Asian Cardiovasc Thorac Ann 1998;6:127-128
© 1998 Asia Publishing EXchange Pte Ltd
Refractory Left Ventricular Failure Due to Large Left Ventricular Thrombus
Filiz Özerkan, MD,
Meral Kayikçio
lu, MD,
Azem Akilli, MD
Department of Cardiology Ege University Medical School  zmir, Turkey
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For reprint information contact: Filiz Özerkan, MD 1468 Sokak 16/A Alsancak, zmir, Turkey Tel: 90 232 422 1348 Fax: 90 232 374 6618 or 422 4537
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ABSTRACT
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Mural thrombi are common in patients with acute myocardial infarction and can cause refractory left ventricular failure as a rare complication. We report a case of large postinfarction ventricular thrombus resulting in left ventricular failure resistant to medical therapy. After echocardiographic diagnosis, thrombectomy and coronary bypass grafting were performed and the symptoms subsided.
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INTRODUCTION
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Mural thrombi are common in patients succumbing to acute myocardial infarction. The most convenient and accurate method for diagnosing left ventricular thrombus is two-dimensional echocardiography. Clinical studies suggest that the incidence of left ventricular thrombi identified echocardiographically is 20% to 40%, with the vast majority occurring in anterior myocardial infarction.1 Although a mural thrombus adheres to the endocardium overlying the infarcted myocardium, superficial portions can become detached and produce systemic arterial emboli.2 Refractory left ventricular failure is a rare complication of mural thrombi.3 We recently encountered a case of anterior myocardial infarction in which a large mural thrombus was demonstrated echocardiographically and surgically removed.
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CASE REPORT
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A 65-year-old woman who had an extensive anterior myocardial infarction 3 months before admission, was referred to our clinic for left ventricular failure unresponsive to medical therapy. In the acute phase of infarction she was not given any thrombolytic therapy. She had hypertension, smoking habit, hyperlipidemia, and a family history of coronary artery disease as risk factors. She suffered from dyspnea, orthopnea, and cough since the infarction. She did not have any clinical finding of thromboembolism. In spite of intensive medical therapy she was in New York Heart Association functional class IV and in severe respiratory distress on admission.
Physical examination showed a regular tachycardia of 112 beats per minute with a systemic blood pressure of 100/70 mm Hg. Inspiratory crepitations were heard over the lower third of both lung bases. The cardiac rhythm was regular and S3 was present. Abdominal examination revealed a slightly palpable hepatomegaly. There was slight jugular venous distention and pretibial pitting edema. All blood and urine biochemical findings were within the normal limits.
The patient's resting electrocardiogram showed sinus tachycardia with right axis deviation. There were Q waves and ST-segment elevations in leads I1, AVL, and V2 to V6 (Figure 1
). Chest radiograph revealed moderate cardiac enlargement with pulmonary congestion. The anterior wall, septum, and apex were found to be akinetic by echocardiography. The left ventricular ejection fraction was 25%. A large intraventricular thrombus measuring 3.8 x 6.5 cm (20 cm2 in area) was seen at the apex (Figure 2). Subsequent coronary angiography showed total occlusion of the proximal left anterior descending coronary artery (Figure 3). The patient was transferred to the cardiovascular surgery department for thrombectomy and coronary artery bypass grafting. Two weeks after the operation, she was in New York Heart Association functional class II. She was symptom-free at the 6-month follow-up.
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Figure 1. Electrocardiogram at rest. Note the QS formation and ST-segment elevations in I1, AVL, and V1 to V6.
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Figure 2. Transthoracic echocardiogram in the apical four-chamber view showing a large thrombus in the apex of the left ventricle. A = apex, LA = left atrium, LV = left ventricle, RA = right atrium, RV = right ventricle.
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Figure 3. Coronary angiogram showing proximal total occlusion of the left anterior descending artery in the right anterior oblique projection.
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DISCUSSION
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Left ventricular mural thrombi are a common complication of acute myocardial infarction. They are usually located in the left ventricle, particularly at the apex but they may overlie infarcted septum, inferior wall, or posterior wall.2 Although systemic arterial emboli from mural thrombi are found frequently, refractory left ventricular failure due to thrombus is seen rarely in patients with acute myocardial infarction.3,4 Echocardiography is the most valuable noninvasive method for demonstrating wall-motion abnormalities of the infarcted area, ventricular function, and mural thrombi after acute myocardial infarction.5 Heparin or thrombolytic therapy can reduce the incidence and extent of mural thrombi.2 Anticoagulation for 3 to 6 months with warfarin is advocated for patients with demonstrable mural thrombi.6 Our patient did not receive thrombolytic therapy.
Cheng3 reported a similar case where a large left ventricular thrombus was revealed by two-dimensional echocardiography following an anteroseptal transmural infarction complicated by recurrent tachycardia and severe left ventricular failure. The patient died in spite of oral anticoagulant treatment and medical therapy for left ventricular heart failure. The clinical picture in our patient was similar. She had a delayed diagnosis of mural thrombus and her left ventricular cavity size was decreased, leading to a low ejection fraction and left heart failure. She was promptly given intravenous heparin followed by thrombectomy and coronary artery bypass grafting. Early surgery in our patient led to a favorable outcome.
In patients with large myocardial infarctions who develop refractory heart failure, echocardiographic examination should be performed as soon as possible to diagnose the underlying etiology. Early surgery should be considered in patients who have recurrent systemic emboli and refractory left ventricular failure due to thrombus. Early identification and appropriate therapy for left ventricular thrombus may have life-saving implications.
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REFERENCES
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Spirito P, Bellotti P, Chiarella F, et al. Prognostic significance and natural history of left ventricular thrombi in patients with acute anterior myocardial infarction: a two-dimensional echocardiographic study. Circulation
1985;72:774.[Abstract/Free Full Text]
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Pasternak RC, Braunwald E, Sobel BE. Acute myocardial infarction. In: Braunwald E, editor. Heart disease. 4th ed. Philadelphia: Saunders, 1992:1261–2.
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Cheng TC. Refractory left ventricular failure: use of two-dimensional echocardiography in identification of thrombi. Postgrad Med
1982;72:135–8.
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Arvan S. Left ventricular mural thrombi secondary to acute myocardial infarction: predisposing factors and embolic phenomenon. J Clin Ultrasound
1983;11:467–73.[Medline]
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Jugdutt BI, Sivaram CA. Prospective two-dimensional echocardiographic evaluation of left ventricular thrombus and embolism after acute myocardial infarction. J Am Coll Cardiol
1989;13:54.[Medline]
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Mooe T, Teien DE, Karp KH, Eriksson P. Dynamics of left ventricular thrombi in acute anterior myocardial infarction treated with thrombolytics. Coronary Artery Dis
1995; 6:703–7.[Medline]
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ABSTRACT
INTRODUCTION
