The distinctive structure and composition of arterial and venous thrombi and pulmonary emboli

被引:0
作者
Irina N. Chernysh
Chandrasekaran Nagaswami
Sofia Kosolapova
Alina D. Peshkova
Adam Cuker
Douglas B. Cines
Carolyn L. Cambor
Rustem I. Litvinov
John W. Weisel
机构
[1] University of Pennsylvania School of Medicine,
[2] Kazan Federal University,undefined
来源
Scientific Reports | / 10卷
关键词
D O I
暂无
中图分类号
学科分类号
摘要
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.
引用
收藏
相关论文
共 139 条
[1]  
Hirsh J(1996)Management of deep vein thrombosis and pulmonary embolism. A statement for healthcare professionals. Council on Thrombosis (In consultation with the Council on Cardiovascular Radiology), American Heart Association Circulation 93 2212-2245
[2]  
Hoak J(2018)Risk Stratification Model: Lower-Extremity Ultrasonography for Hospitalized Patients with Suspected Deep Vein Thrombosis J. Gen. Intern. Med. 33 21-25
[3]  
Alper EC(2017)Heart Disease and Stroke Statistics—2017 Update, American Heart Association Circulation 135 146-603
[4]  
Benjamin EJ(1985)Plaque fissuring–the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina Br. Heart J. 53 363-373
[5]  
Davies MJ(2012)Procoagulant activity in hemostasis and thrombosis: Virchow’s triad revisited Anesth. Analg. 114 275-285
[6]  
Thomas AC(2017)Thrombus composition in sudden cardiac death from acute myocardial infarction Resuscitation 113 108-114
[7]  
Wolberg AS(2011)Composition of coronary thrombus in acute myocardial infarction J. Am. Coll. Cardiol. 57 1359-1367
[8]  
Aleman MM(2006)Altered fibrin architecture is associated with hypofibrinolysis and premature coronary artery atherothrombosis Arterioscler. Thromb. Vasc. Biol. 26 2567-2573
[9]  
Leiderman K(2011)Fibrin clot structure and function: a role in the pathophysiology of arterial and venous thromboembolic diseases Arterioscler. Thromb. Vasc. Biol. 31 e88-99
[10]  
Machlus KR(2014)Time-dependent hardening of blood clots quantitatively measured Thromb. Res. 133 265-271