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Journal articles on the topic 'Microthrombi'

Author: Grafiati

Published: 21 December 2024

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1

Olson, Timothy M., David J. Driscoll, William D. Edwards, Francisco J. Puga, and Gordon K. Danielson. "Pulmonary microthrombi." Journal of Thoracic and Cardiovascular Surgery 106, no. 4 (October 1993): 739–44. http://dx.doi.org/10.1016/s0022-5223(19)33719-5.

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2

Fitzpatrick, James E., Carl Johnson, M. C. Major, Paul Simon, James Owenby, and Lieutenant Colonel. "Cutaneous Microthrombi." American Journal of Dermatopathology 9, no. 5 (October 1987): 419–22. http://dx.doi.org/10.1097/00000372-198710000-00008.

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3

Mihalko, Emily P., Megan Sandry, Nicholas Mininni, Kimberly Nellenbach, Halston Deal, Michael Daniele, Kamrouz Ghadimi, Jerrold H. Levy, and Ashley C. Brown. "Fibrin-modulating nanogels for treatment of disseminated intravascular coagulation." Blood Advances 5, no. 3 (January 29, 2021): 613–27. http://dx.doi.org/10.1182/bloodadvances.2020003046.

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Abstract Disseminated intravascular coagulation (DIC) is a pathological coagulopathy associated with infection that increases mortality. In DIC, excessive thrombin generation causes symptoms from formation of microthrombi to multiorgan failure; bleeding risks can also be a concern because of clotting factor consumption. Different clinical events lead to DIC, including sepsis, trauma, and shock. Treatments for thrombotic episodes or bleeding presentation in DIC oppose each other, thus creating therapeutic dilemmas in management. The objective of this study was to develop fibrin-specific core-shell nanogels (FSNs) loaded with tissue-type plasminogen activator (tPA) to treat the microcirculatory complications of DIC, which would facilitate targeted clot dissolution to manage microthrombi and the potential consumptive coagulopathy that causes bleeding. FSNs enhance formation of actively polymerizing clots by crosslinking fibrin fibers, but they can also target preexisting microthrombi and, when loaded with tPA, facilitate targeted delivery to lyse the microthrombi. We hypothesized that this dual action would simultaneously address bleeding and microthrombi with DIC to improve outcomes. In vivo, tPA-FSNs decreased the presentation of multiorgan microthrombi, recovered platelet counts, and improved bleeding outcomes in a DIC rodent model. When incorporated with human DIC patient plasma, tPA-FSNs restored clot structure and clot growth under flow. Together, these data demonstrate that a fibrinolytic agent loaded into fibrin-targeting nanogels could improve DIC outcomes.

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4

Shao, Bojing, Mark G. Wahrenbrock, Longbiao Yao, Tovo David, Shaun R. Coughlin, Lijun Xia, Ajit Varki, and Rodger P. McEver. "Carcinoma mucins trigger reciprocal activation of platelets and neutrophils in a murine model of Trousseau syndrome." Blood 118, no. 15 (October 13, 2011): 4015–23. http://dx.doi.org/10.1182/blood-2011-07-368514.

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Abstract Trousseau syndrome is classically defined as migratory, heparin-sensitive but warfarin-resistant microthrombi in patients with occult, mucinous adenocarcinomas. Injecting carcinoma mucins into mice generates platelet-rich microthrombi dependent on P- and L-selectin but not thrombin. Heparin prevents mucin binding to P- and L-selectin and mucin-induced microthrombi. This model of Trousseau syndrome explains resistance to warfarin, which inhibits fluid-phase coagulation but not selectins. Here we found that carcinoma mucins do not generate microthrombi in mice lacking P-selectin glycoprotein ligand-1 (PSGL-1), the leukocyte ligand for P- and L-selectin. Furthermore, mucins did not activate platelets in blood from PSGL-1–deficient mice. Mucins induced microthrombi in radiation chimeras lacking endothelial P-selectin but not in chimeras lacking platelet P-selectin. Mucins caused leukocytes to release cathepsin G, but only if platelets were present. Mucins failed to generate microthrombi in cathepsin G-deficient mice. Mucins did not activate platelets in blood from mice lacking cathepsin G or protease-activated receptor-4 (PAR4), indicating that cathepsin G activates platelets through PAR4. Using knockout mice and blocking antibodies, we found that mucin-triggered cathepsin G release requires L-selectin and PSGL-1 on neutrophils, P-selectin on platelets, and Src family kinases in both cell types. Thus, carcinoma mucins promote thrombosis through adhesion-dependent, bidirectional signaling in neutrophils and platelets.

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5

Park, Sohyung, and Byung-Ha Choi. "Acute Myocardial Infarction with Microthrombi in Cardiac Small Vessels after COVID-19 Vaccination (ChAdOx1 nCov-19): A Case Report." Korean Journal of Legal Medicine 45, no. 4 (November 30, 2021): 127–32. http://dx.doi.org/10.7580/kjlm.2021.45.4.127.

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We present the postmortem findings of an unexpected death due to acute myocardial infarction (AMI) with microthrombi and thrombosis in other vessels after the first dose of coronavirus disease 2019 (COVID-19) vaccination (ChAdOx1 nCov-19). The deceased was a 69-year-old woman who complained of nonspecific symptoms shortly after vaccination and was found dead on the sixth day. Postmortem examination revealed AMI and complications (left ventricular rupture, hemopericardium) with microthrombi in small cardiac vessels, which are similar to the characteristic findings of myocardial injury caused by microthrombi in patients with COVID-19. Nonobstructive thromboembolism in the pulmonary arteries and inferior vena cava, and fibrin microthrombi in some small vessels in the brain were also observed. It is unclear whether these findings are associated with COVID-19 vaccination, and further comprehensive studies are needed.

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6

Neil, Desley A. H. "CD31 highlights platelet-rich microthrombi." Histopathology 54, no. 3 (February 2009): 387–88. http://dx.doi.org/10.1111/j.1365-2559.2008.03215.x.

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7

Dienel, Ari, Remya Ammassam Veettil, Sung-Ha Hong, Kanako Matsumura, Peeyush Kumar T., Yuanqing Yan, Spiros L. Blackburn, et al. "Microthrombi Correlates With Infarction and Delayed Neurological Deficits After Subarachnoid Hemorrhage in Mice." Stroke 51, no. 7 (July 2020): 2249–54. http://dx.doi.org/10.1161/strokeaha.120.029753.

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Background and Purpose: Delayed neurological deficits are a devastating consequence of subarachnoid hemorrhage (SAH), which affects about 30% of surviving patients. Although a very serious concern, delayed deficits are understudied in experimental SAH models; it is not known whether rodents recapitulate the delayed clinical decline seen in SAH patients. We hypothesized that mice with SAH develop delayed functional deficits and that microthrombi and infarction correlate with delayed decline. Methods: Adult C57BL/6J mice of both sexes were subjected to endovascular perforation to induce SAH. Mice were allowed to survive for up to 1 week post-ictus and behavioral performance was assessed daily. Postmortem microthrombi, large artery diameters (to assess vasospasm), and infarct volume were measured. These measures were analyzed for differences between SAH mice that developed delayed deficits and SAH mice that did not get delayed deficits. Correlation analyses were performed to identify which measures correlated with delayed neurological deficits, sex, and infarction. Results: Twenty-three percent of males and 47% of females developed delayed deficits 3 to 6 days post-SAH. Female mice subjected to SAH had a significantly higher incidence of delayed deficits than male mice with SAH. Mice that developed delayed deficits had significantly more microthrombi and larger infarct volumes than SAH mice that did not get delayed deficits. Microthrombi positively correlated with infarct volume, and both microthrombi and infarction correlated with delayed functional deficits. Vasospasm did not correlate with either infarction delayed functional deficits. Conclusions: We discovered that delayed functional deficits occur in mice following SAH. Sex differences were seen in the prevalence of delayed deficits. The mechanism by which microthrombi cause delayed deficits may be via formation of infarcts.

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8

Redfern, Andrew, Huda Mahmoud, Tom McCulloch, Adam Shardlow, Matthew Hall, Catherine Byrne, and Nicholas M. Selby. "Renal Arcuate Vein Microthrombi-Associated AKI." Clinical Journal of the American Society of Nephrology 10, no. 2 (December 1, 2014): 180–86. http://dx.doi.org/10.2215/cjn.01540214.

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9

Skjørten, Fredrik. "ON THE NATURE OF HYALINE MICROTHROMBI." Acta Pathologica Microbiologica Scandinavica 73, no. 4 (August 17, 2009): 489–501. http://dx.doi.org/10.1111/j.1699-0463.1968.tb03208.x.

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10

Skjørten, Fredrik. "HYALINE MICROTHROMBI IN AN AUTOPSY MATERIAL." Acta Pathologica Microbiologica Scandinavica 76, no. 3 (August 18, 2009): 361–75. http://dx.doi.org/10.1111/j.1699-0463.1969.tb03267.x.

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11

Huber, Alfred, Alexander Dorn, Alfred Witzmann, and Jorge Cerv�s-Navarro. "Microthrombi formation after severe head trauma." International Journal of Legal Medicine 106, no. 3 (May 1993): 152–55. http://dx.doi.org/10.1007/bf01225238.

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12

Fernández-Ruiz, Irene. "Microthrombi cause cardiac injury in COVID-19." Nature Reviews Cardiology 18, no. 5 (February 4, 2021): 306. http://dx.doi.org/10.1038/s41569-021-00524-5.

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13

Aikawa, Tadao, Jiro Ogino, Yuichi Kita, and Naohiro Funayama. "Myocardial microthrombi after COVID-19 mRNA vaccination." European Heart Journal 42, no. 43 (October 8, 2021): 4501. http://dx.doi.org/10.1093/eurheartj/ehab727.

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14

Spurlock, Ben O., and A. B. Chandler. "Microthrombi in Human Atherogenesis: A Sem Report." Proceedings, annual meeting, Electron Microscopy Society of America 43 (August 1985): 690–91. http://dx.doi.org/10.1017/s042482010012014x.

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The response to injury hypothesis for the pathogenesis of atherosclerosis as outlined by Ross and associates focuses on three major events: 1) that lesions of athero sclerosis are initiated in response to some form of injury to the arterial endothelium; 2) that focal sites of injury permit circulating blood elements; i.e., platelets, monocytes and lipoproteins to adhere to the subendothelial connective tissue; 3) that adherent platelets release platelet derived growth factor (PDGF) from their granules and lead to the proliferation of smooth muscle cells in the intima. if there is early repair of the endothelial surface the process ceases; if however, the connective tissue components remain exposed to the circulating elements there is a continuation of the process with progressive smooth muscle cell proliferation and development of an atherosclerotic plaque.

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15

Fox, S. B., C. A. Day, and K. C. Gatter. "Association between platelet microthrombi and finger clubbing." Lancet 338, no. 8762 (August 1991): 313–14. http://dx.doi.org/10.1016/0140-6736(91)90452-u.

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16

Kincaid-Smith, P. "Points: Myocardial microthrombi in systemic lupus erythematosus." BMJ 297, no. 6646 (August 13, 1988): 489. http://dx.doi.org/10.1136/bmj.297.6646.489-d.

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17

Zhen, Zhu-Yin, Yu-Cheng Guo, Zhi-Gao Zhang, Liang-Yan, Pin-Ji Ge, and Hui-Ming Jin. "Experimental Study on Microthrombi and Myocardial Injuries." Microvascular Research 51, no. 1 (January 1996): 99–107. http://dx.doi.org/10.1006/mvre.1996.0010.

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18

Geys, Lotte, Dries Bauters, Elien Roose, Claudia Tersteeg, Karen Vanhoorelbeke, Marc F. Hoylaerts, Ilse Scroyen, and Roger H. Lijnen. "ADAMTS13 deficiency promotes microthrombosis in a murine model of diet-induced liver steatosis." Thrombosis and Haemostasis 117, no. 01 (2017): 19–26. http://dx.doi.org/10.1160/th16-03-0195.

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SummaryADAMTS13 cleaves ultralarge multimeric von Willebrand Factor (VWF), thereby preventing formation of platelet-rich microthrombi. ADAMTS13 is mainly produced by hepatic stellate cells, and numerous studies have suggested a functional role of ADAMTS13 in the pathogenesis of liver diseases. The aim of our study was to investigate a potential role of ADAMTS13 in formation of hepatic microthrombi and development of non-alcoholic steatohepatitis (NASH), and furthermore to evaluate whether plasmin can compensate for the absence of ADAMTS13 in removal of thrombi. Therefore, we used a model of high-fat diet-induced steatosis in Adamts13 deficient (Adamts13−/−) and wild-type (WT) control mice. Microthrombi were more abundant in the liver of obese Adamts13−/− as compared to obese WT or to lean Adamts13−/− mice. Obese Adamts13−/− mice displayed lower platelet counts and higher prevalence of ultra-large VWF multimers. Hepatic plasmin-α2-antiplasmin complex levels were comparable for obese WT and Adamts13−/− mice and were lower for lean Adamts13−/− than WT mice, not supporting marked activation of the fibrinolytic system. High fat diet feeding, as compared to normal chow, resulted in enhanced liver triglyceride levels for both genotypes (p < 0.0001) and steatosis (p < 0.0001 for WT mice, p = 0.002 for Adamts13−/− mice) without differences between the genotypes. Expression of markers of inflammation, oxidative stress, steatosis and fibrosis was affected by diet, but not by genotype. Thus, our data confirm that obesity promotes NASH, but do not support a detrimental role of ADAMTS13 in its development. However, Adamts13 deficiency in obese mice promotes hepatic microthrombosis, whereas a compensatory role of plasmin in removal of microthrombi in the absence of ADAMTS13 could not be demonstrated.

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19

MOHANAKRISHNAN, BALAJI PRASAD ELLAPPAN, KATHERINE G HOLDER, SARIA TASNIM, MANISH L PATEL, and NICOLE L DAVEY-RANASINGHE. "A RARE MICROTHROMBI DISEASE: CATASTROPHIC ANTIPHOSPHOLIPID ANTIBODY SYNDROME." Chest 162, no. 4 (October 2022): A982. http://dx.doi.org/10.1016/j.chest.2022.08.774.

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20

Simon, David, Laura Finn, and Allison Eddy. "Subepithelial Humps and Microthrombi: Looking for a Mechanism." American Journal of Kidney Diseases 47, no. 2 (February 2006): 365–70. http://dx.doi.org/10.1053/j.ajkd.2005.07.052.

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21

Heye, N., C. Paetzold, R. Steinberg, and J. Cervos-Navarro. "The topography of microthrombi in ischemic brain infarct." Acta Neurologica Scandinavica 86, no. 5 (November 1992): 450–54. http://dx.doi.org/10.1111/j.1600-0404.1992.tb05122.x.

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22

Sabri, M., J. Ai, K. Lakovic, J. D’abbondanza, D. Ilodigwe, and R. L. Macdonald. "Mechanisms of microthrombi formation after experimental subarachnoid hemorrhage." Neuroscience 224 (November 2012): 26–37. http://dx.doi.org/10.1016/j.neuroscience.2012.08.002.

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23

Fernando, Deepani D., Simone L. Reynolds, Gunter Hartel, Bernard Cribier, Nicolas Ortonne, Malcolm K. Jones, and Katja Fischer. "A unique group of scabies mite pseudoproteases promotes cutaneous blood coagulation and delays plasmin-induced fibrinolysis." PLOS Neglected Tropical Diseases 15, no. 1 (January 6, 2021): e0008997. http://dx.doi.org/10.1371/journal.pntd.0008997.

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Background Scabies, a highly contagious skin disease affecting more than 200 million people worldwide at any time, is caused by the parasitic mite Sarcoptes scabiei. In the absence of molecular markers, diagnosis requires experience making surveillance and control challenging. Superficial microthrombi in the absence of vasculitis in scabies-affected skin are a recognised, yet unexplained histopathological differential of scabies infection. This study demonstrates that a family of Scabies Mite Inactivated Cysteine Protease Paralogues (SMIPP-Cs) excreted by the mites plays a role in formation of scabies-induced superficial microthrombi. Methodology/Principal findings A series of in vitro and ex vivo experiments involving two representative recombinant SMIPP-Cs was carried out. In the presence of SMIPP-Cs, the thrombin clotting time (TCT), fibrin formation and plasmin induced fibrinolysis were monitored in vitro. The ultrastructure of the SMIPP-C—modulated fibrin was analysed by Scanning Electron Microscopy (SEM). Immuno-histological analyses were performed ex vivo, to localise the SMIPP-C proteins within scabies infected skin biopsies. SMIPP-Cs displayed pro-coagulant properties. They bound calcium ions, reduced the thrombin clotting time, enhanced the fibrin formation rate and delayed plasmin-induced fibrinolysis. The SMIPP-Cs associated with fibrin clots during fibrinogen polymerisation and did not bind to preformed fibrin. Scanning electron microscopy revealed that the fibrin clots formed in the presence of SMIPP-Cs were aberrant and denser than normal fibrin clots. SMIPP-Cs were detected in microthrombi which are commonly seen in scabietic skin. Conclusions/Significance The SMIPP-Cs are the first scabies mite proteins found in sub-epidermal skin layers and their pro-coagulant properties promote superficial microthrombi formation in scabetic skin. Further research is needed to evaluate their potential as diagnostic or therapeutic target.

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24

Pellegrini, Dario, Rika Kawakami, Giulio Guagliumi, Atsushi Sakamoto, Kenji Kawai, Andrea Gianatti, Ahmed Nasr, et al. "Microthrombi as a Major Cause of Cardiac Injury in COVID-19." Circulation 143, no. 10 (March 9, 2021): 1031–42. http://dx.doi.org/10.1161/circulationaha.120.051828.

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Background: Cardiac injury is common in patients who are hospitalized with coronavirus disease 2019 (COVID-19) and portends poorer prognosis. However, the mechanism and the type of myocardial damage associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain uncertain. Methods: We conducted a systematic pathological analysis of 40 hearts from hospitalized patients dying of COVID-19 in Bergamo, Italy, to determine the pathological mechanisms of cardiac injury. We divided the hearts according to presence or absence of acute myocyte necrosis and then determined the underlying mechanisms of cardiac injury. Results: Of the 40 hearts examined, 14 (35%) had evidence of myocyte necrosis, predominantly of the left ventricle. Compared with subjects without necrosis, subjects with necrosis tended to be female, have chronic kidney disease, and have shorter symptom onset to admission. The incidence of severe coronary artery disease (ie, >75% cross-sectional narrowing) was not significantly different between those with and without necrosis. Three of 14 (21.4%) subjects with myocyte necrosis showed evidence of acute myocardial infarction, defined as ≥1 cm 2 area of necrosis, whereas 11 of 14 (78.6%) showed evidence of focal (>20 necrotic myocytes with an area of ≥0.05 mm 2 but <1 cm 2 ) myocyte necrosis. Cardiac thrombi were present in 11 of 14 (78.6%) cases with necrosis, with 2 of 14 (14.2%) having epicardial coronary artery thrombi, whereas 9 of 14 (64.3%) had microthrombi in myocardial capillaries, arterioles, and small muscular arteries. We compared cardiac microthrombi from COVID-19–positive autopsy cases to intramyocardial thromboemboli from COVID-19 cases as well as to aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment–elevation myocardial infarction. Microthrombi had significantly greater fibrin and terminal complement C5b-9 immunostaining compared with intramyocardial thromboemboli from COVID-19–negative subjects and with aspirated thrombi. There were no significant differences between the constituents of thrombi aspirated from COVID-19–positive and –negative patients with ST-segment–elevation myocardial infarction. Conclusions: The most common pathological cause of myocyte necrosis was microthrombi. Microthrombi were different in composition from intramyocardial thromboemboli from COVID-19–negative subjects and from coronary thrombi retrieved from COVID-19–positive and –negative patients with ST-segment–elevation myocardial infarction. Tailored antithrombotic strategies may be useful to counteract the cardiac effects of COVID-19 infection.

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25

Kim, Hee Sung, Yoon-Sun Chun, Sung Nam Chang, and Wook-Hwa Park. "Hypereosinophilic syndrome: correlation between clinical severity and cutaneous microthrombi." International Journal of Dermatology 40, no. 5 (May 2001): 330–32. http://dx.doi.org/10.1046/j.1365-4362.2001.00971.x.

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26

Rapp, Joseph H., Kelsy Hollenbeck, and Xian Mang Pan. "An experimental model of lacunar infarction: Embolization of microthrombi." Journal of Vascular Surgery 48, no. 1 (July 2008): 196–200. http://dx.doi.org/10.1016/j.jvs.2008.01.038.

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27

Hamada, Takahiro. "Hypereosinophilic Syndrome With Peripheral Circulatory Insufficiency and Cutaneous Microthrombi." Archives of Dermatology 143, no. 6 (June 1, 2007): 799. http://dx.doi.org/10.1001/archderm.143.6.812.

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28

Hosseinnejad, Aisa, Nadine Ludwig, Ann-Katrin Wienkamp, Rahul Rimal, Christian Bleilevens, Rolf Rossaint, Jan Rossaint, and Smriti Singh. "DNase I functional microgels for neutrophil extracellular trap disruption." Biomaterials Science 10, no. 1 (2022): 85–99. http://dx.doi.org/10.1039/d1bm01591e.

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Non-fouling DNase I conjugated microgel provide a novel biohybrid platform to disrupt Neutrophil extracellular traps (NETs) and can be used as a non-thrombogenic coating for reduction of NET-mediated inflammation and microthrombi formation.

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29

Ramón y Cajal Agüeras, Santiago. "COVID-19 and pathology: What do we know?" ANALES RANM 137, no. 137(02) (September 30, 2020): 133–39. http://dx.doi.org/10.32440/ar.2020.137.02.rev06.

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The experience of recent months in the study of the pathology associated with COVID-19 infection is showing histological alterations similar to other infections associated with previous pandemics, such as diffuse alveolar damage, signs of endotheliitis, inflammatory infiltrates and fibrin microthrombi. In the samples of patients with COVID-19, a greater number of cases with signs of endothelitis and a greater number of microthrombi stand out, both at the level of the lung parenchyma and in other locations, such as the colon, myocardium, liver … The study of the biopsies of patients who have overcome the acute phases of COVID is showing the presence of interstitial inflammatory infiltrates at the lung level and areas of fibrosis, and various factors that may predict the greater or lesser probability of the development of fibrosis are being studied pulmonary in such patients.

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30

Hoque, Muhammad Mazharul, Motiul Islam, Tarikul Hamid, Rabiul Halim, Rajib Hasan, and Kazi Nuruddin Ahmed. "Tissue plasminogen activator (tPA) treatment for COVID_19 associated acute respiratory distress syndrome (ARDS): A case report." Bangladesh Critical Care Journal 9, no. 1 (April 18, 2021): 49–51. http://dx.doi.org/10.3329/bccj.v9i1.53059.

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Coagulopathy has proven to be a common complication of the novel coronavirus SARS-CoV-21. Some of the COVID-19 associated pneumonia patients exhibit relatively preserved lung compliance and high alveolar‐arterial oxygen gradient. Pathology reports consistently demonstrate diffuse pulmonary microthrombi on autopsy, consistent with a vascular occlusive etiology of respiratory failure rather than the more classic findings of ARDS2. Pulmonary microthrombi induced respiratory failure is very difficult to prove because the patients are so critically ill that transfer to CT suit to do CTPA often becomes unsafe for the patients. Moreover, performing V/Q scan is increasingly difficult in such settings. Here we report a case of severe COVID-19 associated respiratory failure who was treated with tissue plasminogen activator (tPA) on clinical ground. Bangladesh Crit Care J March 2021; 9(1): 49-51

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Bai, Sheng, Jintang Liao, Bo Zhang, Min Zhao, Baiyang You, Pan Li, Haitao Ran, Zhigang Wang, Ruizheng Shi, and Guogang Zhang. "Multimodal and multifunctional nanoparticles with platelet targeting ability and phase transition efficiency for the molecular imaging and thrombolysis of coronary microthrombi." Biomaterials Science 8, no. 18 (2020): 5047–60. http://dx.doi.org/10.1039/d0bm00818d.

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In this article, we constructed PLGA-cRGD-PFH-ICG NPs through emulsification process and then the bi-modal imaging of coronary microthrombi in ischemia/reperfusion rat model and thrombolysis of clots in vitro were both successfully completed by these NPs.

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Stein, Sherman C., Xiao-Han Chen, Grant P. Sinson, and Douglas H. Smith. "Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury." Journal of Neurosurgery 97, no. 6 (December 2002): 1373–77. http://dx.doi.org/10.3171/jns.2002.97.6.1373.

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Object. The goal of this study was to determine the frequency with which cerebral intravascular coagulation (IC) complicates traumatic brain injury (TBI). The authors also investigated the incidence of IC in relation to varying mechanisms, time courses, and severities of TBI and in different species. Methods. Tissue was sampled from surgical specimens of human cerebral contusions, from rats with lateral fluid-percussion injuries, and from pigs with head rotational acceleration injuries. Immunohistochemical fluorescent staining for antithrombin III was performed to detect cerebral intravascular microthrombi. Abundant IC was found in all specimens, and microthrombi had formed in arterioles and venules of all sizes, ranging from 10 to 600 µm. Although it was more pronounced in focal lesions and more severe injuries, considerable IC was also observed in mild and diffuse injuries. The authors found a strong association between the severity of coagulopathy and the density of IC. Conclusions. These results strongly support the contention that IC is a universal response to TBI and an important secondary cerebral insult.

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Islam, Md Motiul, Muhammad Mazharul Hoque, Tarikul Hamid, Muhammad Rabiul Halim, Kazi Nuruddin Ahmed, and Rajib Hasan. "Tissue plasminogen activator (tPA) treatment for COVID 19 associated respiratory failure: A case Series." Bangladesh Critical Care Journal 10, no. 1 (April 25, 2022): 62–67. http://dx.doi.org/10.3329/bccj.v10i1.59207.

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The global pandemic of COVID-19 has oversaturated the medical care facilities with a large proportion of patient associated with acute respiratory distress syndrome (ARDS). ARDS in patients with COVID-19 is associated with high incidence of pulmonary embolism, pulmonary hypertension and microthrombotic complications. Although heparin is frequently used to treat thrombotic pathology COVID-19, pulmonary embolism is still observed in severe cases. Pathology reports consistently demonstrate diffuse pulmonary microthrombi on autopsy, consistent with vascular occlusive etiology of respiratory failure rather than the more classic finding in ARDS. Pulmonary microthrombi induced respiratory failure is very difficult to prove because the patients are so critically ill that transfer to CT suit to do CT pulmonary angiogram (CTPA) often become unsafe for the patients. Moreover, performing V/Q scan is increasingly difficult in these settings. Here we report a case series of 10 patients with severe COVID-19 associated respiratory failure who were treated with tissue plasminogen activator (tPA). Bangladesh Crit Care J March 2022; 10 (1): 62-67

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34

Wang, Xue-Feng, Pei-Pei Jin, Tong Zhou, Ya-Peng Zhao, Qiu-Lan Ding, Deng-Bin Wang, Guang-Ming Zhao, Jing-Dai, Hong-Li Wang, and Hai-Liang Ge. "MR Molecular Imaging of Thrombus: Development and Application of a Gd-based Novel Contrast Agent Targeting to P-selectin." Clinical and Applied Thrombosis/Hemostasis 16, no. 2 (January 12, 2009): 177–83. http://dx.doi.org/10.1177/1076029608330470.

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Molecular imaging of thrombus formation at initial stage requires a robust thrombus-specific contrast agent with high sensitivity. In this study, we report a novel P-selectin-targeted paramagnetic molecular imaging agent and the agent’s potential to sensitively detect occult microthrombi on the intimal surface of endothelium. Platelet clots and blood clots targeted in vitro with paramagnetic nanoparticles presented a highly detectable, homogeneous T1-weighted contrast enhancement that was improved with increasing gadolinium level. In vivo contrast enhancement under part of circulation conditions was assessed in dogs. The micro-thrombi around the femoral vein of dog demonstrated higher signal intensities than the control clots and the adjacent muscle. Histology was performed on regions likely to contain thrombus as indicated by MRI. These results suggest that molecular imaging of P-selectin-targeted paramagnetic nanoparticles can provide sensitive detection and localization of P-selectin and may allow for early, direct identification of microthrombi, leading to early diagnosis.

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35

Zuo, Yu, Yogendra Kanthi, Jason S. Knight, and Alfred H. J. Kim. "The interplay between neutrophils, complement, and microthrombi in COVID-19." Best Practice & Research Clinical Rheumatology 35, no. 1 (March 2021): 101661. http://dx.doi.org/10.1016/j.berh.2021.101661.

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Giles, W., D. Pepperall, and N. Wilson. "Abnormal placental doppler studies not related to platelet microthrombi formation." Placenta 15, no. 7 (October 1994): A19. http://dx.doi.org/10.1016/0143-4004(94)90079-5.

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Shehi, Elona, Sridhar Chilimuri, Dongmin Shin, Madanmohan Patel, Nisha Ali, and Masooma Niazi. "Microthrombi in skin biopsy of a patient with COVID-19." JAAD Case Reports 6, no. 12 (December 2020): 1327–29. http://dx.doi.org/10.1016/j.jdcr.2020.10.009.

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Guagliumi, Giulio, Aurelio Sonzogni, Irene Pescetelli, Dario Pellegrini, and Aloke V. Finn. "Microthrombi and ST-Segment–Elevation Myocardial Infarction in COVID-19." Circulation 142, no. 8 (August 25, 2020): 804–9. http://dx.doi.org/10.1161/circulationaha.120.049294.

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Chavanon, Olivier, Monsef Hlal, Abderhamane Bakkali, Géraldine Dessertaine, Claire Haffner-Dubus, Sylvie Lantuejoul, and Aude Boignard. "Multiple Microthrombi on a Papillary Fibroelastoma of the Aortic Valve." Annals of Thoracic Surgery 93, no. 1 (January 2012): 304–6. http://dx.doi.org/10.1016/j.athoracsur.2011.06.043.

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Wehn, Antonia, Andrey Klymchenko, Nikolaus Plesnila, and Igor Khalin. "Microthrombi-Mediated Blood-Brain-Barrier Dysfunction after Traumatic Brain Injury." Brain and Spine 4 (2024): 103402. http://dx.doi.org/10.1016/j.bas.2024.103402.

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Thorp, K. E., James A. Thorp, Elise M. Thorp, Margery M. Thorp, and Paul R. Walker. "COVID-19: Energy, Protein Folding & Prion Disease." Gazette of Medical Sciences 3, no. 1 (September 13, 2022): 179–206. http://dx.doi.org/10.46766/thegms.neuro.22083101.

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The recent recognition of intravascular amyloid formation with deposition of insoluble microthrombi throughout the circulatory system in primary COVID-19 infection or following administration of mRNA vaccines is a pivotal discovery that alters conventional notions about the nature of the underlying pathologic process at play in SARS-CoV-2 infection.

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Linneweber, J., T. Chow, T. Takano, T. Maeda, K. Nonaka, S. Schulte-Eistrup, S. Kawahito, J. Moake, and Y. Nose. "FLOW CYTOMETRIC ASSAY TO QUANTIFY PUMP INDUCED MICROTHROMBI DURING CARDIOPULMONARY BYPASS." ASAIO Journal 46, no. 2 (March 2000): 182. http://dx.doi.org/10.1097/00002480-200003000-00127.

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Muto, Yuko, Kokichi Suzuki, Eriko Sato, and Hidemi Ishii. "Carboxypeptidase B inhibitors reduce tissue factor-induced renal microthrombi in rats." European Journal of Pharmacology 461, no. 2-3 (February 2003): 181–89. http://dx.doi.org/10.1016/s0014-2999(03)01297-4.

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Brown, J. H., C. C. Doherty, D. C. Allen, and P. Morton. "Fatal cardiac failure due to myocardial microthrombi in systemic lupus erythematosus." BMJ 296, no. 6635 (May 28, 1988): 1505. http://dx.doi.org/10.1136/bmj.296.6635.1505.

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Guria, G. T., M. A. Herrero, and K. E. Zlobina. "Ultrasound detection of externally induced microthrombi cloud formation: a theoretical study." Journal of Engineering Mathematics 66, no. 1-3 (October 14, 2009): 293–310. http://dx.doi.org/10.1007/s10665-009-9340-9.

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Todorov, S. S., A. S. Kazmin, V. Yu Deribas, and S. S. Todorov Jr. "Pathological anatomy of lung vessels in COVID-19." CLINICAL AND EXPERIMENTAL MORPHOLOGY 11, no. 2 (2022): 6–12. http://dx.doi.org/10.31088/cem2022.11.2.6-12.

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Pathological anatomy of pulmonary vascular lesions plays a key role in understanding the patho-genesis and morphogenesis of COVID-19. This review focuses on morphological features of pulmonary vascular injury in COVID-19. The virus is known to be capable of causing not only cytopathic cell damage of various organs and tissues (type II pneumocytes, cardiomyocytes, neurons, epithelial cells of the gas-trointestinal tract) but also endotheliotropic damage that aggravates the development and course of acute alveolar damage to the lungs. We studied the literature on microscopic changes in the vessel walls in lung tissue for 2020–2022. This review discusses the issues of local or systemic vascular lesions, morphologi-cal changes in the vessels over time, the likelihood of the development of microangiopathy, vasculitis, and endotheliitis in COVID-19 patients. Particular attention is paid to possible mechanisms of endotheliopathy in COVID-19 patients and its role in the microthrombi genesis. We speculate that in the future, postmor-tem lung examination in COVID-19 patients using histological, histochemical, and immunohistochemical methods will clarify the features of alterative and inflammatory changes and reparative processes in the blood vessel walls, as well as neoangiogenesis at different stages of the disease. Keywords: pathological anatomy, COVID-19, lungs, endotheliopathy, endotheliitis, microthrombus formation

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Andereggen, Lukas, Volker Neuschmelting, Michael von Gunten, Hans Rudolf Widmer, Javier Fandino, and Serge Marbacher. "The Role of Microclot Formation in an Acute Subarachnoid Hemorrhage Model in the Rabbit." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/161702.

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Background.Microvascular dysfunction and microthrombi formation are believed to contribute to development of early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (SAH).Objective.This study aimed to determine (i) extent of microthrombus formation and neuronal apoptosis in the brain parenchyma using a blood shunt SAH model in rabbits; (ii) correlation of structural changes in microvessels with EBI characteristics.Methods.Acute SAH was induced using a rabbit shunt cisterna magna model. Extent of microthrombosis was detected 24 h post-SAH (n=8) by fibrinogen immunostaining, compared to controls (n=4). We assessed apoptosis by terminal deoxynucleotidyl transferase nick end labeling (TUNEL) in cortex and hippocampus.Results.Our results showed significantly more TUNEL-positive cells (SAH: 115 ± 13; controls: 58 ± 10;P=0.016) and fibrinogen-positive microthromboemboli (SAH: 9 ± 2; controls: 2 ± 1;P=0.03) in the hippocampus after aneurysmal SAH.Conclusions.We found clear evidence of early microclot formation in a rabbit model of acute SAH. The extent of microthrombosis did not correlate with early apoptosis or CPP depletion after SAH; however, the total number of TUNEL positive cells in the cortex and the hippocampus significantly correlated with mean CPP reduction during the phase of maximum depletion after SAH induction. Both microthrombosis and neuronal apoptosis may contribute to EBI and subsequent DCI.

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Shaikh, M. Faizan, Subhan Ahmed Sajjad, Owais Ramzan, Shua Nasir, Lal Shehbaz, Hafsa Tahir Shaikh, and S. Muhammad Irtiza Hashmi. "Comparison of histopathological findings of patients presenting with acute appendicitis in COVID-19 infected and non-COVID-19 infected patients." International Journal of Endorsing Health Science Research (IJEHSR) 10, no. 2 (June 1, 2022): 233–41. http://dx.doi.org/10.29052/ijehsr.v10.i2.2022.233-241.

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Background: COVID-19 disease has been associated with multiple organs and causes various symptoms depending on the organ involved. Histological findings in the lungs, such as microthrombi, perivascular lymphocytic infiltrate, and necrosis/infarction, can also be seen in the histopathology of the appendix of COVID-19 +ve patients. Methodology: This cross-sectional study was conducted in Dr. Ziauddin Hospital, a tertiary care center in Karachi, Pakistan. In this research article, the histopathology reports of the appendix of COVID-19 +ve patients presenting with acute appendicitis, either antigen or PCR positive, are compared with those of non-COVID patients who presented with acute appendicitis. The data was analyzed using SPSS 20.0, and Pearson’s Chi-Square and Cramer's V tests were performed for analysis. Results: Comparing the histopathology reports of COVID-19 +ve and non-COVID patients presenting with acute appendicitis, an appendix of COVID-19 +ve patients shows microthrombi; perivascular lymphocytic infiltrates, and necrosis/infarction. Conclusion: Patients who are COVID-19 +ve presenting with acute appendicitis should be treated surgically as soon as possible to reduce the risk of acute presentation, ultimately leading to perforation, and not wait for the patient to recover from COVID infection first.

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Vergouwen, Mervyn DI, Marinus Vermeulen, Bert A. Coert, Erik SG Stroes, and Yvo BWEM Roos. "Microthrombosis after Aneurysmal Subarachnoid Hemorrhage: An Additional Explanation for Delayed Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 28, no. 11 (July 16, 2008): 1761–70. http://dx.doi.org/10.1038/jcbfm.2008.74.

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Patients with aneurysmal subarachnoid hemorrhage (SAH) who experience delayed cerebral ischemia (DCI) have an increased risk of poor outcome. Delayed cerebral ischemia is considered to be caused by vasospasm. However, not all patients with DCI have vasospasm. Inversely, not all patients with vasospasm develop clinical symptoms and signs of DCI. In the past, treatments aiming at vasospasm were not successful in preventing ischemia. The purpose of this review is to give an overview of clinical data showing that DCI cannot always be attributed to vasospasm, and to present an in-depth analysis of clinical and autopsy studies on the role of microthrombosis in the pathogenesis of DCI. Clinical studies show that DCI is associated with an activation of the coagulation cascade within a few days after SAH, preceding the time window during which vasospasm occurs. Furthermore, impaired fibrinolytic activity, and inflammatory and endothelium-related processes, lead to the formation of microthrombi, which ultimately result in DCI. The presence of microthrombi is confirmed by autopsy studies. Insight in the pathophysiology of DCI is crucial for the development of effective therapies against this complication. Because multiple pathways are involved, future research should focus on drugs with pleiotropic effects.

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Karrer, L., J. Duwe, A. H. Zisch, E. Khabiri, M. Cikirikcioglu, A. Napoli, A. Goessl, et al. "PPS-PEG Surface Coating to Reduce Thrombogenicity of Small Diameter ePTFE Vascular Grafts." International Journal of Artificial Organs 28, no. 10 (October 2005): 993–1002. http://dx.doi.org/10.1177/039139880502801006.

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Aims Patency failure of small vascular synthetic grafts is still a major problem for coronary and peripheral revascularization. Thus, three new surface coatings of small synthetic grafts were tested in an acute pig model to evaluate their thrombogenicity (extracorporeal arterio-venous shunt) and in a chronic rat model to evaluate the tissue reaction they induced (subcutaneous implantation). Methods In five domestic pigs (25–30 kg) an extracorporeal femoro-femoral arterio-venous shunt model was used. The study protocol included first a non-heparinized perfusion sequence followed by graft perfusion after 10,000 UI iv heparin. Grafts were perfused for 3 and 9 minutes. The following coatings were tested on ePTFE grafts: poly-propylene sulphide (PPS) – poly-ethylene glycol (PEG) (wet and dry applications) as well as carbon. Two sets of control were used, one dry and one wet (vehicle only). After perfusion grafts were examined by scanning electron microscopy for semiquantitative assessment (score 0–3) of cellular and microthrombi deposition. To assess tissue compatibility, pieces of each material were implanted subcutaneously in 16 Wistar rats. At 2, 4, 8, 12 weeks four animals each were sacrificed for semi-quantitative (score 0–3) histologic evaluation of tissue reaction. Results In the pig model, cellular deposition and microthrombi formation increased over time. In non-heparinized animals, the coatings did not improve the surface characteristics, since they did not prevent microthrombi formation and cellular deposition. In heparinized animals, thrombogenicity was lowest in coated grafts, especially in PPS–PEG dry (P&0.05), and highest in controls. Cell deposition was lowest in PPS–PEG dry, but this difference was not statistically significant vs. controls. In the rat model, no significant differences of the tissue reaction could be shown between materials. Conclusion While all coatings failed to add any benefit for lowering tissue reaction, surface coating with PPS–PEG (dry application) reduced thrombogenicity significantly (in heparinized animals) and thus appears to be promising for improving graft patency of small synthetic vascular prostheses.

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