Table 1

Thrombus composition and aetiology

Ref.
(year)
No of patients% of patients w.r.t aetiologyStaining techniqueMain findings
Marder et al 7
2006
25LAA:16
CE:64
ODE:12
UDE:8
H&ESimilar histological components in CE and LAA
Ogata et al 20
2008
142LAA:12
CE:75
SVO:1
ODE:9
UDE:3
H&E, Masson’s trichrome, Mallory’s phosphotungstic acid haematoxylinMost LAA thrombi are fibrin and platelet rich at plaque site and become fibrin and RBC rich while occluding brain arteries
CE strokes have RBC rich thrombi
Niesten et al 19
2014
22LAA:36
CE:27
ODE:14
UDE:23
H&E, Mallory’s phosphotungstic acid- haematoxylin (fibrin)
IHC: glycophorin A (RBCs) and CD31 (platelets)
LAA thrombi are RBC rich
No differences in platelets and fibrin content between stroke subtypes
Boeckh-Behrens et al 9
2014
34LAA:9
CE:47
ODE:18
UDE:26
H&E, Elastica van Gieson stainingHigher percentage of WBCs in the thrombus indicates organised thrombi of CE origin
Kim et al 35
2015
37LAA:22
CE:59
UDE:19
H&E,
IHC: CD61(platelet glycoprotein IIIa)
CE thrombi are RBC rich and have lower fibrin content compared with LAA thrombi
Simons et al 23
2015
40CE: 53H&E
IHC:CD34
Comparatively higher RBC content in CE thrombi
No significant association between CE stroke and thrombus composition
Ahn et al 15
2016
36LAA: 22
CE: 61
UDE: 17
H&E, MSB
IHC: CD42b (platelet glycoprotein Ib)
LAA thrombi were RBC rich and CE thrombi were fibrin rich with platelets clustered within the rich fibrin
UDE thrombi (5/6) had histologic features and composition like CE thrombi
Boeckh-Behrens et al 8
2016
137LAA:16
CE:49
ODE:8
UDE:27
H&ECE thrombi had higher proportions of fibrin/platelets, less erythrocytes, and more leucocytes than noncardioembolic thrombi
UDE strokes had thrombus histology and interventional and clinical outcome parameters similar to CE strokes
Dargazanli et al 36
2016
54LAA:19
CE:46
ODE:24
UDE:11
H&E,
IHC: CD3 (T cells)
High CD3 +T cells count associated with LAA thrombi
Schuhmann et al 12
2016
37LAA: 37
CE:51
UDE:12
H&E, MSB
IHC: CD4 (T cells), CD68 (monocytes) and vWF
Stroke subtype and clinical outcome had no association with immune cell or platelet % or distribution in thrombi
RBC rich clots had higher T cells and monocytes
Sporns et al 32
2017
187LAA:19
CE:41
ODE:6
UDE:34
H&E, Elastica van Gieson, Prussian blue
IHC: CD3, CD20, and CD68/KiM1P
CE thrombi are fibrin/platelet rich with more WBCs than non CE thrombi (LAA+ODE)
Cryptogenic strokes and CE strokes showed similar thrombus histology
The IHC parameters showed no noticeable differences between stroke subtypes
Maekawa et al 33
2018
43LAA: 12
CE: 70
ODE: 2
UDE: 16
H&ERBC rich thrombi are associated with non CE aetiology
Berndt et al 57
2018
133LAA: 12
CE: 53
ODE: 2
UDE: 33
H&E
(NCCT and CTA for clot perviousness)
Pervious thrombi are fibrin/platelet rich.
Pervious thrombi were significantly associated with CE compared with non-CE thrombi
Shin et al 31
2018
37LAA:19
CE:59
UDE:22
H&ERBC-rich clots associated with CE stroke aetiology
Fibrin/platelet rich thrombi were more frequent in LAA and undetermined subtypes whereas mixed type was more frequent in CE patients
Fitzgerald et al 34
2019
105LAA:19
CE:50
ODE:11
UDE:20
H&E, MSBPlatelet-rich clots and % of platelet content significantly higher in LAA than CE thrombi
No correlation between stroke aetiology and the other major thrombus components
Staessens et al 5
2020
177 thrombiNAH&E, MSB, Feulgen’s reaction (DNA staining)
IHC and IFC: vWF, platelets (GPIbα), fibrin, leukocytes (CD45), RBCs (autofluorescence)
AIS thrombi composed of two main types of areas: RBC rich areas and platelet rich areas. RBC-rich areas are with densely packed RBCs within a meshwork of thin fibrin strands, and very few nucleated cells or vWF. Dense fibrin structures together with vWF, delineate platelet-rich areas.
Leukocytes and DNA chiefly present at the interface between RBC rich and platelet rich areas
  • *All studies used TOAST classification of stroke except for reference 20.

  • CE, cardioembolism; CTA, CT angiography; IA, intra-arterial; IFC, immunofluorescence staining; IHC, immunohistochemical staining; LAA, large-artery atherosclerosis; MSB, Martius scarlet blue; NCCT, non-contrast CT; ODE, stroke of other determined aetiology; RBC, red blood cell; SVO, small-vessel occlusion; SVS, susceptibility vessel sign; TOAST, Trial of Org 10 172 in Acute Stroke Treatment; UDE, stroke of undetermined aetiology; vWF, von Willebrand factor; WBC, white blood cell.