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Table of Contents
Year : 2014  |  Volume : 17  |  Issue : 3  |  Page : 237-239
Asymptomatic type B right atrial thrombus in a case with protein S deficiency

1 Medanta Institute of Critical Care and Anesthesiology, Medanta -The Medicity, Gurgaon, Haryana, India
2 Medanta Heart Institute, Medanta -The Medicity, Gurgaon, Haryana, India

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Date of Submission19-Oct-2013
Date of Acceptance28-Feb-2014
Date of Web Publication3-Jul-2014


Thirty seven year old asymptomatic male underwent routine medical examination which revealed an abnormal mass in the right atrium. Family history was not suggestive of any cardiac or malignant disease. Detailed investigation detected deficiency of protein S, which is a vitamin K dependent protein and a cofactor for activated protein C mediated cleavage of factor Va and VIIIa. The deficiency of protein S predisposes to venous thrombosis. Further investigation revealed that it was an organized calcified thrombus in right atrium occupying almost whole of the cavity. Various approaches including surgical excision, thrombolysis and anticoagulation has been used to manage such thrombosis. However therapeutic approach is still a question of debate. Atriotomy and excision of mass was done using cardiopulmonary bypass.

Keywords: Cardiopulmonary bypass; Protein S; Thrombus

How to cite this article:
Rawat RS, Mehta Y, Arora D, Trehan N. Asymptomatic type B right atrial thrombus in a case with protein S deficiency. Ann Card Anaesth 2014;17:237-9

How to cite this URL:
Rawat RS, Mehta Y, Arora D, Trehan N. Asymptomatic type B right atrial thrombus in a case with protein S deficiency. Ann Card Anaesth [serial online] 2014 [cited 2020 Sep 28];17:237-9. Available from:

   Introduction Top

Right atrial (RA) thrombus is potentially dangerous and has high mortality [1] and their management is also challenging. [2] Patient with protein S deficiency are prone for thromboembolic phenomenon. [3] There are high chances of formation of calcium in the thrombus. Such thrombus can embolize to lungs. There is a need to find out the most suitable therapy to manage such patients.

   Case report Top

A 37-year-old diabetic asymptomatic man underwent routine pre-employment medical examination. Physical examination and routine laboratory investigations were within the normal limits. Transthoracic Echocardiography (TTE) revealed a large heterogeneous mass in RA. The patient was referred to our hospital, for the management of mass in RA. The patient is a nonsmoker, nonalcoholic, and do not have a history of any prolonged illness, surgery, syncopal attack, or thrombotic problem including deep vein thrombosis (DVT). Family history was negative for any cardiac or malignant disease. There was no deficiency of antithrombin III and protein C. The glucose-6-phosphate dehyrogenase levels were within normal limits. Factor V Leiden mutation was not detected. Homocysteine level, thyroid function, and lipid profile were normal. The reticulocyte count, coombs test (direct and indirect), irregular antibody screening, anticardiolipin antibodies, and lupus anticoagulants were negative. The protein S level was 44% only. Doppler study of carotid arteries and vessels at groin showed normal diameter and there was no atheromatous plaque, DVT, or stenosis. TTE was repeated which confirmed presence of mass in RA. In addition, in view of presence of dense white shadow in the mass, the cardiologist opined that the mass is a calcified one. The mass was extending up to the superior vena cava (SVC) and was protruding through the tricuspid valve in diastole. As a result, patient had mild tricuspid regurgitation; however, the pulmonary artery systolic pressure (22 mmHg) was normal. Tricuspid annular plane systolic excursion was 2.1 cm. Patient had normal left ventricular function with ejection fraction of 55%. Patient had normal chamber dimension, valves anatomy and no other significant abnormalities. Atheroma was not present in ascending and descending aorta. Cardiac magnetic resonance imaging revealed a large well-defined lobulated altered signal intensity mass lesion (5.2 × 5.2 × 2.4 cm) floating within the RA lumen, attached to its posterior wall. Superiorly, it extended into SVC for a distance of 2 cm and downward it projected through the tricuspid valve into the right ventricular lumen. Left atrium, both ventricles, ascending and descending thoracic aorta appeared normal. Coronary angiography showed insignificant blockages of coronary arteries. Ultrasound of the abdomen was normal. A diagnosis of thrombus or neoplastic lesion with calcium deposits in RA was made. We planned for surgical removal of this RA mass.

After overnight fasting, patient was taken for surgery. A 20 G catheter was inserted in left radial artery for arterial pressure monitoring. A 7 F triple lumen catheter was inserted in left femoral vein for central venous pressure monitoring, and for central venous access for infusion of inotropes and electrolyte solutions. Inotropes were connected to the central venous catheter before induction of anesthesia. A standard technique for induction and maintenance of anesthesia was followed. One 16 G catheter (Laeder cath-2, VYGON, France) was inserted in right internal jugular vein (IJV) to a length of 10 cm from the site of insertion under ultrasound guidance keeping in mind not to push this catheter too deep to avoid dislodgment of the mass. The aim was to provide access for SVC cannulation if the surgeon does not find a suitable site for SVC cannulation. In that case, we could guide a 17 F SVC cannula from head-end using Seldinger technique. The trans-esophageal echocardiography (TEE) performed in operation theatre showed similar finding as TTE [Figure 1].

The cardiopulmonary bypass (CPB) was established using an inferior vena cava cannula inserted through right femoral vein and an adequately sized cannula inserted in the SVC. The right IJV access for SVC cannulation was not required; the surgeon was able to insert the cannula from the surgical site. All these procedures were performed under continuous monitoring of the RA mass with TEE. A right atriotomy was performed and mass was excised. The mass was occupying the entire RA and it was adherent to the posterior wall of RA. The CPB and aortic cross clamp times were 91 and 71 min, respectively. The mass was an organized and heavily calcified thrombus [Figure 2]. After surgery, patient was transferred to intensive care unit for monitoring and observation. The trachea was extubated after 10 hr of elective ventilation. On the following day, anticoagulation therapy with intravenous heparin 5000 units was started 6 hourly to prevent any thromboembolic phenomenon. Histopathology revealed an organized and calcified thrombus. Subsequently, the patient was discharged home and anticoagulation therapy with acitram was continued.
Figure 1: The trans-esophageal echocardiography image shows calcified mass in the right atrium

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Figure 2: Well-defined calcified thrombus

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   Discussion Top

The presence of thrombus in RA is rare and an indication of potentially fatal pulmonary embolism. They are classified according to their origin, as type A when they originate in the deep peripheral veins and type B when they originates in situ in the right cardiac chamber and are of local origin. [4] The patients present with syncope, but occasionally have an insidious clinical presentation. [5] The patients are at constant risk of pulmonary embolization leading to hemodynamic instability and has a high mortality rate. [6] Such patients carry a high risk and may require emergency treatment.

We investigated possible prothrombotic risk factors and detected protein S deficiency. No abnormality was detected in other coagulation factors. Protein S, a vitamin K dependent protein, is a cofactor for activated protein C-mediated cleavage of factors Va and VIIIa. The deficiency of plasma protein S, genetic or acquired, predisposes to venous thrombosis. [3] Diagnosis is based on antigenic assay of total or free plasma protein S level. TTE is useful imaging method for diagnosis of RA thrombus. These patients may have venous thrombosis of lower limbs or pulmonary embolus and hence venous Doppler of great vessels, lung scintigraphy, CT scan, pulmonary angiography is performed to look for the sites of thromboembolism.

The therapeutic approach is still the subject of debate [7] and includes thrombolytic therapy, surgical or percutaneous embolectomy and anticoagulation with heparin. [8] Urgent surgical treatment with exploration of right chamber and embolectomy under CPB is the standard treatment. Rose et al. reported lower mortality rate in the patients who received thrombolytic therapy when compared to the patients who underwent surgery or anticoagulation. [9] Theoretically, the thrombolytic therapy has numerous advantages; it accelerates thrombolysis pulmonary reperfusion, reduces pulmonary artery hypertension, and improves right and left ventricle function and reverses cardiogenic shock. Thrombolysis dissolves the clot in three major sites, intracardiac, pulmonary and venous thrombosis. In the present patient, the mass was calcified and was unlikely to dissolve and its chances of embolizing to lung were high, therefore, we chose surgical embolectomy.

   Conclusion Top

The treatment of RA thrombus in an asymptomatic stable patient with protein S deficiency is still not standardized. The choice depends upon physician judgment and few case reports. The most appropriate therapeutic approach for managing RA calcified thrombus seems to be surgical excision of thrombus. The patients with protein S deficiency should undergo regular yearly echocardiography examination to rule out thrombus in heart in order to prevent life-threatening pulmonary embolism.

   References Top

1.Leclercq F, Messner-Pellenc P, Beigbeder JY, Albat B, Thévenet A, Grolleau-Raoux R. Floating thrombus in the right atrium and severe pulmonary embolism. Value of intravenous thrombolysis. Arch Mal Coeur Vaiss 1994;87:805-11.  Back to cited text no. 1
2.Shah CP, Thakur RK, Ip JH, Xie B, Guiraudon GM. Management of mobile right atrial thrombi: A therapeutic dilemma. J Card Surg 1996;11:428-31.  Back to cited text no. 2
3.Goldman L, Schafer AI. Thrombotic disorders. Goldman′s Cecil Medicine. 24 th ed., Ch. 179; 2012. p. 1148-54.  Back to cited text no. 3
4.Janssens U, Klues HG, Hanrath P. Successful thrombolysis of right atrial and ventricle thrombi in a patient with peripartum cardiomyopathy and extensive thromboembolism. Heart 1997;78:515-6.  Back to cited text no. 4
5.Chartier L, Béra J, Delomez M, Asseman P, Beregi JP, Bauchart JJ, et al. Free-floating thrombi in the right heart: Diagnosis, management, and prognostic indexes in 38 consecutive patients. Circulation 1999;99:2779-83.  Back to cited text no. 5
6.Cordeiro Piçarra B, Santos AR, Dionísio P, Vasconcelos J, Banazol N, Lourenço S, et al. Right atrial thrombus: A rare presentation of plasminogen activator inhibitor deficiency. Rev Port Cardiol 2012;31:171-4.  Back to cited text no. 6
7.Fabi M, Gesuete V, Testa G, Balducci A, Maria P, Gargiulo G. Calcified thrombus in right atrium: Rare but treatable complication of long-term indwelling central venous catheter. Cardiol Res 2011;2:189-92.  Back to cited text no. 7
8.Yang JY, Williams S, Brandão LR, Chan AK. Neonatal and childhood right atrial thrombosis: Recognition and a risk-stratified treatment approach. Blood Coagul Fibrinolysis 2010;21:301-7.  Back to cited text no. 8
9.Rose PS, Punjabi NM, Pearse DB. Treatment of right heart thromboemboli. Chest 2002;121:806-14.  Back to cited text no. 9

Correspondence Address:
Yatin Mehta
Medanta Institute of Critical Care and Anesthesiology, Medanta - The Medicity, Sector 38, Gurgaon, Haryana - 122 001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.135877

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  [Figure 1], [Figure 2]