Spontaneous echo contrast caused by platelet and leukocyte aggregates?
R J Zotz1, M Müller, S Genth-Zotz
1Leipzig University Heart Center, Leipzig, Germany. rzo@schwalm-eder-kliniken.de
Insights
Spontaneous echocardiographic contrast (SEC) originates from activated platelets and leukocytes in the left atrium, not the right. This finding supports the role of platelet aggregates in SEC pathogenesis and potential thromboembolic events.
Area of Science:
- Cardiology
- Hematology
- Biomedical research
Background:
- Spontaneous echocardiographic contrast (SEC) is a known indicator of thromboembolic events.
- The precise origin and contributing factors to SEC formation remain incompletely understood.
Purpose of the Study:
- To investigate the origin of spontaneous echocardiographic contrast (SEC).
- To analyze blood samples directly from the left atrium to identify cellular components contributing to SEC.
Main Methods:
- Blood samples were collected from the femoral artery/vein and right/left atria of patients with and without SEC.
- Flow cytometry was used to analyze platelet and leukocyte activation and aggregation markers (CD41a, CD42b, CD62p, CD45, CD14).
- Analysis focused on comparing peripheral and cardiac blood samples, and right vs. left atrial samples.
Main Results:
- Peripheral venous blood showed higher platelet and leukocyte activation than arterial blood.
- In patients without SEC, cardiac blood activation mirrored peripheral levels.
- In patients with SEC, significantly higher platelet and leukocyte activation, and leukocyte-platelet aggregates (LTAg) were observed in the left atrium compared to the right atrium.
Conclusions:
- Increased platelet and leukocyte activation in the left atrium is associated with the presence of SEC.
- These findings support the hypothesis that platelet aggregates in the left atrium play a role in the pathogenesis of SEC.
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.
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