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CASE REPORT |
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Year : 2013 | Volume
: 6
| Issue : 4 | Page : 459-461 |
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A case of chronic left ventricular thrombus with ischemic cardiomyopathy
Vikram Bhausaheb Vikhe, Ankur Gupta, Prakash Shende
Department of Medicine, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pimpri, Pune, India
Date of Web Publication | 17-Sep-2013 |
Correspondence Address: Vikram Bhausaheb Vikhe Department of Medicine, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pimpri, Pune India
Source of Support: None, Conflict of Interest: None | Check |
DOI: 10.4103/0975-2870.118289
Left ventricular (LV) thrombus is a serious complication of anterior wall myocardial infarction (MI), especially in patients with severe LV dysfunction. LV thrombus carries a high risk of causing stroke and other thromboembolic complications despite adequate anticoagulation therapy. There is a benefit of anticoagulation in patients with ischemic cardiomyopathy to reduce thromboembolic events or in resolution of LV thrombus. Two-dimensional (2D) echocardiography is the most commonly used technique for the diagnosis and follow-up of such cases. Our patient developed a chronic LV thrombus with ischemic cardiomyopathy post anterior wall MI and was managed well on anticoagulants to prevent the thromboembolic events under strict vigilance and follow-up. Keywords: 2D echocardiography, anticoagulation, LV dysfunction, LV thrombus, myocardial infarction
How to cite this article: Vikhe VB, Gupta A, Shende P. A case of chronic left ventricular thrombus with ischemic cardiomyopathy. Med J DY Patil Univ 2013;6:459-61 |
Introduction | | |
Left ventricular (LV) thrombus occurs in case of impaired LV dysfunction as a result of ischemic cardiomyopathy, aneurysm, or a myocardial infarction (MI). [1],[2] LV thrombus is a well-recognized complication of acute MI. [2],[3] Approximately 40-60% of patients with extensive anterior wall MI (AWMI) develop LV thrombus. [3] Due to the high risk of thromboembolic events, early and accurate detection of LV thrombus is very important. [3] These thromboembolic events can be prevented by long-term use of systemic anticoagulation. [2],[4] Two-dimensional (2D) echocardiography plays a pivotal role in determining the natural course of LV thrombus formation in post-MI patients. [3]
Case Report | | |
We report the case of a 50-year-old male who presented with acute-onset left-sided chest pain, constricting type, non-radiating, associated with profuse sweating, restlessness, and palpitations. His general, physical, and systemic examination was unremarkable. His electrocardiogram (ECG) was suggestive of antero-septal and lateral wall MI. His serum creatine phosphokinase-MB CPK-MB levels were elevated and troponin-T was positive. After this, he was thrombolysed with streptokinase. Rest of the hematological investigations were within normal limits. His past history revealed that he was a tobacco chewer for past 30 years and hypertensive since 2 years and was taking Tab. amlodipine 5 mg OD. 2D echocardiography revealed anterior wall, anterior septum, and lateral wall akinesia. Left ventricular ejection fraction (LVEF) was 20%. There was presence of an LV thrombus measuring 2.3 × 3.5 cm at the apex. His coronary angiography (CAG) showed right coronary artery (RCA) dominance. CAG revealed a plaque causing 40% stenosis in the proximal RCA and diffuse disease followed by total occlusion in the mid RCA, whereas the distal RCA showed retrograde filling from the left anterior descending (LAD) artery. In the left coronary artery, the LAD showed minor plaques, whereas the mid, distal, and diagonals were normal. Patient was discharged on ramipril, aspirin, clopidogrel, atorvastatin, furosemide, spironolactone, and warfarin. He was advised for a regular follow-up and lifestyle modifications. His prothrombin time/international normalized ratio PT/INR and warfarin dose were monitored and adjusted accordingly in the follow-up visits. Patient was stable for 4 months after which he developed unstable angina. This time he was treated with enoxaparin 60 mg BD for 5 days. 2D echocardiography this time revealed ischemic cardiomyopathy with all four chambers dilated. LVEF was 25%. A large thrombus measuring 3.2 × 3.0 cm was seen at the apex. Inferior vena cava was dilated and there was severe pulmonary hypertension with tricuspid regurgitation. The anterior wall and interventricular septum of LV were akinetic and apex was dyskinetic. Patient's symptoms were relieved in the next few days and he was discharged on the same above-mentioned treatment. Oral warfarin was continued and adjusted according to the PT/INR values [Figure 1] and [Figure 2]. | Figure 2: Image showing the big left ventricular clot with measurements and dilated left ventricle
Click here to view |
Discussion | | |
LV thrombus is a serious complication of the anterior wall MI, especially in patients with severe LV dysfunction as it was the case in our patient. [5] The development of most thrombi takes place within the first 2 weeks after acute MI or within few hours after extensive AWMI. [3] LV thrombus in our patient was diagnosed by 2D echocardiography after 2 days of acute MI. LV thrombus carries a high risk of causing stroke and other thromboembolic complications despite adequate anticoagulation therapy. [6] In patients with cardiomyopathy, the incidence of LV thrombus has been reported in the literature as 11-44%. [6] The definitive treatment of LV thrombus is controversial. The main treatment options include thrombectomy, anticoagulation, and thrombolysis. [1],[2] Many studies report a benefit of anticoagulation in patients with ischemic cardiomyopathy to reduce the thromboembolic events or in resolution of LV thrombus. [1],[2] In case of mobile and pedunculated thrombi, surgical removal is generally recommended because they have a significantly higher risk of systemic embolization. [1],[7] 2D echocardiography is the most commonly used technique for diagnosis and follow-up of such cases. It has a sensitivity of 92-95% and a specificity of 86-88% for the diagnosis of LV thrombus. [8]
Conclusion | | |
In our case, the patient was admitted again with unstable angina. He had stenosis in RCA and an episode of acute MI 4 months back; therefore, he is prone for such events in future also. Furthermore, LV thrombus by itself can complicate MI, where akinesia causes blood stasis and the formation of LV thrombus. [9] Our patient had developed a chronic LV thrombus probably due to LV dysfunction and ischemic cardiomyopathy causing blood stasis. [9] The incidence of LV thrombus in patients with cardiomyopathy has been reported in the literature as 11-44%. [1],[6] He was managed well on anticoagulants to prevent the thromboembolic events, but he is still at high risk of developing thromboembolic events in future as embolization to the peripheral vessels, especially cerebral vessels being the most common, is well known. [10]
Consent
Written informed consent was obtained from the patient for publication of this case report and any accompanying images.
References | | |
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[Figure 1], [Figure 2]
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