Left Atrial Thrombus - A Review

LEFT ATRIUM THROMBUS

23-12-2014

Introduction

Determinants

Classification

Management

Conclusions

Patients with severe symptomatic MS, 50% or more have chronic AF.

The incidence of thromboembolic complications is higher in patients with rheumatic mitral stenosis and is a major cause of morbidity and mortality.

The left atrium and left atrial appendage are well recognised sites of clot formation in these patients.

Patients with a clot in the left atrium and left atrial appendage had a higher incidence of systemic embolization.

LA thrombi are reported to occur in 26-33% of patients with severe mitral stenosis.

LA thrombi were found in 20% of patients who underwent surgery for mitral stenosis.

The presence of LA thrombi was associated with a threefold increase in embolic events.

Fifty percent of LA thrombi in patients with rheumatic valvular disease, and nearly 90% of LA thrombi in patients with non-valvular AF are limited to the LA appendage

DETERMINANTS Various factors determine the individual risk for the

development of left atrial clot and thromboembolization in patients with rheumaticmitral valve disease which include

Atrial fibrillation Left atrial size Duration of symptoms Older age Severity of mitral stenosis

However the presence of moderate to severe mitral regurgitation has a negative predictive value for the development of clot in the left atrium.

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CLASSIFICATION The thrombus in the left atrium can be

classified as (Manjunath et al.) -

Ia (thrombus confined to LAA) Ib (thrombus in LAA and protruding into LA cavity) IIa (attached to LA roof but above the plane of

fossa ovalis) IIb (reaching below plane of fossa ovalis) III (attached to interatrial septum) IV (mobile with attachment to roof or lateral wall) V (ball valve thrombus)

SPONTANEOUS ECHO CONTRAST The incidence of spontaneous echo contrast in

mitral stenosis varies from 21 to 67%.

Previous reports have shown that in majority or all, left atrial clot and systemic thromboembolization were associated with spontaneous echo contrast in left atrium on transesophageal echocardiography.

Spontaneous echo contrast was also found to be an important predictor of systemic embolization, independent of the presence of clot in LA clot.

Fatkin et al, in a group of 140 patients who underwent transesophageal echocardiography found that the presence of SEC, not the presence of clot in LA correlated significantly with previous history thromboembolism.

Acarturk et al, found that the presence of both (spontaneous echo contrast and left atrial clot) correlated significantly with thromboembolism.

MANAGEMENT Anticoagulation is conventionally used to

reduce the risks of thromboembolic events associated with atrial fibrillation, particularly in the pericardioversion period.

The benefit is balanced by the high cost and risk of anticoagulation.

The mechanism by which warfarin achieves the reported risk reduction is speculative.

Earlier reports supported the hypothesis of "thrombus maturation," by which the thrombus endothelializes and adheres to the atrial wall.

Coumarin anticoagulants such as warfarin act by inhibiting the synthesis of vitamin Kdependent coagulation factors II, VII, IX, and X.

The primary effect of this form of anticoagulation is to prevent further thrombus extension and development.

It has been suggested that this will facilitate the action of the endogenous fibrinolysis (ie, tissue plasminogen activator).

Thrombus resolution has been demonstrated in clinical reports on patients with left ventricular thrombi treated with 12 weeks of warfarin.

CONCLUSIONS It can be stated that more than one third of

the patients with severe rheumatic MS and AF will have LA thrombi.

In a subgroup of the patients with normal sinus rhythm, patients with larger left atrium (≥40 cm2 ) and spontaneous echo contrast have a higher risk of clot formation in the LA/LAA.

Anticoagulation appears to be facilitating LAC and LA thrombus resolution, with an 80% short term success rate.