatora, klini~ke posljedice, di-jagnosti~ke i terapijske mogu}nosti.D. Fabijani} et al.: Pacemaker Lead Thrombosis, Coll. Antropol. 29 (2005) 1: 159–161161U:\coll-antropolo\coll-antro-1-2005\fabijanic.vp17. lipanj 2005 08:24:21Plate: 3 of 3Color profile: DisabledBlack  150 lpi at 45 degrees

Right Atrial Pacemaker Lead Thrombosis Incidentally Detected by Transesophageal Echocardiography

HRČAK - Portal of Croatian Scientific and Professional Journals

Coll. Antropol. 29 (2005) 1: 159–161UDC 616.125-005.6:616-073Case ReportRight Atrial Pacemaker Lead ThrombosisIncidentally Detected by TransesophagealEchocardiographyDamir Fabijani}, Lovel Giunio, Marija Vuji~i}, Ivica Vukovi}, Ratko Ermacora and Neboj{a Kne`evi}Department of Medicine, Division of Cardiology, University Hospital »Split«, Split, CroatiaA B S T R A C TIn a 62-year-old man with permanent atrial fibrillation and recurrent stroke, a large right atrial thrombus at-tached to a permanent pacemaker lead was incidentally identified by transesophageal echocardiography. Surgicaltreatment, recommended because of the large dimensions of the mass, was refused by the patient, and thrombus wassuccessfully dissolved by anticoagulant treatment. Pathogenesis of pacemaker lead thrombosis, clinical implications,diagnostic and therapeutic options are discussed.Key words: pacemaker, stroke; thrombosis; transesophageal echocardiographyIntroductionPacemaker lead induced venous thrombosis is awell-known phenomenon that occurs in approximately30–45% of patients after implantation of a permanenttransvenous pacemaker1. However, development of right-heart thrombosis in the presence of permanent pace-maker leads has been rarely described. We report a caseof a large right atrial thrombus attached to a pacemakerlead incidentally diagnosed by transesophageal echo-cardiography (TEE).Patient and MethodsA 62-year old man had an echocardiographic exami-nation done four weeks after the recurrence of an ische-mic stroke. He had been treated because of arterial hy-pertension, ischemic cardiomyopathy, and permanentatrial fibrillation. A single-chamber pacemaker (Med-tronic SPECTRAX S) with steroid eluting unipolartransvenous lead with silicone insulation was implan-ted, because of symptomatic bradyarrhythmia, thirteenyears ago. CT of the brain confirmed several smallerischemic cerebral insults in the left parietal, right occip-ital and temporal region. The patient was receiving as-pirin 100 mg daily, as well as antihypertensive therapy.Clinical and laboratory parameters (including coagula-tion parameters) were within normal limits. The elec-trocardiogram confirmed atrial fibrillation and normalfunction of the pacemaker in the VVI mode. Transtho-racic echocardiogram (Vivid 3, General Electric, Mil-waukee, WI, USA) with a 2.5 to 3.5 MHz ultrasoundtransducer demonstrated increased left atrial diameter(LA = 46 mm) as well as a reduced left ventricular sys-tolic function (LVEF = 45%). A mobile mass was seen inthe right atrium, but its echocardiographic evaluationwas difficult because of the patient’s obesity. TEE usinga 5-MHz multiplane imaging transducer, which wasperformed owing to poor transthoracic echocardiogra-phic images and inability to exclude an intracardiac em-bolic source showed a large thrombus (25  21 mm) at-tached to the atrial segment of the pacemaker lead(Figure 1). The thrombotic mass did not propagatethrough tricuspide orifice, and there were no sign ofacute or chronic right ventricular inflow or outflow ob-struction. A spontaneous echocontrast in the left atriumand left atrial appendage, as well as reduced emptyingflow velocity of left atrial appendage (0.22 m/s) was de-tected. The superior vena cava was free of thrombus. Noother intracardiac masses were found. TEE examina-tion with bubble contrast study (0.9% saline) and Val-salva maneuvre did not show intracardiac shunt on theatrial and/or ventricular level. Other intracardiac mas-ses, atrial or ventricular septal defect were not found.Three-dimensional ultrasonography with Doppler study159Received for publication August 24, 2004U:\coll-antropolo\coll-antro-1-2005\fabijanic.vp17. lipanj 2005 08:24:18Plate: 1 of 3Color profile: DisabledBlack  150 lpi at 45 degreesof the carotid arteries that is a reliable diagnostic me-thod in evaluating atherosclerotic lesions of carotid ar-teries 2, as well as a TEE imaging of the thoracic aortadid not show plaques that could be potential sources ofembolization. Lung scintigraphy by technetium 99 didnot reveal any perfusion defects.Because of the thrombus size and mobility surgicalremoval of thrombus was recommended to our patient,but was refused. Thrombolytic therapy was not admin-istered because of the recent stroke, and the patient wastreated with low-molecular weight heparin followed byper os anticoagulant therapy with target INR within therange of 2.5 to 3.5. Echocardiographic follow-up con-firmed gradual dissolution of the thrombus after 6weeks. After complete resolution of thrombus chronicanticoagulant therapy was continued according to Euro-pean Society of Cardiology (ESC) guidelines for perma-nent atrial fibrillation with recommended INR between2.0 and 3.0.DiscussionSerious thrombotic and embolic complications are re-ported to occur in 0.6–3.5 % of patients with permanenttransvenous pacing leads1. Right atrial pacemaker leadthrombosis has been less frequently described, present-ing either as an incidental echocardiographic finding3 orby symptoms of right-sided heart failure4, obstruction orembolization of pulmonary artery5.Several mechanisms have been postulated in thepathogenesis of pacemaker lead induced thrombosis6.The long-term residence of permanent pacemaker leadsmay act as a continous nidus for the formation of throm-bus. In cases of dual-chamber pacing multiple pace-maker wires increase the total surface area of foreignmaterial at risk for thrombus formation. Pacemakerleads may produce a foreign-body-type reaction withsubsequent inflammation and fibrosis along the courseof the wire, and this may lead to thrombus propagationalong the pacing lead. Furthermore, congestive heartfailure, hypercoagulable states such as antithrombinIII, protein C and S deficiencies, thrombocytosis, malig-nancies, and possibly pacemaker lead material itself,may predispose to thrombosis7–9. It has been shown thatpacemaker leads with different types of insulation havevarious thrombogenicity. Namely, thrombogenicity ofpolyurethane leads may be lower than that of siliconeleads9.Intracardiac, generally right atrial lead thrombosisis more dangerous and difficult to manage. The hemo-dynamic significance of the intracardiac clot depends onits size, ranging from one to several centimeters in di-ameter, and location10. Atrial arrhythmias can occur ifthe sinoatrial area is involved. Similar to atrial myxo-mas, intracardiac thrombus may cause functional tri-cuspid stenosis or insufficiency, and should be conside-red when refractory right ventricular failure is present4.Systemic embolization can be related with perma-nent pacing in several ways. Paradoxical embolus canresult in the presence of an established or transientintracardiac right-to-left shunt (i.e. latent foramenovale)11. Transvenous pacemaker leads may be placedunintentionally into the left ventricle via a patent fora-men ovale or through atrial septal defect, resulting inthromboembolic complications, primarily embolic stro-ke12,13. Finally, patients in a VVI pacing mode have ahigher incidence of paroxysmal and permanent atrial fi-brillation, which independently predisposes to embolicevents. Patients with VVI pacing mode have a signifi-cantly higher incidence of reduced left atrial appendagefunction than patients with atrioventricular sequential(VDD, DDD) pacing14–16.D. Fabijani} et al.: Pacemaker Lead Thrombosis, Coll. Antropol. 29 (2005) 1: 159–161160Fig. 1. Transesophageal echocardiographic image: large thrombus (thick arrow) attached to the atrial portion of thepacemaker lead (thin arrow). LA = left atrium; RA = right atrium; LV = left ventricle; RV = right ventricle.U:\coll-antropolo\coll-antro-1-2005\fabijanic.vp17. lipanj 2005 08:24:20Plate: 2 of 3Color profile: DisabledBlack  150 lpi at 45 degreesDespite accepted clinical guidelines for the strokeprevention in patients with atrial fibrillation, our pa-tient was treated only with aspirin 100 mg daily. Carls-son et al.17 have reported that only 28% of the patientswith permanent pacemaker and atrial fibrillation wereanticoagulated; only 10.8% of those who were not anti-coagulated had contraindications to the therapy. Theyconcluded that the majority of pacemaker patients withatrial fibrillation, for whom anticoagulation is indi-cated, failed to receive it. Those caring for these patientsare urged to ensure its much widely use.In spite of the considerable size of the thrombus ourpatient was asymptomatic, and thrombosis of the pace-maker lead was detected incidentally. The position ofthe pacemaker lead in the right ventricle was confirmedby TEE, and the existence of a right-to-left shunt wasexcluded by contrast echocardiography. Therefore, thepacemaker lead thrombus could not be related with theprevious ischemic strokes in our patient. Probable so-urces of recurrent stroke were thromboemboli due topermanent atrial fibrillation, as suggested by the re-duced emptying flow velocity of the left atrial append-age (0.22 m/s), the spontaneous echocontrast in leftatrium and left atrial appendage defined as a 3+ = mod-erate (dense swirling pattern during the entire cardiaccycle), according the criteria of Fatkin et al.18. Our pa-tient was treated with a low-molecular weight heparinand gradual dissolution of the thrombotic formation wasdocumented by echocardiography. Chronic anticoagu-lant therapy with warfarin was administered because ofthe increased risk of a repeated ischemic stroke.We recommend that all patients with permanentpacemakers who have an increased risk for lead throm-bosis, including those with congestive heart failure,hypercoagulable states, and immobilization, should beconsidered for systemic anticoagulation. However, be-cause a case of the pacemaker lead thrombosis withmassive pulmonary embolism within 12 hours after apermanent transvenous pacemaker implantation hasbeen reported19, anticoagulant therapy should be star-ted early.R E F E R E N C E S1. BARAKAT, K., N. M. ROBINSON, R. A. SPURRELL, Cardiology,93 (2000) 142. — 2. TETICKOVIC, E., M. GAJSEK-MARCHETTI, J.MATELA, V. FLIS, Coll. Antropol., 25 (2001) 511. — 3. SCHIFTER, R.D., M. L. KOZER, I. B. SAUL, C. V. R. REDDY, Angiology, 50 (1999) 855.— 4. WIERZBOWSKA, K., M. KRZEMINSKA-PAKULA, M. MARS-ZAL-MARCINIAK, J. DROZDZ, J. ZASSLONKA, J. D. KASPRZAK, Pa-cing. Clin. Electrophysiol., 24 (2001) 391. — 5. HUNG, M. J., C. H.WANG, L. T. KUO, W. J. CHERNG, Echocardiography, 17 (2000) 329. —6. DA COSTA, S. S., A. SCALABRINI NETO, R. COSTA, J. G. CALDAS,M. MARTINELLI FILHO, Pacing. Clin. Electrophysiol., 25 (2002) 1301.— 7. GODEC, D., M. BALIJA, Coll. Antropoll., 20 Suppl. (1996) 27. — 8.TISKARUDMAN, L., G. KRAJACIC-KARAS, J. DELAC, R. SABOL, F.J. RUDMAN, Coll. Antropoll., 18 Suppl. (1994) 15. — 9. PALATIANOS,G. M., M. K. DEWANJEE, G. PANOUTSOPOULOS, M. KAPADVANJ-WALA, S. NOVAK, G. N. SFAKIANAKIS, Pacing. Clin. Electrophysiol.,17 (1994) 141. — 10. NICOLOSI, G. L., P. A. CHARMET, D. ZANUT-TINI, Br. Heart. J., 43 (1980) 199. — 11. LOUTOLAHTY, M., M. SARA-STE, J. HARTIALA, Clin. Physiol., 15 (1995) 265. — 12. ALTUN, A., O.AKDEMIR, O. ERDOGAN, O. ASLAN, G. OZBAY, Angiology, 53 (2002)609. — 13. ARBANE, M., J. SCHLAPFER, N. AEBISHER, L. KAPPEN-BERGER, Europace, 1 (1999) 202. — 14. YOSHITOMI, H., K. TANABE,T. ASANUMA, H. SHIMIZU, M. KOBAYASHI, Y. MURAKAMI, K. SA-NO, Y. ISHIBASHI, T. SHIMADA, Echocardiography, 15 (1998) 473. —15. SIMANTIRAKIS, E. N., F. I. PARTENAKIS, S. I. CHRYSOSTOMA-KIS, E. G. ZURIDAKIS, N. E. IGOUMENIDIS, P. E. VARDAS, Heart, 77(1997) 428. — 16. LEE, T. M., S. F. SU, K. L. CHIEN, Y. J. LIN, W. J.CHEN, M. F. CHEN, C. S. LIAU, Y. T. LEE, Heart, 78 (1997) 262. — 17.CARLSSON, J., S. MIKETIC, G. DEES, S. HAUN, A. CUNEO, U. TEB-BE, Europace, 2 (2000) 115. — 18. FATKIN, D., R. P. KELLY, M. P. FE-NELEY, J. Am. Coll. Cardiol., 23 (1994) 961. — 19. KARAVIDAS, A., G.LAZAROS, E. MATSAKAS, N. KOUVOUSIS, C. SAMARA, E. CHRI-STOFORATOU, A. ZACHAROULIS, Echocardiography, 21 (2004) 429.D. Fabijani}Department of Internal Medicine – Kri`ine, University Hospital Split, [oltanska 2, 21000 Split, Croatiae-mail: damir.fabijanic@st.htnet.hrTROMB NA VODI^U ELEKTROSTIMULATORA SRCA U DESNOM ATRIJU – SLU^AJAN NALAZTRANSEZOFAGUSNOM EHOKARDIOGRAFIJOMS A @ E T A KU 62-godi{njeg mu{karca s permanentnom fibrilacijom atrija i ponavljaju}im mo`danim infarktom, transezofa-gusnom ehokardiografijom je u desnom atriju na elektrodi trajnog elektrostimulatora srca prikazan ve}i ugru{ak.Zbog veli~ine ugru{ka preporu~en je operativni zahvat kojeg je bolesnik odbio, pa je ugru{ak otopljen primjenomantikoagulansa. U radu se razmatra patogeneza ugru{ka na elektrodi elektrostimulatora, klini~ke posljedice, di-jagnosti~ke i terapijske mogu}nosti.D. Fabijani} et al.: Pacemaker Lead Thrombosis, Coll. Antropol. 29 (2005) 1: 159–161161U:\coll-antropolo\coll-antro-1-2005\fabijanic.vp17. lipanj 2005 08:24:21Plate: 3 of 3Color profile: DisabledBlack  150 lpi at 45 degrees

Right Atrial Pacemaker Lead Thrombosis Incidentally Detected by Transesophageal Echocardiography

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