Kanji Iga MD, Hirokazu Kondou MD, Toshihiro Tamura MD, Chisato Izumi MD, Moriaki Inoko MD, Shouji Kitaguchi MD, Toshirou Hirozane MD, Yoshihiro Himura MD, Hiromitsu Gen MD and Takashi Konishi MD

Key words; left ventricular thrombus, echocardiography, clinical background

Department of Cardiology, Tenri Hospital

200 Mishimacho, Tenri City, 632-8852, Japan

Address correspondence to:

Takashi Konishi MD, Department of Cardiology, Tenri Hospital,

200 Mishimacho, Tenri City, 632-8552 Japan

E-mail: igakan@kcn.ne.jp

Fax 81-743-62-1903

We analyzed the clinical backgrounds of 9 patients with fresh left ventricular thrombus detected by two-dimensional echocardiography during the past 5 years in our hospital. Patients with acute myocardial infarction were excluded. Left ventricular systolic function was disturbed diffusely or segmentally in all patients with a mean ejection fraction of 33%. In 7 patients, echocardiography was performed shortly after furosemide therapy for New York Heart Association class IV congestive heart failure; echocardiography was also performed just before treatment in 4 of the 7 patients and there was no left ventricular thrombus detected in any patient. Two patients died of underlying disorders within 2 months after the detection of the thrombus, however, in the other 7 patients left ventricular thrombus disappeared after starting anticoagulant therapy in the next 6 months without thromboembolic episodes. As fresh left ventricular thrombus developed shortly following diuretic therapy in patients with severe congestive heart failure associated with left ventricular systolic dysfunction, concomitant anticoagulant therapy is recommended.

Thromboembolism is one of the major complications of acute myocardial infarction because of new thrombus formation in akinetic left ventricle (1,2). In addition to acute myocardial infarction, predisposing factors for thromboembolism with known left ventricular dysfunction and sinus rhythm are congestive heart failure and decreased left ventricular ejection fraction (3,4). However, there have been no large-scale studies of fresh thrombus in relation to thromboembolism although there have been isolated case reports.

In this paper, we analyzed clinical backgrounds of patients with fresh left ventricular thrombus except for patients with acute myocardial infarction to discuss committing factors to induce left ventricular thrombus formation.

We selected 9 patients who had a fresh thrombus in the left ventricle referred to the echo-lab of Tenri Hospital in the past 5 years. Patients within two weeks of acute myocardial infarction were excluded. Clinical characteristics of the patients are summarized in Table 1.

Left ventricular thrombus was diagnosed as fresh if the thrombus was low-echoic and two cardiologists familiar with echocardiography concurred in the diagnosis; the thrombus was protruding in 8 patients and floating in one patient. Only two patients were receiving anticoagulation therapy at the time of detection; one patient had just begun receiving anticoagulants the previous day, and in the other patient prothrombin time was not sufficient at 10.5 sec.

Left ventricular systolic function was disturbed diffusely or segmentally with apex predominance in all patients. Left ventricular ejection fraction was measured by cineangiography in 7 patients and the other 2 patients by echocardiography using Simpson’s method and was 33% on average. Underlying heart disorders were old myocardial infarction in 4 patients, idiopathic dilated cardiomyopathy in 3 patients, cardiomyopathy due to sarcoidosis and systemic lupus erythematosis in one each. All patients were in sinus rhythm. Echo-equipment were Toshiba 140A with a transducer of 2.5, 3.75 and 5.0 MHz or Aquison sequoia 3.5 MHz. We used the same machine in the same patients.

In 7 patients, echocardiography was done shortly after furosemide therapy for New York Heart Association (NYHA) class IV congestive heart failure (CHF); echocardiography was also done just before the treatment in four of the 7 patients and there was no left ventricular thrombus in any patient. Physicians in charge were medical trainees in all the four patients. Furosemide was administered with dosage ranging from 40mg to 80mg orally in 2 patients and intravenously in the other 5 patients. The mean time interval was 5.4 days (range 1-7 days) and the body weight loss was 3.2 kg (range 2-5 kg) between the two echocardiographic studies. The hematocrit increased after diuretic therapy in all four cases from 41.3% to 44.8% on average. The other causes of referral to the echo-lab were regular follow-up study in a patient with old myocardial infarction, looking for the cause of cardiac thrombus in a patient shortly after cerebral infarction.

In all 4 patients who were not receiving anticoagulant therapy, thrombin-antithrombin III complex (TAT) was above 10ng/ml (range 10.7-36.3 ng/ml).

After detection of the thrombus, we administered a small amount of heparin and/or warfarin without fibrinolytic therapy in all patients. Two patients died of underlying disorders within 2 months after thrombus detection, but in the other 7 patients, the left ventricular thrombus disappeared on follow-up study. No patients developed thromboembolism after starting heparin and/or warfarin therapy.

Case presentation (case 3)

A 70-year-old man was admitted to our hospital because of paroxysmal nocturnal dyspnea lasting for two weeks. Chest x-ray showed severe pulmonary congestion and two-dimensional echocardiography revealed large apical akinesis without thrombus in it. After admission, oral furosemide 40mg was given resulting in 1kg weight loss during the first 24 hours as well as improvement of symptoms. Follow-up echocardiograms obtained 7 days after admission revealed a low-echoic and protruding thrombus in the akinetic left ventricular apex (Fig.1). TAT was 16.8 ng/ml.

The risk of cerebral infarction is high in patients with left ventricular systolic dysfunction such as dilated cardiomyopathy and old myocardial infarction (5,6). This may be due to concomitant atherosclerosis of the cerebral artery or thromboembolism. The source of emboli is atheroma of the aortic arch and/or thrombus in an akinetic left ventricle. As left ventricular systolic function worsens when congestive heart failure develops, blood in the left ventricle may become more stagnant.

Left ventricular segmental dysfunction is associated with organized thrombus, which is firmly attached to the left ventricle wall and is usually of the laminar type (7). Although there is no clear criteria for fresh thrombus, we regarded it as fresh when the thrombus was low-echoic and was not laminar. In addition to the character of the thrombi, thrombus was not seen a few days earlier in four patients who had undergone echocardiography at that time. As the cardiac apex is difficult to visualize entirely, small thrombus might have been present before treatment. However, it is at least evident that the thrombus increased in size after diuretic therapy.

Thrombin-antithrombin III complex (TAT) is a marker of thrombin generation indicating increased coagulation. In our study, TAT of all 4 patients measured without anticoagulation showed more than 10ng/dl. TAT could be an excellent marker for detecting left ventricular thrombus as well as deep vein thrombosis in the absence of anticoagulation (8).

Treatment of fresh left ventricular thrombus is controversial. Surgery is recommended if the patient’s general condition is good enough and the thrombus is markedly protruding or floating type. However, the majority of the patients are too aged and frail to tolerate surgery. As fresh thrombus in the left ventricle may become fragmented and develop emboli by fibrinolytic therapy, we used only anticoagulant therapy (4). Subsequently, as there were no signs and symptoms of further thromboembolism later, we were able to avoid thromboembolism during the lytic process of the thrombus.

Transthoracic echocardiography can detect left ventricular thrombus relatively easily and can be repeated in a short period of time because it is a non-invasive method (9,10). Most of the qualified cardiologists would not obtain repeated echocardiograms shortly after treatment of CHF. Medical trainees would repeat echocardiograms more often than qualified cardiologists do. If more experienced cardiologists had been in charge of these patients, these new thrombi would not have been discovered. Left ventricular thrombus is often detected by two-dimensional echocardiography if serial echocardiograms are taken within 2 weeks of acute myocardial infarction (11). Similarly, if serial echocardiograms had been taken for patients with severe congestive heart failure caused by left ventricular systolic dysfunction, more patients of fresh thrombus would have been discovered.

The first-line treatment for congestive heart failure caused by poor left ventricular systolic function is diuretics. We expect rapid diuresis by either oral or intravenous administration of furosemide that is a common drug. As hematocrit increased after diuretic therapy, hemoconcentration was one of the factors committing to new thrombus formation. Anticoagulant therapy deserves to consider when diuretic therapy is scheduled for patients with congestive heart failure.

1. Asinger RW, Mikekk FL, Elsperger J, Hodges M. Incidence of left-ventricular thrombus after acute transmural myocardial infarction. N Engl J Med 1981;305:297-302
2. Keren A, Mazouz B, Moriel M, Tzivoni D, Stern S. Use of streptokinase for lysis of a mobile left ventricular thrombus--report of a case and review of the literature. Cardiology 1988;75:444-447
3. Keren A, Goldberg S, Gottlieb S, Klein J, Schuger C, Medina A, Tzivoni D, Stern S. Natural history of left ventricular thrombi: their appearance and resolution in the posthospitalization period of acute myocardial infarction. J Am Coll Cardiol. 1990 15;15:790-800
4. Kessler KM, Cotler RP, Bilsker MS, Myerburg RJ. Narrow-based left ventricular thrombus. Am J Cardiol. 1984 ;53:645-6
5. Stratton JR, Resnick AD. Increased embolic risk in patients with left ventricular thrombi. Circulation 1987;75:1004-11
6. Gunthard J, Stocker F, Bolz D, Jaggi E, Ghisla R, Oberhansli I, Wyler F. Dilated cardiomyopathy and thrombo-embolism. Eur J Pediatr. 1997;156:3-6
7. Takamoto T, Kim D, Urie PM, Guthaner DF, Gordon HJ, Keren A, Popp RL. Comparative recognition of left ventricular thrombi by echocardiography and cineangiography. Br Heart J. 1985;53:36-42.
8. Sassa H, Sone T, Tsuboi H, Kondo J, Yabashi T. Diagnostic significance of TAT and D dimer in patients with deep vein thrombosis. J Cir J 1996;60:201-206
9. Kneissl D, Bubenheimer P, Roskamm H. Ventricular thrombi in the chronic infarct stage: echocardiographic findings, clinical aspects, relations to anticoagulation. Z Kardiol. 1985;74:639-47
10. Reeder GS, Tajik AJ, Seward JB. Left ventricular mural thrombus: two-dimensional echocardiographic diagnosis. Mayo Clin Proc. 1981;56:82-6
11. 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.

Figure legends

Table 1

Background data in this series

Fig. 1

Two-dimensional echocardiogram on admission (left panel) showed large akinetic area without thrombus. However, large thrombus at the cardiac apex developed 7 days after diuretic therapy (right panel, arrows).