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Статті в журналах з теми "Thrombus Formation Risk"
1
Jiroušková, Markéta, Igor Chereshnev, Heikki Väänänen, Jay L. Degen та Barry S. Coller. "Antibody blockade or mutation of the fibrinogen γ-chain C-terminus is more effective in inhibiting murine arterial thrombus formation than complete absence of fibrinogen". Blood 103, № 6 (15 березня 2004): 1995–2002. http://dx.doi.org/10.1182/blood-2003-10-3401.
Повний текст джерелаАнотація:
Abstract An elevated plasma fibrinogen level is a risk factor for thrombotic cardiovascular disease, but which of fibrinogen's functions is responsible for the increased risk is unknown. To define better the contribution of fibrinogen to large vessel thrombus formation, we studied carotid artery thrombosis in wild-type mice, mice lacking fibrinogen (fbg–/–), mice treated with 7E9 (a blocking antibody to the fibrinogen γ-chain C-terminus), and mice expressing a mutant fibrinogen (γΔ5) that lacks the γ-chain platelet-binding motif QADGV. In control mice, thrombus formation resulted in occlusion in 8 ± 2 minutes (mean ± SD). In fbg–/– mice, thrombi grew to large sizes, but then they abruptly embolized, confirming previous observations by others in an arteriolar thrombus model. In contrast, mice treated with 7E9 and γΔ5 mice developed only small, nonoclusive mural thrombi and embolization was limited. These findings reveal that a fibrinogen antibody, 7E9, or a fibrinogen mutant retaining clotting function, can limit thrombus formation more effectively than the complete absence of fibrinogen. We hypothesize that the smaller thrombi in these animals result from the ability of fibrin to bind and sequester thrombin and/or the ability of the altered fibrinogen molecules, which cannot recruit platelets, to bind to and passivate the surface.
2
Sugita, Chihiro, Atsushi Yamashita, Yunosuke Matsuura, Takashi Iwakiri, Nozomi Okuyama, Shuntaro Matsuda, Tomoko Matsumoto, et al. "Elevated plasma factor VIII enhances venous thrombus formation in rabbits: Contribution of factor XI, von Willebrand factor and tissue factor." Thrombosis and Haemostasis 110, no. 07 (2013): 62–75. http://dx.doi.org/10.1160/th13-01-0069.
Повний текст джерелаАнотація:
SummaryElevated plasma levels of factor VIII (FVIII) are associated with increased risk of deep venous thrombosis. The aim of this study is to elucidate how elevated FVIII levels affect venous thrombus formation and propagation in vivo. We examined rabbit plasma FVIII activity, plasma thrombin generation, whole blood coagulation, platelet aggregation and venous wall thrombogenicity before and one hour after an intravenous infusion of recombinant human FVIII (rFVIII). Venous thrombus induced by the endothelial denudation of rabbit jugular veins was histologically assessed. Thrombus propagation was evaluated as indocyanine green fluorescence intensity. Argatroban, a thrombin inhibitor, and neutralised antibodies for tissue factor (TF), factor XI (FXI), and von Willebrand factor (VWF) were infused before or after thrombus induction to investigate their effects on venous thrombus formation or propagation. Recombinant FVIII (100 IU/kg) increased rabbit plasma FVIII activity two-fold and significantly enhanced whole blood coagulation and total plasma thrombin generation, but did not affect initial thrombin generation time, platelet aggregation and venous wall thrombogenicity. The rFVIII infusion also increased the size of venous thrombus 1 hour after thrombus induction. Argatroban and the antibodies for TF, FXI or VWF inhibited such enhanced thrombus formation and all except TF suppressed thrombus propagation. In conclusion, elevated plasma FVIII levels enhance venous thrombus formation and propagation. Excess thrombin generation by FXI and VWF-mediated FVIII recruitment appear to contribute to the growth of FVIII-driven venous thrombus.
3
Yoshida, Hideo, Janice Russell, and D. Neil Granger. "Thrombin mediates the extraintestinal thrombosis associated with experimental colitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 5 (November 2008): G904—G908. http://dx.doi.org/10.1152/ajpgi.90400.2008.
Повний текст джерелаАнотація:
Recent evidence implicating tissue factor and the protein C pathway in the hypercoagulable state associated with intestinal inflammation suggests that thrombin is likely to contribute to this response. The objective of this study was to assess the role of thrombin in the extraintestinal thrombosis associated with experimental colitis. Thrombus formation was quantified in microvessels of the cremaster muscle in mice with dextran sodium sulfate (DSS)-induced colonic inflammation. The light/dye endothelial injury model was used to elicit thrombus formation in DSS colitic mice treated with either hirudin, heparin, or antithrombin III. The initiation and propagation/stabilization phases of thrombus formation were quantified using the time of onset of the thrombus and time to blood flow cessation, respectively. Thrombus formation was accelerated in arterioles of DSS colitic mice, as exhibited by significant reductions in the time of thrombus initiation and propagation/stabilization. Colitic mice treated with hirudin, heparin, or antithrombin III did not exhibit a significant change in the time of onset of the thrombus compared with untreated colitic mice. However, all three antithrombin agents largely prevented the DSS-induced reduction in the time to flow cessation following light/dye injury, with hirudin offering complete protection. These findings indicate that thrombin plays a major role in the extraintestinal thrombus formation associated with experimental colitis. Thrombin appears to contribute to the propagation/stabilization, rather than initiation, phase of the colitis-associated thrombogenesis at the distant vascular site. The results support the therapeutic use of antithrombin agents for reducing the risk of thromboembolism in patients with inflammatory bowel disease.
4
Gorter, Karin A. M., Marco C. Stehouwer, Bart P. Van Putte, Eline A. Vlot, and Rolf T. Urbanus. "Acidosis induced by carbon dioxide insufflation decreases heparin potency: a risk factor for thrombus formation." Perfusion 32, no. 3 (October 27, 2016): 214–19. http://dx.doi.org/10.1177/0267659116677307.
Повний текст джерелаАнотація:
Background: Since the introduction of CO2 insufflation during open heart surgery in our hospital, we incidentally observed thrombus formation in the dissected heart, in the pericardium and in the cardiotomy reservoir of the cardiopulmonary bypass system. Furthermore, we measured very high levels of pCO2, causing severe acidosis, in stagnant blood in the pericardium and cardiotomy reservoir. Objectives: In this in vitro study, we assessed the influence of acidosis and hypothermia on heparin potency and thrombin formation. Methods: We assessed heparin potency in function of pH (pH 5.0-7.4) and temperature (24-37°C) by comparing the activated partial thromboplastin time in platelet-poor plasma between samples with and without unfractionated heparin. We measured thrombin formation in platelet-poor plasma by means of fluorescent, calibrated, automated thrombography in function of pH (pH 5.0-7.4) and temperature (24-37°C). The parameters of interest were the endogenous thrombin potential and the peak amount of thrombin generation. Results: The major finding of this study is the significant decrease in the efficiency of unfractionated heparin in delaying thrombus formation at acidotic (pH 5.0-7.0) conditions (p=0.034-0.05). Furthermore, we found that thrombin formation is significantly increased at hypothermic (24-34°C) conditions (p=<0.001-0.01). Conclusions: Based on the results of our in-vitro study, we conclude that acidosis may lead to a decreased heparin potency. Acidosis, as induced by CO2 insufflation, may predispose patients to incidental thrombus formation in stagnant blood in the open thorax and in the cardiotomy reservoir. Hypothermia might further increase this risk. Therefore, we recommend reconsidering the potential advantages and disadvantages of using CO2 insufflation during cardiopulmonary bypass.
5
Kraft, Peter, Michael K. Schuhmann, Melanie Dittmeier, Felix Fluri, and Christoph Kleinschnitz. "Pretreatment with rivaroxaban attenuates stroke severity in rats by a dual antithrombotic and anti-inflammatory mechanism." Thrombosis and Haemostasis 115, no. 04 (2016): 835–43. http://dx.doi.org/10.1160/th15-08-0631.
Повний текст джерелаАнотація:
SummaryStroke outcome is more favourable in patients receiving oral anticoagulants compared with non-anticoagulated patients. The reasons for this “stroke-attenuating” property of oral anticoagulants are largely unknown. This study examined whether prestroke anticoagulation with rivaroxaban, a novel direct factor Xa inhibitor, influences stroke severity, thrombin-mediated intracerebral thrombus formation and pro-inflammatory processes in a rat model of brain ischaemia/reperfusion injury. Male Wistar rats were anticoagulated with rivaroxaban and subjected to 90 minutes of transient middle cerebral artery occlusion. Infarct size, functional outcome and the occurrence of intracranial haemorrhage (ICH) were assessed until day 7. Thrombin generation was determined by measuring the amount of thrombin/antithrombin complex. Intracerebral thrombus formation was evaluated by histology and Western blot. CD68-immunoreactivity and the expression of cytokines and adhesion molecules were investigated to assess postischaemic inflammation. The integrity of the blood–brain barrier was analysed using fluorescein isothiocyanate-dextran. Rats pretreated with rivaroxaban developed significantly smaller strokes and less severe functional deficits compared with controls. Although rivaroxaban strongly reduced thrombin-mediated thrombus formation, this was not accompanied by an increased risk of ICH. In addition, rivaroxaban dampened the inflammatory response in the ischaemic brain by downregulating ICAM-1 expression and the activation of CD68+-immune cells. In contrast, rivaroxaban had no effect on the integrity of the blood–brain barrier after stroke. Here, we identified reduced thrombo-inflammation as a major determinant of the stroke-protective property of rivaroxaban in rats. Further studies are needed to assess the therapeutic potential of novel oral anticoagulants in the acute phase after a stroke.
6
Irkin, O. I., and D. O. Bilyi. "Thrombosis in the cavity of the left ventricle. Part 1. Causes, diagnosis, prevention of formation." Ukrainian Journal of Cardiology 29, no. 5-6 (January 11, 2023): 52–58. http://dx.doi.org/10.31928/2664-4479-2022.5-6.5258.
Повний текст джерелаАнотація:
More than 100 years have passed since the first description of intracavitary thrombi, but the problem of diagnosis of thrombi, risk factors for development, as well as the impact of myocardial revascularization remain is a very relevant problem today, which definitely affects the prevalence of thrombi formation in the cavity of the left ventricle (LV). This review is devoted to the description and analysis of the main methods of diagnosing the presence of a thrombus in the cavity of the LV and factors affecting the formation of a thrombus. The most adequate method for diagnosing left ventricular thrombosis is a cardiac magnetic resonance imaging, but a simpler method such as transthoracic echocardiography can be used as a screening method for most patients. Determining the causes of LV thrombosis, such as reduced ventricular mobility, local myocardial damage, the presence of hyper coagulation and inflammatory phenomena, contributes to the adequate treatment of patients and the necessary prevention of thrombus formation.
7
Sagan, Agnieszka, Wojciech Mrowiecki, Tomasz Mikolajczyk, Karol Urbanski, Mateusz Siedlinski, Ryszard Nosalski, Ryszard Korbut, and Tomasz Guzik. "Local inflammation is associated with aortic thrombus formation in abdominal aortic aneurysms." Thrombosis and Haemostasis 108, no. 11 (2012): 812–23. http://dx.doi.org/10.1160/th12-05-0339.
Повний текст джерелаАнотація:
SummaryIntraluminal thrombus formation in aortic abdominal aneurysms (AAA) is associated with adverse clinical prognosis. Interplay between coagulation and inflammation, characterised by leukocyte infiltration and cytokine production, has been implicated in AAA thrombus formation. We studied leukocyte (CD45+) content by flow cytometry in AAA thrombi from 27 patients undergoing surgical repair. Luminal parts of thrombi were leukocyte-rich, while abluminal segments showed low leukocyte content. CD66b+ granulocytes were the most prevalent, but their content was similar to blood. Monocytes (CD14+) and T cells (CD3+) were also abundant, while content of B lymphocytes (CD19+) and NK cells (CD56+CD16+) were low. Thrombi showed comparable content of CD14highCD16− monocytes and lower CD14highCD16+ and CD14dimCD16+, than blood. Monocytes were activated with high CD11b, CD11c and HLA-DR expression. Total T cell content was decreased in AAA thrombus compared to peripheral blood but CD8 and CD3+CD4-CD8− (double negative T cell) contents were increased in thrombi. CD4+ cells were lower but highly activated (high CD69, CD25 and HLA-DR). No differences in T regulatory (CD4+CD25+FoxP3+) cell or pro-atherogenic CD4+CD28null lymphocyte content were observed between thrombi and blood. Thrombus T cells expressed high levels of CCR5 receptor for chemokine RANTES, commonly released from activated platelets. Leukocyte or T cell content in thrombi was not correlated with aneurysm size. However, CD3+ content was significantly associated with smoking in multivariate analysis taking into account major risk factors for atherosclerosis. In conclusion, intraluminal AAA thrombi are highly inflamed, predominantly with granulocytes, CD14highCD16− monocytes and activated T lymphocytes. Smoking is associated with T cell infiltration in AAA intraluminal thrombi.
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Stolla, Moritz, Lucia Stefanini, Jessica Hirsch, Claire Roden, Timothy Daniel Ouellette, Mortimer Poncz, and Wolfgang Bergmeier. "The Signaling Molecule CalDAG-GEFI Represents a Novel Target for Antithrombotic Therapy." Blood 114, no. 22 (November 20, 2009): 1077. http://dx.doi.org/10.1182/blood.v114.22.1077.1077.
Повний текст джерелаАнотація:
Abstract Abstract 1077 Poster Board I-99 Background/Objective: The signaling molecule Ca2+ and diacylglycerol regulated guanine nucleotide exchange factor I (CalDAG-GEFI) plays a crucial role in the immediate, Ca2+ dependent activation of Rap1 and intergrin αaIIbβ3 in stimulated platelets. Our previous studies demonstrated that signaling by protein kinase C and the Gi-coupled receptor for ADP, P2Y12, provides an alternative pathway that facilitates the delayed but prolonged activation of Rap1. P2Y12 inhibitors such as clopidogrel bisulfate (Plavix) are currently considered the gold standard for the prevention and treatment of thrombotic complications. The aims of the study were to: 1) evaluate CalDAG-GEFI signaling as a potential new target for antithrombotic therapy and 2) to compare the contribution of CalDAG-GEFI and P2Y12 signaling to thrombus formation in pre-clinical models of models of thrombotic disease. Methods/Results: Thrombus formation was compared in: wildtype (WT), CalDAG-GEFI-/-, WT treated with clopidogrel (clopidogrel was administered orally 24h and 3h prior to the experiment at a dosage of 0,075mg/g bodyweight) and CalDAG-GEFI-/- mice treated with clopidogrel. Thrombosis was studied in three different models: 1) laser-induced thrombosis in the microcirculation of the cremasteric muscle (thrombin-dependent, localized), tissue factor-induced pulmonary thromboembolism (thrombin-dependent, systemic) and FeCl3-induced thrombosis in the mesentery (collagen/thrombin-dependent, localized). As shown previously, clopidogrel treatment significantly reduced but did not abolish laser-induced thrombus formation in WT mice. Laser induced thrombosis was completely inhibited in arterioles of CalDAG-GEFI -/- mice, while significant thrombus formation was observed in venules. Clopidogrel treatment of CalDAG-GEFI-/- mice further reduced venous thrombus formation, providing in vivo confirmation that platelet aggregation in the absence of CalDAG-GEFI requires P2Y12 signaling. In line with these findings, we observed that CalDAG-GEF-/- mice were partially protected from tissue factor-induced pulmonary thromboembolism when compared to clopidogrel-treated CalDAG-GEF-/- mice. In the model of FeCl3-induced thrombosis, CalDAG-GEFI-/- platelets adhered to the damaged vascular wall but failed to form thrombi in both venules and arterioles. In contrast clopidogrel-treated WT mice were protected from FeCl3-induced vessel occlusion but continuously formed embolizing thrombi of considerable size that contained activated platelets. This phenomenon was detectable in both arterioles and venules and might be of clinical relevance. Conclusion: Our studies identify CalDAG-GEFI as a promising new target for antiplatelet therapy. CalDAG-GEFI inhibition will have a strong antithrombotic effect as it is a critical component of the near-immediate platelet response to exposed extracellular matrix and/or soluble agonists. However, backup by PKC/P2Y12 signaling should allow for the formation of small but stable mural thrombi, especially under low flow conditions as found in veins and in venules, thus limiting the risk of bleeding complications. Disclosures: Poncz: Diagnostica Stago: Patents & Royalties.
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Lindenblatt, Nicole, Michael D. Menger, Ernst Klar, and Brigitte Vollmar. "Sustained hypothermia accelerates microvascular thrombus formation in mice." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 6 (December 2005): H2680—H2687. http://dx.doi.org/10.1152/ajpheart.00425.2005.
Повний текст джерелаАнотація:
Cold is supposed to be associated with alterations in blood coagulation and a pronounced risk for thrombosis. We studied the effect of clinically encountered systemic hypothermia on microvascular thrombosis in vivo and in vitro. Ferric chloride-induced microvascular thrombus formation was analyzed in cremaster muscle preparations from hypothermic mice. Additionally, flow cytometry and Western blot analysis was used to evaluate the effect of hypothermia on platelet activation. To test whether preceding hypothermia predisposes for enhanced thrombosis, experiments were repeated after hypothermia and rewarming to 37°C. Control animals revealed complete occlusion of arterioles and venules after 742 ± 150 and 824 ± 172 s, respectively. Systemic hypothermia of 34°C accelerated thrombus formation in arterioles and venules (279 ± 120 and 376 ± 121 s; P < 0.05 vs. 37°C). This was further pronounced after cooling to 31°C (163 ± 57 and 281 ± 71 s; P < 0.05 vs. 37°C). Magnitude of thrombin receptor activating peptide (TRAP)-induced platelet activation increased with decreasing temperatures, as shown by 1.8- and 3.0-fold increases in mean fluorescence after PAC-1 binding to glycoprotein (GP)IIb-IIIa and 1.6- and 2.9-fold increases of fibrinogen binding on incubation at 34°C and 31°C. Additionally, tyrosine-specific protein phosphorylation in platelets was increased at hypothermic temperatures. In rewarmed animals, kinetics of thrombus formation were comparable to those in normothermic controls. Concomitantly, spontaneous and TRAP-enhanced GPIIb-IIIa activation did not differ between rewarmed platelets and those maintained continuously at 37°C. Moderate systemic hypothermia accelerates microvascular thrombosis, which might be mediated by increased GPIIb-IIIa activation on platelets but does not cause predisposition with increased risk for microvascular thrombus formation after rewarming.
10
Ding, Katharina J., Victoria L. Cammann, Konrad A. Szawan, Barbara E. Stähli, Manfred Wischnewsky, Davide Di Vece, Rodolfo Citro, et al. "Intraventricular Thrombus Formation and Embolism in Takotsubo Syndrome." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 1 (January 2020): 279–87. http://dx.doi.org/10.1161/atvbaha.119.313491.
Повний текст джерелаАнотація:
Objective: Takotsubo syndrome (TTS) is characterized by acute left ventricular dysfunction, which can contribute to intraventricular thrombus and embolism. Still, prevalence and clinical impact of thrombus formation and embolic events on outcome of TTS patients remain unclear. This study aimed to investigate clinical features and outcomes of patients with and without intraventricular thrombus or embolism. Additionally, factors associated with thrombus formation or embolism, as well as predictors for mortality, were identified. Approach and Results: TTS patients enrolled in the International Takotsubo Registry at 28 centers in Australia, Europe, and the United States were dichotomized according to the occurrence/absence of intraventricular thrombus or embolism. Patients with intraventricular thrombus or embolism were defined as the ThrombEmb group. Of 1676 TTS patients, 56 (3.3%) patients developed intraventricular thrombus and/or embolism following TTS diagnosis (median time interval, 2.0 days [range, 0–38 days]). Patients in the ThrombEmb group had a different clinical profile including lower left ventricular ejection fraction, higher prevalence of the apical type, elevated levels of troponin and inflammatory markers, and higher prevalence of vascular disease. In a Firth bias-reduced penalized-likelihood logistic regression model apical type, left ventricular ejection fraction ≤30%, previous vascular disease, and a white blood cell count on admission >10×10 3 cells/μL emerged as independent predictors for thrombus formation or embolism. Conclusions: Intraventricular thrombus or embolism occur in 3.3% of patients in the acute phase of TTS. A simple risk score including clinical parameters associated with intraventricular thrombus formation or embolism identifies patients at increased risk. Clinical Trial Registration: URL: http://www.clinicaltrials.gov . Unique identifier: NCT01947621.
Дисертації з теми "Thrombus Formation Risk"
1
TASSO, PAOLA. "Morphometric and Hemodynamic Characterization of Patient-Specific Post-EVAR Models: A Computational Study." Doctoral thesis, Politecnico di Torino, 2020. http://hdl.handle.net/11583/2823949.
Повний текст джерела
2
Lobo, Inês de Castro Gonçalves de Almada. "Molecularly engineered materials for selective albumin binding to reduce the risk of thrombus formation." Doctoral thesis, 2009. http://hdl.handle.net/10216/61628.
Повний текст джерела
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Lobo, Inês de Castro Gonçalves de Almada. "Molecularly engineered materials for selective albumin binding to reduce the risk of thrombus formation." Tese, 2009. http://hdl.handle.net/10216/61628.
Повний текст джерелаКниги з теми "Thrombus Formation Risk"
1
Lancellotti, Patrizio, and Bernard Cosyns. Cardiac Source of Embolism (SOE) and Cardiac Masses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0014.
Повний текст джерелаАнотація:
Embolism of cardiac origin accounts for around 15–30 per cent of ischaemic strokes. The diagnosis of a cardio-embolic source of stroke is frequently uncertain and relies on the identification of a potential cardiac source of embolism in the absence of significant cerebrovascular occlusive disease. In this respect, echocardiography (both transthoracic and/or transoesophageal) serves as a cornerstone in the evaluation, diagnosis, and managementof these patients. A clear understanding of the various types of cardiac conditions associated with cardio-embolic stroke and their intrinsic risk is therefore very important. This chapter describes three categories of cardio-embolic sources of embolism: conditions predisposing to thrombus formation; cardiac masses; and cardiac conduits for paradoxical embolization. It focuses on cardiac masses and potential sources of embolism including vegetations, thrombi, cardiac tumours, non-neoplastic masses, extracardiac masses, suggesting differential diagnosis with structures that may mime pathologic conditions.
2
Jones, Michael, Norman Qureshi, and Kim Rajappan. Atrial fibrillation. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0116.
Повний текст джерелаАнотація:
Atrial fibrillation is a tachycardia arising in the atria, with atrial electrical activity occurring chaotically and continuously, without any effective atrial contraction occurring. The effects of this are an irregular ventricular rate, loss of the atrial contribution to ventricular filling, and the pooling of blood in the atria, thus increasing the risk of thrombus formation. The ventricular rate may be fast, slow, or of normal speed, depending on the state of the patient’s atrioventricular conduction. Atrial fibrillation is classified as paroxysmal (self-terminating within 7 days), persistent (lasting longer than 1 week, or requiring cardioversion to terminate) or permanent (cardioversion unable to terminate durably to sinus rhythm).
3
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.
Повний текст джерелаАнотація:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
4
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.
Повний текст джерелаАнотація:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
5
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.
Повний текст джерелаАнотація:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
6
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.
Повний текст джерелаАнотація:
Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
7
van Lier, Felix, and Robert Jan Stolker. Preoperative assessment and optimization. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0040.
Повний текст джерелаАнотація:
Perioperative cardiovascular complications (including myocardial ischaemia and myocardial infarction) are the predominant cause of morbidity and mortality in patients undergoing non-cardiac surgery. The pathophysiology of perioperative myocardial infarction is complex. Prolonged myocardial ischaemia due to the stress of surgery in the presence of a haemodynamically significant coronary lesion, leading to subendocardial ischaemia, and acute coronary artery occlusion after plaque rupture and thrombus formation contribute equally to these devastating events. Perioperative management aims at optimizing the patient’s condition by identification and modification of underlying cardiac risk factors and diseases. The first part of this chapter covers current knowledge on preoperative risk assessment. Current risk indices, the value of additional testing, and new preoperative cardiac risk makers are investigated. During recent decades there has been a shift from the assessment and treatment of the underlying culprit coronary lesion towards a systemic medical therapy aiming at prevention of myocardial oxygen supply–demand mismatch and coronary plaque stabilization. In the second part of this chapter, risk-reduction strategies are discussed, including β-blocker therapy, statins, and aspirins. A central theme in this chapter will focus on long-term cardiovascular risk reduction. Patients who undergo non-cardiac (vascular) surgery are particularly prone to long-term adverse cardiac outcomes. The goal of perioperative cardiovascular risk identification and modification should not be limited to the perioperative period, but should extend well into the postoperative period.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
Повний текст джерелаАнотація:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
9
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
Повний текст джерелаАнотація:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
10
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
Повний текст джерелаАнотація:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
Частини книг з теми "Thrombus Formation Risk"
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Morales, Xabier, Jordi Mill, Kristine A. Juhl, Andy Olivares, Guillermo Jimenez-Perez, Rasmus R. Paulsen, and Oscar Camara. "Deep Learning Surrogate of Computational Fluid Dynamics for Thrombus Formation Risk in the Left Atrial Appendage." In Statistical Atlases and Computational Models of the Heart. Multi-Sequence CMR Segmentation, CRT-EPiggy and LV Full Quantification Challenges, 157–66. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39074-7_17.
Повний текст джерела
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Andina Munawar, Dian, Anggia Chairuddin Lubis, and Muhammad Munawar. "Left Atrial Appendage Occlusion: Current and Future." In Atrial Fibrillation - Diagnosis and Management in the 21st Century [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105776.
Повний текст джерелаАнотація:
Patients with non-valvular atrial fibrillation (NVAF) are at an increased risk of ischemic stroke due to the risks of thrombus formation. The left atrial appendage (LAA) is shown to be “the culprit” of thromboembolic events in NVAF and is currently a therapeutic target to prevent stroke. The absolute benefit of oral anticoagulation in the management of NVAF to improve cardiovascular outcomes has been well established. However, some patients are not good long-term candidates for oral anticoagulation for many reasons, including risks of bleeding, noncompliant to oral anticoagulation (OAC). Left atrial appendage occlusion (LAAO) provides an attractive alternative to reduce the risk of stroke for those who are contraindicated to OAC therapy.
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Miranda, Haley Goucher. "An LVAD Patient Presenting With Intracranial Hemorrhage." In Critical Care, 245–54. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/med/9780190885939.003.0032.
Повний текст джерелаАнотація:
Abstract Patients with implanted durable left ventricular assist devices (LVADs) are increasing in prevalence as expertise with surgical implantation and subsequent management continues to improve. LVAD patients require chronic anticoagulation due to the risk of thrombus formation in the pump motor. They are thus at risk of both hemorrhagic and thromboembolic events, which pose significant challenges for the intensivist. LVAD patients are at high risk for hemorrhagic expansion due to their multiple mechanisms of coagulopathy, but reversal of anticoagulation must be done cautiously due to the risk of LVAD pump thrombosis. Management may also be complicated due to reduced pulsatility associated with continuous-flow devices in addition to the lack of formal guidelines for blood pressure goals in the setting of acute stroke.
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Guttmann, Oliver P., Ronald Binder, Oliver Gämperli, and Andreas Baumbach. "Antithrombotics for Acute and Chronic Coronary Syndromes." In Manual of Cardiovascular Medicine, 117–24. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198850311.003.0014.
Повний текст джерелаАнотація:
Thrombus formation involves activation of aggregating platelets as well as the formation of fibrin after activation of the coagulation cascade. Fibrin eventually binds to glycoprotein IIB/IIIA receptors on platelets thereby forming a very solid occlusive clot. There are several molecules interfering with platelet activation: (1) aspirin, which blocks the formation of thromboxane A2; (2) clopidogrel, prasugrel, and ticagrelor which block P2Y12 receptors and their activation by ADP; (3) glycoprotein inhibitors that interfere with glycoprotein IIB/IIIA on platelets, the final common pathway of platelet activation, and finally (4) thrombin inhibitors blocking PAR-1 receptors on platelets. Commonly, after an acute coronary syndrome (ACS) or after percutaneous coronary interventions (PCI) or even bypass surgery, dual antiplatelet therapy (DAPT) is recommended consisting of aspirin plus a P2Y12 inhibitor. The duration of treatment after the acute event is commonly 12 months for those with ACS and 6 months for those with a high bleeding risk. In patients with high ischaemic risk, prolonged DAPT treatment can be considered, but often such patients also have a high bleeding risk. Intravenous platelet inhibitors, such as Reopro, tirofiban, and others, are used mainly during PCI, particularly in patients with ACS. Inhibitors of coagulation cascade, such as factor Xa or factor II inhibitors or vitamin K antagonists are mainly used in patients with ACS and concomitant atrial fibrillation. In these patients, mainly aspirin or in some the P2Y12 inhibitor is skipped for some weeks or months.
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Myat, Aung, and Tony Gershlick. "The contemporary use of antiplatelet therapy in interventional cardiology." In Oxford Textbook of Interventional Cardiology, 418–40. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199569083.003.024.
Повний текст джерелаАнотація:
Accepting that the adhesion, activation, and aggregation of platelets plays a central role in the initial formation and subsequent propagation of intracoronary thrombi, antiplatelet therapy (APT) has become central to the management of a number of manifestations of cardiovascular (CV) disease; not least in preventing the deleterious effects of stent thrombosis (ST) that can follow percutaneous coronary intervention (PCI) with stent deployment. PCI causes significant local trauma to the vessel wall leading to exposure of the subendothelium and release of its thrombogenic constituents into the intravascular environment resulting in an increased risk of vaso-occlusive complications. Exposure of the stent struts can further stimulate platelet adherence to the non-endothelialized vessel wall and accelerate activation and aggregation. Furthermore, PCI can also potentiate the release of vasoactive agents from the platelet-rich thrombus. This may be of particular importance when PCI is undertaken in those presenting with acute coronary syndromes (ACS) where plaque disruption has already locally activated platelets by exposing the flowing blood constituents to thrombogenic plaque contents.
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Haldar, Shouvik. "Removal (Extraction) of Pacemakers and ICD Leads." In Manual of Cardiovascular Medicine, 259–64. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198850311.003.0032.
Повний текст джерелаАнотація:
Most cardiac implantable electronic devices (CIEDs) use leads or electrodes to connect the device generator to cardiac tissues, and as such, they are foreign bodies that can activate coagulation, thrombus formation, or be a site of infection, as bacteria attached to leads are difficult for the immune system to reach. Risk factors for complications are diabetes, renal disease, and COPD among others. Suspected infection has to be evaluated carefully using transoesophageal echocardiography, blood cultures, wound swabs inflammatory markers and often the CIEDs have to be removed if suspicion is confirmed. Removal can be achieved today with special technology and requires the experience and skills of the operator to avoid major complications, particularly bleeding.
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Panikker, Sandeep, Tim Betts, and Milena Leo. "Left atrial appendage occlusion." In Oxford Textbook of Interventional Cardiology, edited by Simon Redwood, Nick Curzen, and Adrian Banning, 703–14. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754152.003.0047.
Повний текст джерелаАнотація:
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, affecting 1.5–2% of the general population and more than 8% of those older than 80 years. Because of the progressive ageing of our population, an exponential increase in incidence is expected over the next few decades. Patients with AF have an increased mortality and morbidity, particularly owing to fatal or disabling stroke. The risk of embolic stroke is five times higher in the presence of AF, with an average annual rate around 5%, but there is a progressive increase with age and the presence of other risk factors, such as prior stroke or transient ischaemic attack, hypertension, diabetes mellitus, congestive heart failure, female sex, and vascular disease, as predicted by the CHADS2 and the CHA2DS2-VASc scores. Moreover, strokes associated with AF are more severe, with a 50% greater likelihood of becoming disabled or handicapped and more than 50% likelihood of death. Intracardiac thrombus formation due to the Virchow triad of events (endothelial or endocardial damage or dysfunction, abnormal blood stasis, and altered haemostasis, platelet function, and fibrinolysis) followed by distal embolization leads to thromboembolic events manifest as transient ischaemic attack, ischaemic stroke, and peripheral embolism in patients with AF.
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Badimon, Lina, and Gemma Vilahur. "Atherosclerosis and thrombosis." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 447–62. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0037.
Повний текст джерелаАнотація:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to extracellular vesicles (mainly microvesicles) a role in all stages of atherosclerosis development and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Becker, Richard C., and Frederick A. Spencer. "Atherosclerosis and Arterial Thrombosis." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0007.
Повний текст джерелаАнотація:
The development of atherosclerotic vascular disease represents a major risk for myocardial infarction, stroke, and occlusive peripheral vascular events. Although unique in their own right, atherosclerosis and arterial thrombosis share common origins and are linked by genetic, pathologic, and environmental factors. An increased knowledge base and in-depth understanding of vascular biology has laid the groundwork for prevention and targeted therapies. Coronary atherosclerosis has been described macroscopically over the past century and a half by renowned pathologists and clinicians ranging from Von Rokitansky and Virchow to Osler. The pathologic sequence of events includes an initiating step, defined as the fatty streak, followed by plaque maturation and transition, setting the stage for intravascular thrombosis. The progression of coronary atherosclerosis varies widely among individuals, as does the time course and influence of recognized risk factors. Observations at the microscopic and cellular levels have contributed substantially to unraveling several of the mysteries that surround human atherosclerosis and fostering a clearer view of the mechanisms leading to intravascular thrombosis. It is now evident that the atherosclerotic plaque and its cellular components represent an ideal substrate for thrombus formation. Thus, the term “atherothrombosis” appears fitting. In experimental animals, focal sites of predilection for either spontaneous or dietary induced atherosclerosis can be determined reliably prior to plaque development. These areas are delineated by their in vivo uptake of the protein-binding azo dye Evans blue. Salient features of these lesion-prone areas include increased endothelial permeability and intimal accumulation of plasma proteins, including albumin, fibrinogen, and low-density lipoproteins (LDLs). There is also increased endothelial cell turnover. Overall, the “prelesion” area within endothelial cells takes on a unique appearance, and the surface glycocalyx is two- to fivefold thinner than normal endothelial cells (Caplan et al., 1974). Lesion-prone areas within blood vessel walls exhibit a unique property of blood monocyte recruitment, followed by accumulation of these cells in the subendothelial space, a process that is accelerated in the presence of hyperlipidemia.
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Mogensen, Jens, and Torsten B. Rasmussen. "Left ventricular non-compaction: diagnosis and clinical management." In ESC CardioMed, 1509–12. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0364.
Повний текст джерелаАнотація:
Left ventricular non-compaction (LVNC) is characterized by a specific morphological appearance of the myocardium with an inner non-compacted hypertrabeculated layer and deep recesses communicating with the left ventricular cavity, and an outer compacted myocardium. LVNC is a specific morphological finding and may be present in healthy individuals with apparently normal hearts and in patients with various cardiac and systemic conditions including X-linked Barth syndrome, cardiomyopathies, congenital heart diseases, and non-cardiac systemic diseases. Recent investigations have revealed that LVNC may appear as the sole manifestation of disease in carriers of genetic mutations associated with dilated and hypertrophic cardiomyopathies. Therefore, it is important to consider the possibility of familial disease when diagnosing LVNC and explore the family history of the patient. Clinical screening of relatives should be offered when familial disease is suspected or when LVNC remains unexplained. Anticoagulation should be considered when LVNC appears in patients with impaired systolic function of the left ventricle to avoid formation of thrombi and cardiac embolization following an assessment of the entire risk profile of the individual patient.
Тези доповідей конференцій з теми "Thrombus Formation Risk"
1
Chesnutt, Jennifer K. W., and Hai-Chao Han. "Contributions of Platelet Activation and Collision to Thrombus Formation in Tortuous Venules." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80579.
Повний текст джерелаАнотація:
Vessel tortuosity is often seen in humans in association with various conditions, including thrombosis.1–3 Thrombosis is a major contributor to cardiovascular disease, which is the leading cause of death in the U.S. Tortuosity can increase shear stress that can activate platelets, which can lead to thrombosis.4 A fundamental gap exists in understanding how vessel tortuosity regulates thrombosis through such microscale physical mechanisms. Solving this problem is essential to assess the risk of thrombosis and to develop new treatment strategies.
2
Hame, C. W., R. L. Lorenz, H. Kuooer, N. Bleifeld, and P. C. Weber. "BIOCHEMICAL EVIDENCE OF THROMBUS FORMATION IN PATIENTS NITH PERSISTENT UNSTABLE ANGINA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643780.
Повний текст джерелаАнотація:
Thromboxane released from activated platelets and prostacyclin of the vessel wall may act as potent antagonistic modulators of platelet aggregability and coronary vascular tone. Therefore we studied urinary excretion of their major metabolites, 2,3-dinor-throeboxane B2 (TX-M)and 2,3-dinor-6-keto prostaglandin F, (PGI-H), in 16 patients presenting Mith prolonged angina at rest. The 10 patients who did not improve under vigorous antianginal treatment within 48 hours exhibited higher TX-M excretion than 6 patients responding to therapy (2208 ± 1542 vs 609 ± 312 ng/g creatinine) p<0.01). Elevated TX-H excretion Mas also found in 4/8 patients Mith sustained post-infarction angina. Mhen 9 patients Mere re-studied in a stable phase after 11 ± 5 Months TX-H Mas consistently in the norial or high normal range. Excretion of PGI-M Mas not depressed in any patient but correlated Meakly Mith TX-M (r=0.408). Thus, enhanced TX-M excretion as index of platelet activation lay identify patients Mho are at increased risk of active throsbus formation and Mho could benefit lost froi anti-aggregatory treatment.
3
Qureshi, Ahmed, Omar Darwish, Desmond Dillon-Murphy, Henry Chubb, Steven Williams, Dmitry Nechipurenko, Fazoil Ataullakhanov, David Nordsletten, Oleg Aslanidi, and Adelaide de Vecchi. "Modelling Left Atrial Flow and Blood Coagulation for Risk of Thrombus Formation in Atrial Fibrillation." In 2020 Computing in Cardiology Conference. Computing in Cardiology, 2020. http://dx.doi.org/10.22489/cinc.2020.219.
Повний текст джерела
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Reuter, Steven P., Ian R. Prechtl, Steven W. Day, and Jason R. Kolodziej. "Left Ventricular Assist Device Thrombus Detection Using Wavelets and Image Classification." In ASME 2020 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/imece2020-24465.
Повний текст джерелаАнотація:
Abstract Cardiac related diseases are a common health risk for adults. Consequently, therapies such as heart transplants and medication exist to treat these ailments. Heart transplants remain the gold standard for treating severe heart failure, however, left ventricular assistive devices, a cardiac blood pump, are gaining popularity and not just as a bridge for long term care. Unfortunately, with the benefits of these devices come risks of clot formation. These occlusions can cause strokes, further cardiac damage, or even death. Therefore, these occlusions must be detected at the onset. This work presents a method to non-invasively monitor the condition of a Thoratec HeartMate II ventricular device. The application of a neural network and a classification tree are designed to detect the presence of an aortic graft occlusion that has been seeded into an in vitro cardiac simulator. Using acoustic digital heart sounds, the classification tree showed the most favorable results, outperforming the existing support vector machine method by roughly 20%.
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Gårdhagen, Roland, Fredrik Carlsson, and Matts Karlsson. "Large Eddy Simulation of Steady and Pulsating Flow in Asymmetric Stenosed Pipe." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19474.
Повний текст джерелаАнотація:
Local hemodynamics and its impact on the development of cardiovascular disease and the blood itself have gained increasing attention during the last decades. Regions with low and/or oscillatory Wall Shear Stress (WSS) have been correlated with increased risk for development of atherosclerosis [1]; and turbulence in the cardio vascular system is suggested to increase the risk for hemolysis as well as platelet activation and thrombus formation [2, 3]. Furthermore, turbulent flows are inherently oscillatory with large spatial as well as temporal fluctuation, and hence possibly a risk for atherosclerosis development per se.
6
Falk, E. A. "UNSTABLE ANGINA PECTORIS: PATHOLOGIC ASPECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643711.
Повний текст джерелаАнотація:
Unstable angina pectoris represents a common and important manifestation of acute ischemic heart disease encompassing the broad spectrum of clinical syndromes between stable effort angina and acute myocardial infarction. This group of patientsisfar from uniform concerning underlying pathogenetic mechanisms and prognosis, but generally the risk of infarction or deathis increased during the unstable period. Most patients are presenting with new or worsening effort angina or angina at rest,and especially patients with rest anginaassociated with transient ECG changes seem to constitute a high risk subgroup. Transient reductions in coronary blood flow,rather than increases in myocardial oxygen demand, seem to play the major role in rest angina, indicating an underlying 'dynamic' coronary stenosis.Furthermore, unstable angina seems to beagood clinicalmarker for actively progressing coronary-artery disease.Pathologically, a rapidly evolving coronary-artery lesion represented by a disrupted atherosclerotic plaque with variable degree of plaque hemorrhage and luminalthrombosis usually is present in patientscoming to autopsy after a period of rest angina. The thrombus at the rupture site may be mural and limited (just sealing therupture) or occlusive depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less tha15% stenosis (histologic area stenosis), but is found with increasing frequency when stenosis severety increases beyond 15%.Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits. Aggregated platelets usually can be identified in the mostrecent part of the thrombus, while older parts are more homogeneous due to fibrin infiltration/stabilization. Additionally,microemboli and microinfarcts are frequently found in the myocardium downstream tocoronary thrombi. So, the period of unstable angina preceding a fatal heart attackseems to be characterized by an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation alternates with intermittent thrombus fragmentation and peripheral embolization. Such a dynamic thrombosis (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other clearly thrombus-related acute ischemic events: myocardial infarction or sudden death.Clinical studies using coronary angiography and coronary angioscopy during the acute phase of unstable angina have revealed a high frequency of ulcerated (unstable) atherothrombotic lesion in arteries responsible for the acute ischemia. Furthermore, episodic platelet activation (usually associated with chest pain) has recently been demonstrated in patients with unstable angina.The mechanism underlying pain/ischemia(predominantly spasm?) and the rapid plaque progression (plaque hemorr.hage/luminal thrombosis?) during unstable angina maydiffer. Accordingly, therapy directed against a possible spasm (nitrates, calcium antagonists) usually relieves pain effectively without having any documented effect on infarction/survival, while antithr-ombotic therapy (aspirin, heparin) clearlyimproves the prognosis without apparent antianginal effect. Therefore, with the objective not only of relieving pain but also of improving the prognosis, more attention should be paid to the potentially fatal thrombotic process that apparently isgoing on in a major coronary artery of many patients with unstable angina.
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Girdhar, Gaurav, Yared Alemu, Michalis Xenos, Jawaad Sheriff, Jolyon Jesty, Shmuel Einav, and Danny Bluestein. "Design Optimization of a Mechanical Heart Valve for Reducing Valve Thrombogenicity: A Case Study With ATS Valve." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19309.
Повний текст джерелаАнотація:
Flow past mechanical heart valves (MHV) in mechanical circulatory support devices including total artificial hearts and ventricular assist devices, is primarily implicated in thromboembolism due to non-physiological flow conditions where the elevated stresses and exposure times are sufficiently high to cause platelet activation and thrombus formation. Mitigation of this risk requires lifelong anticoagulation therapy and less thrombogenic MHV designs should therefore be developed by device manufacturers [1].
8
Donohue, Eilis M., Kevin B. Heraty, and Nathan J. Quinlan. "A Scaled-Up Mechanical Prosthetic Heart Valve Model for High-Resolution Flow Field Measurements." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176495.
Повний текст джерелаАнотація:
Every year, over 250,000 patients undergo heart valve implantation [1]. Approximately 55% of implanted prosthetic heart valves (PHV) are mechanical. Patients must undergo lifelong anticoagulant medication in order to alleviate the risk of thrombus formation. In order to understand the complex fluid dynamics underpinning problems such as thrombosis, detailed high-resolution quantitative information on the flow field in PHVs is essential [2]. High-resolution data is also needed for the validation of Computational Fluid Dynamics (CFD) studies.
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Sengupta, Dibyendu, Jane C. Burns, Andrew Kahn, and Alison L. Marsden. "Patient-Specific Hemodynamic Simulations in a Group of Patients With Coronary Artery Aneurysms Caused by Kawasaki Disease." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14842.
Повний текст джерелаАнотація:
Kawasaki disease (KD) is an acute febrile illness that can result in life threatening coronary artery aneurysms in up to 25% of untreated patients. These aneurysms put patients at risk for thrombus formation, myocardial infarction and sudden death. Currently, clinical decisions are made based on anatomy alone, with aneurysm diameter > 8mm as the arbitrary cutoff for anticoagulation therapy, despite a lack of evidence for this choice. We postulate that patient specific hemodynamics may be a better predictor for the risk of thrombosis than maximum diameter alone. To quantify hemodynamics, we performed computational fluid dynamics (CFD) simulations using patient specific models with custom coronary boundary conditions.
10
Lantz, Jonas, Johan Renner, and Matts Karlsson. "Wall Shear Stress in an MRI-Based Subject-Specific Human Aorta Using Fluid-Structure Interaction." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19346.
Повний текст джерелаАнотація:
Wall shear stress (WSS) is well established as an indicator of increased risk for development of atherosclerotic plaques, platelet activation and thrombus formation [1]. Prediction and simulation of the sites of wall shear stresses that are deemed dangerous before intervention would be of great aid to the surgeon. However, the geometries used for these types of simulations are often approximated to be rigid. To more accurately capture the flow and arterial wall response of a realistic human aorta, fluid-structure interaction (FSI) which allows movement of the wall, is needed. Hence, the pressure wave and its effect on the wall motion are resolved and enables a more physiological model as compared to a rigid wall case.