Abstract
Although arterial and venous thromboembolic disorders are among the most frequent causes of mortality and morbidity, there has been little description of how the composition of thrombi and emboli depends on their vascular origin and age. We quantified the structure and composition of arterial and venous thrombi and pulmonary emboli using high-resolution scanning electron microscopy. Arterial thrombi contained a surprisingly large amount of fibrin, in addition to platelets. The composition of pulmonary emboli mirrored the most distal part of venous thrombi from which they originated, which differed from the structure of the body and head of the same thrombi. All thrombi and emboli contained few biconcave red blood cells but many polyhedrocytes or related forms of compressed red blood cells, demonstrating that these structures are a signature of clot contraction in vivo. Polyhedrocytes and intermediate forms comprised the major constituents of venous thrombi and pulmonary emboli. The structures within all of the thrombi and emboli were very tightly packed, in contrast to clots formed in vitro. There are distinctive, reproducible differences among arterial and venous thrombi and emboli related to their origin, destination and duration, which may have clinical implications for the understanding and treatment of thrombotic disorders.
Highlights
Arterial and venous thromboembolic disorders are among the most frequent causes of mortality and morbidity, there has been little description of how the composition of thrombi and emboli depends on their vascular origin and age
We selected representative images from randomly chosen portions of 6 arterial thrombi, 5 venous thrombi, and 6 pulmonary emboli that contained all the typical structural elements seen in all the specimens, and the overall composition and structural elements contained in these portions were quantified
The following structural elements were included in the analysis: fibrin; individual platelets, platelet aggregates and degranulated platelets; red blood cells (RBCs); white blood cells (WBCs); cellular microvesicles; and space between structures
Summary
Arterial and venous thromboembolic disorders are among the most frequent causes of mortality and morbidity, there has been little description of how the composition of thrombi and emboli depends on their vascular origin and age. The formation of venous thrombi is generally attributed to a combination of hypercoagulability together with injured or activated endothelium and impaired blood flow (Virchow’s triad)[5,6] Whether these perceived differences in pathogenesis affect thrombus structure has received relatively little investigation but may be important for the risk of extension and embolization and approach to therapy. The composition of coronary artery thrombi obtained from patients with ST-elevation myocardial infarction evolve over time such that fibrin content doubles each hour during clinically manifesting ischemia, whereas the relative platelet content halves each hour[7,8] These changes have been associated with formation of a dense, stiff fibrin network that impairs responsiveness to anti-platelet therapy and thrombolysis over time[9,10]. In vitro studies of clot contraction have demonstrated that the kinetics of clot contraction are accelerated and extent of contraction is enhanced by higher platelet levels and inhibited by RBCs and higher fibrinogen concentrations[21]
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