LA thrombus formation in mitral valve disease.

To the Editor,

Nonvalvular atrial fibrillation (AF) and mitral valve disease with AF are important causes of left atrial thrombus (1). Abnormal left atrial volume, changed left atrial anatomy, abnormal atrial contraction, abnormal blood flow into the atrium, impaired endothelial function in left atrium, and low mitral valve area are major predisposing factors consisting of thrombus in left atrium and also arrhythmia (2). These factors cause thrombogenic and arrhythmogenic tendencies in the atrium.

We have read with great interest the article by Belen entitled “Relationship between the presence of left atrial thrombus in patients with mitral stenosis and platelet-to-lymphocyte ratio” published in Anatol J Cardiol 2016; 16: 673-7 (3). The authors concluded that the presence of AF is an important risk factor for thrombus development in patients with mitral stenosis. A higher incidence of AF was determined in the left atrial thrombus group in their study [LA thrombus (+) group: 38 (41.3%), n=92 and LA thrombus (−) group: 31 (12%), n=259]. Presence of AF was found to be independently associated with the presence of LA thrombus. We agree with these statements. However, we observed that the patient population between the groups was not equal. Therefore, we cannot associate platelet-to-lymphocyte ratio with the presence of left atrial thrombus in these non-homogenous groups. If we want to investigate the platelet-to-lymphocyte ratio and thrombus, we have to equalize thrombogenic variables, such as AF, mitral valve area, mean gradient, and left atrial volume, between the two groups for obtaining more significant comments.

They concluded that there was a relationship between the presence of left atrial thrombus and platelet-to-lymphocyte ratio, which was independent of other important factors, including AF, in multivariate analysis. However, Table 2 shows that there is no significant difference between AF and platelet-to-lymphocyte ratio in univariate and multivariate analyses (AF-multivariate, p=0.014; platelet-to-lymphocyte ratio: univariate, p=0.02 and multivariate, p=0.016). We think that abnormal surface formation as in left atrial enlargement, inflammatory activation and stasis as in rheumatic valve disease and atrial fibrillation, and inflammatory capacity are not independent of each other (1, 2). Biological markers, such as platelet-to-lymphocyte ratio and red cell distribution width, are affected by inflammatory reactions and abnormal blood flow dynamics in the vessels. It is difficult to determine these markers as independent markers, and we believe that all these anatomic and biochemical variables affect each other. These variables are indicators of diseases with low specificity.