Extensive coronary thrombosis in thrombotic–thrombocytopenic purpura

Hasper, Dietrich; Schrage, D.; Niesporek, Silvia; Knollmann, Friedrich D; Barckow, D.; Oppert, Michael

doi:10.1016/j.ijcard.2004.12.095

Cited by 20 publications

(29 citation statements)

References 6 publications

(4 reference statements)

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“…One of the typical signs of TTP is MI/R injury, suggesting a link between low ADAMTS13 activity and MI/R injury. [12][13][14][15][16] Clinical studies revealed that low ADAMTS13 (and high VWF) levels are associated with an increased risk of MI. 6,[17][18][19][20][21][22] ADAMTS13 polymorphisms that decrease ADAMTS13 activity are also associated with an increased risk of death in patients with coronary artery Figure 2.…”

Section: Discussionmentioning

confidence: 99%

Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice

Meyer

Savchenko

Haas

et al. 2012

Blood

105

123

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Coronary heart disease is a major cause of death in the western world. Although essential for successful recovery, reperfusion of ischemic myocardium is inevitably associated with reperfusion injury. To investigate a potential protective role of ADAMTS13, a protease cleaving von Willebrand factor multimers, during myocardial ischemia/reperfusion, we used a mouse model of acute myocardial infarction. We found that Adamts13 ؊/؊ mice developed larger myocardial infarctions than wild-type control mice, whereas treatment of wild-type mice with recombinant human ADAMTS13 (rhADAMTS13) led to smaller infarctions. The protective effect of ADAMTS13 was further confirmed by a significant reduction of cardiac troponin-I release and less myocardial apoptosis in mice that received rhADAMTS13 compared with controls. Platelets adherent to the blood vessel wall were observed in few areas in the heart samples from mice treated with vehicle and were not detected in samples from mice treated with rhADAMTS13. However, we observed a 9-fold reduction in number of neutrophils infiltrating ischemic myocardium in mice that were treated with rhADAMTS13, suggesting a potent anti-inflammatory effect of ADAMTS13 during heart injury. Our data show that ADAMTS13 reduces myocardial ischemia/reperfusion injury in mice and indicate that rhADAMTS13 could be of therapeutic value to limit myocardial ischemia/reperfusion injury. (Blood. 2012;120(26):5217-5223) IntroductionCoronary heart disease is the leading cause of death in the western world with approximately 1 million myocardial infarctions (MIs) each year just in the United States. 1,2 Acute myocardial infarction (AMI) is caused by thrombotic occlusion of a coronary artery. Although rapid restoration of the coronary circulation is critical for successful treatment, reperfusion itself exacerbates injury of previously ischemic myocardium. 1 The exact mechanisms of myocardial ischemia/reperfusion (MI/R) injury are not fully understood. 1 Given that cardiac ischemia is either unpredictable (MI) or inevitable (in patients undergoing cardioplegic arrest), there is great interest in developing strategies to minimize injury. von Willebrand factor (VWF) and its cleaving protease ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type-1 motif, member 13) play a pivotal role in platelet adhesion and thrombus formation. By specifically cleaving the VWF A2 domain, ADAMTS13 digests the most thrombogenic ultra-large VWF multimers (UL-VWF) into smaller, less hemostatically active VWF molecules. In addition, ADAMTS13's action on VWF downregulates inflammatory responses. As a result, using experimental mouse models, ADAMTS13 was shown to reduce both thrombosis and inflammation, including atherosclerosis. [3][4][5] An increasing amount of clinical evidence points to the possibility that VWF and ADAMTS13 are involved in MI pathogenesis. 6 To test this experimentally, we used a mouse model of acute myocardial infarction. Using mice deficient in ADAMTS13 and treating wild-type mice with human rhADAM...

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Section: Discussionmentioning

confidence: 99%

Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice

Meyer

Savchenko

Haas

et al. 2012

Blood

105

123

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“…41 Usled smanjene aktivnosti metaloproteinaze ADAMTS13 (usled deficita ili prisutnih inhibirajućih antitela na ADAMTS13) u TTP dolazi do akumulacije velikih multimera von Willebrandovog faktora koji agregiraju trombocite preko glikoproteina Ib/IX/V i IIb/IIIa, čak i u odsustvu fibrinogena. 43 Formiranje ovih tromba u TTP se najvećim delom odvija u arteriolama, pa rasprostanjena okluzija arteriola može dovesti do masivne nekroze miokarda. 43 Usporenje protoka krvi kroz miokard usled okludirane mikrocirkulacije može rezultirati nastankom kardiogenog šoka.…”

Section: Trombozna Trombocitopenijska Purpuraunclassified

“…43 Formiranje ovih tromba u TTP se najvećim delom odvija u arteriolama, pa rasprostanjena okluzija arteriola može dovesti do masivne nekroze miokarda. 43 Usporenje protoka krvi kroz miokard usled okludirane mikrocirkulacije može rezultirati nastankom kardiogenog šoka. 43 Pored tipičnih hijalinih mikrovaskularnih tromba u miokardu u TTP se registruju i značajne okluzije glavnih koronarnih arterija.…”

Section: Trombozna Trombocitopenijska Purpuraunclassified

Adequate evaluation of thrombocytopenias as a prerequisite to effective cardiac patient treatment

Antonijević¹,

Živković²,

Jovanović³

et al. 2012

Srce i krvni sudovi

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A dekvatan tretman kardioloških bolesnika nije moguć bez poznavanja osnovnih patogenetskih mehanizama nastanka trombocitopenije. Mada se uvođenjem perkutanih koronarnih intervencija, uz primenu standardnih i novijih antitrombocitnih (antagonista fibrinogenskih receptora -inhibitori GP IIb/ IIIa, ADP antagonista -tienopiridini) i antikoagulantnih lekova prognoza bolesnika sa akutnim koronarnim sindromom značajno poboljšala, suočeni smo i sa dodatnim rizikom od nastanka novih tipova trombocitopenije, etiološki potpuno divergentnih, ali i sa zajedničkim imeniteljem da značajno utiču na nastanak dodatnih komplikacija i povećanje mortaliteta kod inače kompleksnih bolesnika.1 Nalaz trombocitopenije kod bolesnika hospitalizovanih u kardiološkim odeljenjima do skora je predstavljao alarm da treba samo ukinuti standardno primenjene antikoagulantne i antitrombocitne lekove zbog opasnosti nastanaka hemoragijskih komplikacija.Utvrđivanje da li trombocitopenija patogenetski pripada grupi oboljenja koja se predominantno manifestuju hemoragijskim sindromom ili trombotskim manifestacijama presudno će uticati na odluku da li antitrombinsku terapiju treba ukiniti ili modifikovati uvođenjem odgovarajućih antikogulantnih i/ili antitrombocitnih lekova.Među najpoznatija oboljenja koja se ispoljavaju kao trombocitopenija propraćena prevashodno trombotskim manifestacijama spadaju: antifosfolipidni sindrom, heparinom indukovana trombocitopenija tipa II (HIT II), hronična forma diseminovane intravaskularne koagulacije (DIK), trombozna trombocitopenijska purpura (TTP) i još neki oblici o kojima diskutujemo kasnije.2,3 TTP se manifestuje znacima tromboze u mikrocirkulaciji, ali se, zavisno od stepena trombocitopenije, mogu razviti i hemoragijske komplikacije. 4 S obzirom na opasnost od brzog nastanka komplikacija, obaveza je lekara da adekvatnim laboratorijskim monitoringom blagovremeno registruje ovo oboljenje, definiše uzrok i primeni odgovarajuće mere. Definicija i podela trombocitopenijaTrombocitopenija se tradicionalno definiše kao smanjenje broja trombocita u krvi ispod 150x10 9 /L (liberalna definicija). Klinički značajno krvarenje se retko javlja ukoliko je broj trombocita iznad 50x10 Odbor za kardiovaskularnu patologiju, Srpska akademija nauka i umetnosti Poznavanje osnovnih patogenetskih mehanizama nastanka trombocitopenije je preduslov adekvatnog tretmana kompleksnih kardioloških bolesnika. Uvođenje perkutanih koronarnih intervencija uz primenu standardnih i novijih antitrombocitnih i antikoagulantnih lekova značajno je unapredilo prognozu bolesnika sa akutnim koronarnim sindromom, no i dodatno povećalo rizik od nastanka novih tipova trombocitopenije, etiološki potpuno divergentnih, ali i sa zajedničkim imeniteljem da značajno utiču na nastanak novih komplikacija i povećanje mortaliteta. Trombocitopenije koje se javljaju kao posledica perkutanih koronarnih intervencija najčešće su uzrokovane primenom heparina, GP IIb/IIIa inhibitora i jodnim kontrastnim sredstvima. Pored dobro poznate činjenice da znatan broj trombocitopenija po...

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“…Platelets in myelodysplastic syndromes are dysfunctional (3) and, after leukemic transformation and infection, bleeding is the next most common cause of death (4)(5)(6). On the other hand, thrombocytopenia itself is not protective and acute coronary syndromes have been reported in patients who have thrombocytopenia that is associated with various disorders (7)(8)(9). In the setting of cancer and hematologic malignancies, some smaller sized retrospective studies have shown that aspirin may be beneficial in thrombocytopenic patients experiencing acute coronary syndromes (10,11).…”

Section: Introductionmentioning

confidence: 99%

Antiplatelet Therapy in a Patient with Coronary Artery Disease and Myelodysplastic Syndrome with Thrombocytopenia

Fernández–Fernández¹,

Ameneiros-Lago²,

Tuñas-Gesto³

et al. 2017

Acta Med. (Hradec Kralove, Czech Repub.)

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A B ST R AC T To date, there are no sufficient data to make firm recommendations on the treatment of patients with severe thrombocytopenia who require antiplatelet therapy after experiencing acute coronary syndrome. Therefore, we think that it is important to communicate the experience with individual cases. We report the case of a patient who presented with pericardial effusion causing cardiac tamponade. He had thrombocytopenia associated with myelodysplastic syndrome, and ten weeks before this admission, percutaneous transluminal coronary angioplasty with implantation of drug-eluting stents was performed for non-ST-segment elevation acute coronary syndrome. Platelets in myelodysplastic syndromes are dysfunctional, which exacerbates bleeding from thrombocytopenia, and the management of atherosclerotic cardiovascular disease in these patients is challenging.

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Extensive coronary thrombosis in thrombotic–thrombocytopenic purpura

Cited by 20 publications

References 6 publications

Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice

Protective anti-inflammatory effect of ADAMTS13 on myocardial ischemia/reperfusion injury in mice

Adequate evaluation of thrombocytopenias as a prerequisite to effective cardiac patient treatment

Antiplatelet Therapy in a Patient with Coronary Artery Disease and Myelodysplastic Syndrome with Thrombocytopenia

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