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(Stroke. 2001;32:1127.)
© 2001 American Heart Association, Inc.

Original Contributions

Spontaneous Echo Contrast Caused by Platelet and Leukocyte Aggregates?

Rainer J. Zotz, MD; Matthias Müller, MD; Sabine Genth-Zotz, MD Harald Darius, MD

From the Leipzig University Heart Center, Leipzig (R.J.Z., M.M.), and the 2nd Medical Clinic, Johannes Gutenberg University, Mainz (S.G.-Z., H.D.), Germany.

Correspondence to Rainer J. Zotz, MD, Department of Internal Medicine, Klinikum Schwalmstadt, Krankenhausstr. 27, D-34613 Schwalmstadt, Germany. E-mail rzo{at}schwalm-eder-kliniken.de

Background and Purpose—Spontaneous echocardiographic contrast (SEC) is correlated to clinical thromboembolic events. We sought to determine the origin of SEC by utilizing direct analysis of left atrial blood.

Methods—We examined the blood of 13 patients with and 19 without SEC. Blood samples were taken from the femoral vein and artery and from the right and left atria after transseptal puncture. Samples were incubated with fluorescence-labeled antibodies directed against the platelet (CD41a-PE, CD42b-PE, and CD62p-FITC) and leukocyte membrane epitopes (CD45-APC and CD14-FITC). The expressed epitopes were analyzed by dual laser flow cytometry immediately after blood withdrawal.

Results—In the peripheral blood of both groups, more activation and aggregation were found in the venous blood than in the arterial blood (CD41a, P=0.007; CD14neutro, P=0.017; and leukocyte-platelet aggregates [LTAg], P=0.002). In patients without SEC, the degree of activation and aggregation of the cardiac samples closely resembled the results of the peripheral samples. The degree of activation and aggregation was significantly higher in the right atrium than in the left atrium (LTAg, P<0.01; leukocyte activation, P<0.01; CD41a, P<0.01; CD62p, P<0.02). In contrast, in patients with SEC the parameters of platelet and leukocyte activation as well as LTAg was significantly higher in the left atrium than in the right atrium of the same patient (all P<0.01). A correlation between the amount of SEC and platelet-monocyte aggregates could be found (r=0.92, P<0.0001).

Conclusions—The hypothesis that platelet aggregates are involved in the pathogenesis of SEC is supported by the fact that platelets in the left atrium of patients with SEC showed more activation.

Key Words: cardioembolic stroke • leukocytes • platelet activation • spontaneous echo contrast • stroke prevention

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