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Year : 2017  |  Volume : 27  |  Issue : 3  |  Page : 101-103

Left ventricular outflow tract thrombus in a child with dilated cardiomyopathy: An atypical location

1 Department of Paediatrics and Child Health, University of Ilorin; Department of Paediatrics and Child Health, University of Ilorin Teaching Hospital, Ilorin, Kwara State, Nigeria
2 Department of Paediatrics and Child Health, University of Ilorin Teaching Hospital, Ilorin, Kwara State, Nigeria

Date of Web Publication4-Jul-2017

Correspondence Address:
Mohammed Baba Abdulkadir
Department of Paediatrics and Child Health, University of Ilorin, P.M.B. 1515, Ilorin, Kwara State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcecho.jcecho_46_16

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Dilated cardiomyopathy (DCM) may be associated with formation of intracardiac thrombi which may embolize and result in life-threatening complications. We present a 19-month-old female child with DCM who presented with a right hemispheric cerebrovascular accident. Urgent echocardiography revealed poor left ventricular systolic function and a thrombus attached to the interventricular septum along the left ventricular outflow tract. There was resolution of the thrombus following the use of warfarin.

Keywords: Cerebrovascular accident, dilated cardiomyopathy, left ventricle, thrombus

How to cite this article:
Abdulkadir MB, Ibrahim OR, Afolayan FM, Adedoyin OT. Left ventricular outflow tract thrombus in a child with dilated cardiomyopathy: An atypical location. J Cardiovasc Echography 2017;27:101-3

How to cite this URL:
Abdulkadir MB, Ibrahim OR, Afolayan FM, Adedoyin OT. Left ventricular outflow tract thrombus in a child with dilated cardiomyopathy: An atypical location. J Cardiovasc Echography [serial online] 2017 [cited 2021 Dec 2];27:101-3. Available from: https://www.jcecho.org/text.asp?2017/27/3/101/209554

  Introduction Top

Intracardiac thrombi are a complication of dilated cardiomyopathy (DCM).[1] Factors implicated in the formation of thrombi in DCM include low-velocity swirling of blood, abnormal endocardial surfaces, atrial fibrillation, and a hypercoagulable state.[2] Thrombi complicate between 14% and 23% of DCM among children.[1],[3],[4] The most common site for thrombi in DCM is the apex where blood flow is generally slowest.[5] The major risk of the left ventricular thrombi is embolization to critical organs, particularly the brain where they may result in cerebrovascular accidents.[6]

We present a case of the right hemispheric cerebrovascular accident in a 19-month-old Nigerian child with DCM.

  Case Report Top

AH is a 19-month-old female child seen first at 3 months of age on account of recurrent difficulty in breathing, cough, easy fatigability, and poor weight gain. She was small for age with small volume pulses, tachycardia, and hypotension with no cardiac murmurs. An echocardiogram confirmed a diagnosis of DCM, and she was commenced on oral hydrochlorothiazide and spironolactone. She was lost to follow-up 3 months later and presented again at 19 months of age with a 3 days history of sudden weakness of the left arm and leg. She had no similar symptoms in the past. There was no fever, seizures, loss of consciousness, speech difficulty, cough, or difficulty in breathing. On examination, she was conscious, afebrile (axillary temperature −36.0°C), mildly pale, with no cyanosis, jaundice, or pedal edema. Her pulse rate was 116 beats per minute, and blood pressure was 80/40 mmHg with a raised jugular venous pressure. Apex beat was displaced and on auscultation had distant first and second heart sounds. She had nontender hepatomegaly. Pupillary light reflexes were normal. There was left upper motor neuron facial nerve palsy. Power was 1/5 in all muscle groups in the left upper and lower limbs with exaggerated deep tendon reflexes.

She had a sinus tachycardia with increased R amplitude in V5 and V6 on an electrocardiogram. Transthoracic echocardiography revealed a dilated globally hypokinetic left ventricle (LV) with a left ventricular internal diameter in diastole of 5.16 cm and fractional shortening of 10.0%. Other LV parameters are shown in [Table 1]. There was a mild pericardial effusion with maximal depth of 0.8 cm. On parasternal long axis and apical views, an echogenic mass was seen along the interventricular septum 1.8 cm from the aortic valve annulus within the LV [Figure 1]. A modification of the parasternal axis view made the mass more visible [Figure 2]. The mass was immobile and measured 0.86 by 0.49 cm in cross-section with an area of 0.34 cm 2. The mass was suspected to be a thrombus. There was functional mitral regurgitation with a vena contracta width of 0.4 cm, and the mitral valve was not thickened or deformed. Urinalysis was normal, and serial blood cultures revealed no growth. A diagnosis of DCM with right hemispheric cerebrovascular accident and a solitary left ventricular outflow tract (LVOT) thrombus was made. Baseline clotting profile revealed an international normalized ratio (INR) of 0.92. She was commenced on warfarin with close monitoring of INR to achieve a value of between 1.5 and 2.0. Subsequent INR achieved were between 1.11 and 1.96. She gradually recovered neurologic function over a 4-week period and became more ambulant with full power in the upper limbs and power of three in the left lower limb. A repeat echocardiogram done 6 weeks after presentation documented disappearance of the cardiac mass. The left ventricular systolic function still remained poor with a fractional shortening of 16.0%. Other parameters are shown in [Table 1]. She is currently on aspirin, hydrochlorothiazide, spironolactone, and captopril.
Table 1: Selected echocardiographic parameters at presentation and 6 weeks later

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Figure 1: Parasternal long axis view demonstrating dilated left ventricle and thrombus (arrow) at left ventricular outflow tract. AO=Aorta

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Figure 2: Modified parasternal view demonstrating thrombus. LV=Left ventricle

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  Discussion Top

Cerebrovascular accident is not an uncommon complication in individuals with DCM often resulting from embolization of cardiac thrombi.[6] However, it is rare for the thrombus to be located along the LVOT where flow, albeit diminished is not sluggish as compared to the apex or lateral wall.[6] A plausible reason for this abnormal location is the geometry of the LV in this patient [Figure 1] with ballooning of the septum which may have created abnormal forces damaging the endocardium at the site. This mechanism is similar to the formation of nonbacterial thrombotic endocarditis in infective endocarditis following endocardial damage.[7] Another plausible reason for the thrombus is an apical thrombus dislodged and “trapped” at the LVOT. Few authors have described the occurrence of a thrombus in the LVOT.[8],[9] Most of these cases were associated with LVOT obstruction and syncope. This did not occur in this case possibly because of its size and location.

In conclusion, thrombi can arise along the LVOT in children with DCM and may carry a higher risk of embolization.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Günthard J, Stocker F, Bolz D, Jäggi E, Ghisla R, Oberhänsli I, et al. Dilated cardiomyopathy and thrombo-embolism. Eur J Pediatr 1997;156:3-6.  Back to cited text no. 1
Kalaria VG, Passannante MR, Shah T, Modi K, Weisse AB. Effect of mitral regurgitation on left ventricular thrombus formation in dilated cardiomyopathy. Am Heart J 1998;135(2 Pt 1):215-20.  Back to cited text no. 2
Taliercio CP, Seward JB, Driscoll DJ, Fisher LD, Gersh BJ, Tajik AJ. Idiopathic dilated cardiomyopathy in the young: Clinical profile and natural history. J Am Coll Cardiol 1985;6:1126-31.  Back to cited text no. 3
Falk RH, Foster E, Coats MH. Ventricular thrombi and thromboembolism in dilated cardiomyopathy: A prospective follow-up study. Am Heart J 1992;123:136-42.  Back to cited text no. 4
Asinger RW, Mikell FL, Sharma B, Hodges M. Observations on detecting left ventricular thrombus with two dimensional echocardiography: Emphasis on avoidance of false positive diagnoses. Am J Cardiol 1981;47:145-56.  Back to cited text no. 5
Kyrle PA, Korninger C, Gössinger H, Glogar D, Lechner K, Niessner H, et al. Prevention of arterial and pulmonary embolism by oral anticoagulants in patients with dilated cardiomyopathy. Thromb Haemost 1985;54:521-3.  Back to cited text no. 6
Lopez JA, Ross RS, Fishbein MC, Siegel RJ. Nonbacterial thrombotic endocarditis: A review. Am Heart J 1987;113:773-84.  Back to cited text no. 7
Srinivas SK, Subramanyam K, Ramalingam R, Bhat S, Kalpana SR, Manjunath CN. A rare case of left ventricular outflow tract mass. Echocardiography 2013;30:E274-7.  Back to cited text no. 8
Whitson BA, John R, Bradner MW, Liao KK, Missov E, Shumway SJ. Left ventricular outflow tract occluding thrombus after biventricular mechanical circulatory support as a bridge to recovery. ASAIO J 2013;59:324-7.  Back to cited text no. 9


  [Figure 1], [Figure 2]

  [Table 1]


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