Ann Thorac Surg 2003;76:623-625
© 2003 The Society of Thoracic Surgeons
Case report
Left ventricular thrombus sans overt cardiac pathology
Om P. Yadava, DNB*a,
Sumit Yadav, MCha,
Saurabh Juneja, MCha,
Vijay K. Chopra, DMa,
Rajeev Passey, DMa,
Rajen Ghadiok, MDa
a Department of Cardiac Surgery, New Delhi, IndiaDepartment of Cardiology, Dharma Vira Heart Centre, Sir Ganga Ram Hospital, New Delhi, India
Accepted for publication January 26, 2003.
* Address reprint requests to Dr Yadava, Department of Cardiac Surgery, Dharma Vira Heart Centre, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi 110060, India
e-mail: op_yadava{at}yahoo.com
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Abstract
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A 25-year-old man presenting with peripheral and cerebral emboli was incidentally detected as having a left ventricular mass on two-dimensional echocardiographic examination of the heart. In absence of any obvious structural heart disease or hypercoagulable state, the mass was presumptively diagnosed as left ventricular myxoma. The patient was operated on, and histopathology revealed the mass to be a thrombus. The cause and pathogenesis of the left ventricular thrombus, differential diagnosis, and management are discussed. The rarity of the case is highlighted.
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Introduction
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The presence of left ventricular (LV) thrombus in the absence of detectable heart disease is a rare entity. We report a patient with recurrent systemic emboli who was found to have a large LV thrombus in an apparently normal heart and milieu interior.
The 25-year-old man was admitted with 10 days prior history of pain in both lower limbs and sudden onset aphasia. The patient was normotensive, a nonsmoker, and nondiabetic with no symptoms suggestive of cardiac disease. On examination he was in sinus rhythm. His lower extremities were cold with normal popliteal arterial pulses with weakly palpable posterior tibial and dorsalis pedis pulsations bilaterally. His vital measurements were normal, and the rest of the systemic examination was unremarkable with no neurologic deficit except for lone aphasia.
Routine investigations, base line coagulation profile, and cardiac enzymes were all normal. Chest roentgenogram and electrocardiogram were both unremarkable. Computed tomographic scan of the brain revealed left middle cerebral artery territory embolic infarct. To evaluate the source of emboli, a transthoracic two-dimensional (2-D) echocardiography was performed, which revealed a large (3.8 x 1.2 cm) pedunculated, mobile mass with nonhomogenous translucency and an irregular surface. The mass was attached to the apical septum and projected into the LV cavity. There was no regional wall motion abnormality, chamber enlargement, or any valvular pathology. These findings were confirmed on transesophageal echocardiogram (Fig 1).
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Fig 1. A large pedunculated, apical mass in the left ventricle (marked) as visualized by transesophageal echocardiographic imaging.
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A provisional diagnosis of LV myxoma with peripheral and cerebral emboli was made, and the patient was heparinized. Due to the high potential for recurrent embolism, the patient was urgently rushed to surgery without cardiac catheterization or coronary angiography. Cardiopulmonary bypass was established by aortic and single venous cannulation through the right atrium appendage, and the heart was arrested with antegrade cold blood cardioplegia. A 5-cm long left ventriculotomy was made, 3 cm away and parallel to the distal one third of the left anterior descending artery.We located a 4 x 2 cm, pedunculated, friable mass with an irregular surface in the LV cavity that was attached to the apical septum by a stalk.
There were no LV clots or any further pathology. The LV mass was excised en masse by shearing the stalk from the septum. The ventriculotomy was closed, and the patient was weaned off cardiopulmonary bypass uneventfully. Postoperatively the patient’s speech improved dramatically and all peripheral pulsations returned. Postoperative 2D echocardiography revealed normal LV end diastolic and end systolic dimensions (4.4 cm and 3.6 cm, respectively) with well preserved LV function (left ventricular ejection fraction, 0.65). The patient was discharged on postoperative day 6 and was prescribed oral anticoagulants.
Histopathology of the mass revealed a mural thrombus with no evidence of tumor cells. Retrospectively, investigation of a hypercoagulable state, thrombophilic factors protein C, protein S, and antithrombin III, were estimated and found to be within normal limits. In addition, tests for antinuclear antibody, anticardiolipin antibody, and Venereal Disease Research Laboratory were negative.
At 1-year follow-up, the patient is asymptomatic with no evidence of intracardiac thrombus and a 2-D echocardiogram reveals well-preserved LV function.
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Comment
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An intracavitary echodense mass in the left ventricle is usually either a myxoma or a thrombus. We made a presumptive diagnosis of LV myxoma based on 2-D echocardiographic and intraoperative findings of a pedunculated, mobile mass arising from the interventricular septum in the setting of a structurally normal heart. Nonhomogenous echogenicity seen on the 2-D echocardiogram was presumed to be caused by hemorrhages inside the tumor. However, histology revealed the mass to be a thrombus. In retrospect we realize a lot of findings in our patient fit this diagnosis. Major thrombi also can have irregular translucencies due to malacia. Furthermore, most thrombi are located near the apex as was seen in our patient. Thrombi can be of 3 types: (1) perimural, (2) protruding and (3) mobile; and thrombi may even be pedunculated. However, there is no diagnostic feature, either by 2-D echocardiography or by direct inspection, in which the diagnosis can be confirmed, and either pathology may masquerade the other [1]. Histopathology is the final court of appeal and must always be performed.
Left ventricular thrombus has been reported in settings of myocardial infarction, LV aneurysm, cardiomyopathy, and myocarditis. Rare causes of intracardiac thrombus are protein C deficiency, systemic lupus erythematous, hypereosinophilic syndrome, supraventricular tachycardia, trauma, postcardiac surgery, Behçet’s disease, and antiphospholipid syndrome [2]. Report of LV thrombus in the absence of obvious cardiac disease is a rarity and only anecdotally mentioned in the literature [3, 4]. Though exact pathogenesis is unknown, many hypotheses have been advanced. Patchy fibrosis and myofibrillar hypertrophy resulting from diffuse small coronary vessel disease and pathologic coronary spasm causing transient myocardial ischemia may predispose LV thrombus in these patients [4]. In our case, coronary angiography was not performed in view of multiple systemic emboli, large mass with irregular surface, and therefore high embolic potential and preoperative presumptive diagnosis of LV myxoma rather than a thrombus. Therefore, even though there was no evidence of fibrosis or regional wall motion abnormality on 2-D echocardiography, no comments can be made about the briskness of flow through the coronary arteries (indirect evidence of small vessel disease). An endomyocardial biopsy has been suggested for these cases [4] but was not performed by us. Intraoperative myocardial biopsy also was not taken, because we did not think of it at the time. Thus the cause of LV thrombus in our patient could not be ascertained. Whether myocardial biopsy could have helped is conjectural.
There are no established protocols for management of these cases. Though dissolution with anticoagulant therapy is reported in the literature [5], risk of embolization is ever lurking. The rate of embolic episodes in mobile pedunculated thrombi is reported as high as 60% [6]. Therefore we strongly believe that patients with prior embolism must be offered immediate surgery, especially if the thrombus is large with an irregular surface, pedunculated, and multiple in number. The surgical approach to LV masses can be made through the left atrium, aorta, or left ventricle. We believe that it is important to perform a left ventriculotomy to inspect the cavity thoroughly for any further pathology. In addition, if the mass is myxomatous, then it is important to remove the entire tumor, including the stalk, and hence good exposure is mandatory.
We conclude that a careful echocardiographic examination should be performed in patients presenting with peripheral embolism, even in the absence of any clinical evidence of cardiac disease. Emergent surgical removal through a ventriculotomy is recommended in these patients.
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References
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- Kazmierczak M., Kazmierczak E., Sarnowska Z. Left ventricular thrombus imitating cardiac myxoma, successfully treated with clopidogrel. A case report. Kardiol Pol 2001;55:333-335.
- Matitiau A., Tabachnik E., Sthoeger D., et al. Thrombus in the left ventricle of a child with systemic emboli: an unusual presentation of hereditary protein C deficiency. Pediatrics 2001;107:421-422.[Abstract/Free Full Text]
- Verma A.K., Alam M., Rosman H.S., et al. Systemic embolization from thrombus in normal left ventricle. Chest 1988;2:441-442.
- Vaganos S.A., Fox K.R., Kitchen J.G. Left ventricular thrombus in the absence of detectable heart disease. Chest 1989;96:426-427.[Abstract/Free Full Text]
- Sivasankaran S., Harikrishnan S., Tharakan J.M. Left ventricular thrombi in the presence of normal left ventricular function. Indian Heart J 2002;54:196-198.[Medline]
- Haugland J.M., Asinger R.W., Mikell F.L., et al. Embolic potential of left ventricular thrombi detected by two-dimensional echocardiography. Circulation 1987;70:588-598.
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Abstract
Introduction
