Differences in Pathological Composition Among Large Artery Occlusion Cerebral Thrombi, Valvular Heart Disease Atrial Thrombi and Carotid Endarterectomy Plaques

Abstract

Background and Purpose: Acute ischemic stroke (AIS) with large artery occlusion (LAO) may lead to severe disability or death if not promptly treated. To determine the source of cerebral artery occlusion thrombosis, we studied the pathological components of cerebral artery thrombosis with different etiological classifications to guide clinical formulation of preventive treatment. Materials and Methods: Eighty-eight thrombi from AIS patients with LAO, 12 atrial thrombi from patients with valvular heart disease (VHD), and 11 plaques obtained by carotid endarterectomy (CEA) from patients with carotid artery stenosis were included in this retrospective study. The hematoxylin and eosin–stained specimens were quantitatively analyzed for erythrocytes, white blood cells (WBCs) and fibrin; platelets were shown by immunohistochemistry for CD31. Results: The thrombi of VHD showed the highest percentage of fibrin, followed by those of cardioembolism (CE) and stroke of undetermined etiology (SUE), and these values were higher than those of the other groups. Plaques obtained by CEA showed the highest erythrocyte number, followed by the large artery atherosclerosis (LAA) thrombi, and showed significantly noticeable differences between other stroke subtypes. The proportions of fibrin and erythrocytes in the thrombi of CE and SUE were most similar to those in the thrombi of VHD, and the LAA thrombi were the closest to those obtained by CEA. CE thrombi and CEA plaques had a higher percentage of WBCs than thrombi of other stroke thrombus subtypes and VHD. Conclusions: CE and most cryptogenic thrombi may originate from the heart, and the formation of carotid atherosclerotic plaques may be related to atherosclerotic cerebral embolism. Inflammation may be involved in their formation.

Overexpansion of Proteobacteria in the Thrombus of Stroke Patients Treated with Mechanical Thrombectomy and the Risk for Death

“…A total of 58 para n-embedded thrombus samples (50% from the CE group) were collected in the study due to an insu cient amount of tissue. As described previously [35] , the main components of thrombi in stroke patients are red blood cells, white blood cells, brin, and aggregated platelets. The red blood cells, brin, and aggregated platelets were visualized in a purplish red color in FISH slices (Figure 4B), and the blue color represented nucleated cells such as neutrophils and macrophages.…”

“…Two hypotheses may explain the difference in DNA concentration of clot bacteria from different etiological sources. Previous studies have observed that cardiogenic thrombi contain a high level of brin and a large number of white blood cells [35] , and bacteria may be enriched by phagocytosis of white blood cells or by being wrapped in aggregated platelets and brin. The second reason may be that the cardiogenic clot is generally larger due to the anatomical location and hemodynamic reasons, whereas atherosclerotic stroke is possibly the consequence of artery-to-artery embolism arising from the rupture of a proximal in situ atherothrombosis.…”

Histologic differences between in situ and embolized carotid web thrombi: a case report

“…Although the architecture of histology of stroke from other etiologies has been studied, the results are inconsistent. Previous studies have suggested that cardioembolic thrombi have higher proportions of fibrin/platelets, fewer RBCs, and more white blood cells than non-cardioembolic thrombi [ 12 – 14 ]. This was consistent with the in situ thrombus composition in the present case.…”

Clot Composition Analysis as a Diagnostic Tool to Gain Insight into Ischemic Stroke Etiology: A Systematic Review

“…39,57,64,82,96,122-124 Contrastingly, three studies (119 thrombi, median 37) showed higher RBC proportions in CE thrombi. 72,84,125 Seven studies (1,061 thrombi, median 58) showed higher FBR proportions in CE, 39,57,76,82,96,123,124 while in two studies (82 thrombi, median 41) the FBR proportion was higher in LAA. 72,125 CE thrombi also showed a higher FP (FBR+PLTs) proportion in one study (137 thrombi).…”

“…115 Some studies aimed to compare the features of CRY thrombi with those of known TOAST etiology. Most of them found similar proportions of RBCs, 39,57,64,96,122-124,127 FBR, PLTs (or both together), 57,76,96,[122][123][124]127 and WBCs between CRY and CE thrombi. 96,122,127 CRY and CE thrombi also shared smaller ECA and number of retrieved fragments, 39,40 clustering PDP, 51 higher neutrophil counts, 76 and NETosis, 66 temporal profile of eluted thrombin activity, 121 and low expression of IL-1β.…”