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(Circulation. 1997;96:889-896.)
© 1997 American Heart Association, Inc.

Articles

Inhibition of Red Cell Aggregation Prevents Spontaneous Echocardiographic Contrast Formation in Human Blood

Diane Fatkin, MBBS, BSc(Med), FRACP; Thanasis Loupas, PhD; Joyce Low, PhD; ; Michael Feneley, MD, FRACP, FACC

From the Cardiology Department and Victor Chang Cardiac Research Institute (D.F., M.F.), the Hematology Department (J.L.), St Vincent's Hospital, and Ultrasonics Laboratory, CSIRO (T.L.), Sydney, Australia.

Correspondence to Michael Feneley, MD, FRACP, FACC, Cardiology Department, St Vincent's Hospital, Victoria St, Darlinghurst 2010, Australia.

Background Spontaneous echocardiographic contrast (SEC) is a pattern of blood echogenicity that has been attributed to ultrasonic backscatter from blood cell aggregates that form under low shear conditions. Patients with left atrial SEC have an increased thromboembolic risk. This study examined the role of red cell and platelet aggregates in the pathogenesis of SEC in human blood and the effects on SEC of antithrombotic therapy and red cell disaggregatory agents.

Methods and Results Blood echogenicity was examined with the use of quantitative videodensitometry over a controlled range of flow velocities in an in vitro model characterized by nonlaminar flow conditions. One hundred ninety study samples were prepared from single fresh blood donations (40 to 120 mL) from 24 healthy volunteers and 11 patients. Whole blood echogenicity was unaltered by depletion of platelets, stimulation of platelet aggregation with adenosine diphosphate, or inhibition of platelet aggregation with aspirin. Low flow–related echogenicity increased with increasing hematocrit (P<.001) but was abolished when red cells were lysed selectively with saponin (P<.001). In the presence of red cells, low flow–related echogenicity increased with increasing fibrinogen concentration (P<.001) and with plasma paraproteins. Low flow–related echogenicity in whole blood was unaltered by heparin and warfarin but was reduced in a dose-dependent manner by dextran 40 (40 mg/mL, 70% reduction, P<.001) and poloxamer 188 (8 mg/mL, 47% reduction, P<.001), which inhibited red cell aggregation.

Conclusions These results support protein-mediated red cell aggregation as the mechanism of SEC in human blood. Inhibition of red cell aggregation, indexed by resolution of SEC, may provide an alternative to anticoagulant and antiplatelet therapy to reduce cardiac thromboembolic risk.

Key Words: blood cells • platelets • platelet aggregation inhibitors • echocardiography

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