DOCSLIB.ORG

Left Ventricular Thrombus Formation After Acute Myocardial Infarction Ronak Delewi,1 Felix Zijlstra,2 Jan J Piek1

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Education in Heart Heart: first published as 10.1136/heartjnl-2012-301962 on 14 November 2012. Downloaded from ACUTE CORONARY SYNDROMES Left ventricular thrombus formation after acute myocardial infarction Ronak Delewi,1 Felix Zijlstra,2 Jan J Piek1 < Additional references are Cardiovascular disease remains the leading cause of thrombus after discharge, often in association with published online only. To view death in western society. Mortality from acute worsening LV systolic function. Spontaneous or these references please visit the journal online (http://dx.doi.org/ myocardial infarction (AMI) has decreased since the anticoagulant induced resolution is relatively 10.1136/heartjnl-2012-301962). introduction of primary percutaneous coronary common in LV thrombus formation after AMI. 1Department of Cardiology, intervention (PCI), which has proved to be superior Thrombus seems to disappear more often in Academic Medical Center, to thrombolytic therapy by demonstrating lower patients with apical akinesia than those with apical University of Amsterdam, mortality rates and reduced clinical adverse events. aneurysm or dyskinesia.1 Amsterdam, the Netherlands Nevertheless, postinfarct complications still lead to It has been speculated that LV thrombus plays 2 Department of Cardiology, morbidity and mortality in a large number of a positive role in the acutely infarcted myocardium, Erasmus Medical Center, Rotterdam, the Netherlands patients. by offering mechanical support to the infarcted One of the most feared complications is the myocardium and therefore protecting against LV Correspondence to occurrence of thromboembolic events (mostly rupture.w4 The thrombus becomes firmly attached Professor Dr Jan J Piek, cerebrovascular accidents) due to left ventricular to its site of origin, enhancing the underlying Department of Cardiology, (LV) thrombus formation. The risk of LV thrombus myocardial scar, limiting potential infarct expan- Academic Medical Center, fi University of Amsterdam, PO formation is highest during the rst 3 months sion, and partially restoring the thickness of the Box 22660, 1100 DD following acute myocardial infarction, but the myocardial wall. As a consequence, bulging is Amsterdam, The Netherlands; potential for cerebral emboli persists in the large reduced, resulting in a more effective myocardial [email protected] population of patients with chronic LV dysfunc- contraction. Often, however, expansion of the tion. Since these thromboembolic events are infarct zone occurs very early after infarction, usually unheralded by warning signs of transient before the thrombus has time to organise and is cerebral ischaemia, the only truly satisfactory able to prevent formation of LV aneurysm and medical approach is adequate management of these myocardial rupture. high risk groups. This article discusses the inci- dence, diagnosis and management of LV thrombus http://heart.bmj.com/ formation after an AMI. INCIDENCE Early data from the prethrombolytic and throm- bolytic eras suggest that in the setting of AMI, LV PATHOGENESIS OF LV THROMBUS thrombus was present in 7e46% of patients, most The combination of blood stasis, endothelial injury frequently in acute anterior or apical myocardial e e and hypercoagulability, often referred to as infarction.2 4 w3 w5 Differences in diagnostic Virchow’s triad, is a prerequisite for in vivo techniques, timing of examination and use of thrombus formation. In the presence of LV antithrombotic treatment cause substantial varia- on September 26, 2021 by guest. Protected copyright. thrombus formation after AMI, the three compo- tion in the reported frequency of thrombus from nents of this triad can also be recognised (figure 1). different series. In addition, it should be noted that LV regional wall akinesia and dyskinesia result in the incidence as reported in autopsy studies is blood stasis, often recognised on two dimensional consistently higher compared with clinical studies, echocardiography by the occurrence of spontaneous probably due to better accuracy but also due to LV contrast. Prolonged ischaemia leads to suben- patient selection. docardial tissue injury with inflammatory changes. Nowadays the reported incidence is lower. This is Finally, patients with an acute coronary syndrome probably due to (1) more aggressive anticoagulation display a hypercoagulable state with, for example, therapies in the acute phase (eg, the use of heparin, increased concentrations of prothrombin, fibrino- bivalirudin), (2) smaller infarctions, and (3) peptide A, and von Willebrand factor, and decreased improved LV remodelling. Although the use of ACE concentrations of the enzyme responsible for inhibitors is also thought to be associated with cleaving von Willebrand factor (ADAMTS13).w1 w2 improved LV remodelling, the GISSI-3 study found This triad can result in the formation of LV no difference in LV thrombus rates between thrombus composed of fibrin, red blood cells, and patients who did and did not receive lisinopril.5 platelets. There are limited data on the exact frequency of LV thrombus can occur within 24 h after AMI. LV thrombus in PCI treated AMI patients. Two One study performing serial echocardiographic studies found LV thrombus formation in 5.4% and studies showed that about 90% of thrombi are 7.1% of patients with acute anterior wall myocar- formed at a maximum of 2 weeks after the index dial infarctions.w6 w7 However, these studies were event.w3 However, some patients develop a new LV retrospective, non-serial and only assessed LV Heart 2012;98:1743–1749. doi:10.1136/heartjnl-2012-301962 1743 Education in Heart Heart: first published as 10.1136/heartjnl-2012-301962 on 14 November 2012. Downloaded from towards the posterolateral wall. In such cases the prevalence is similar to that observed in anterior wall AMIs of comparable extension.w5 Thrombi can also be found in small apical infarcts, with good global systolic function.w3 The presence of thrombi is significantly related to the region of most severe functional impairment and/or the region with myocardial enhancement (ie, infarction or scarring).7 LV thrombus appears earlier in the course of the disease when initial ejection fraction #40%, in the presence of multi- vessel coronary artery disease, or a high peak crea- tine kinase value.w8 There is conflicting evidence with respect to the influence of b-blockers. Several studies have reported a higher frequency of thrombus develop- Figure 1 The three components of the Virchow’s triad in b left ventricular thrombus formation. ACS, acute coronary ment in patients treated with -blockers which syndrome; LV, left ventricular. could be related to the negative inotropic action of these drugs and thus increased blood stasis. In particular, in a randomised study, Johannessen et al thrombus formation at a single point in time and reported an increased occurrence of thrombus in during the early phase of recovery after myocardial patients with anterior AMI after oral b-blocker infarction. therapy.w9 Turpie et al reported similar results after In the latter study a follow-up echocardiography treatment with b-blockers in a large population of was performed at 1e3 months, showing LV 9 w7 patients with AMI. The GISSI-2 study, however, thrombus in an additional 8% of the patients. observed the same rate of LV thrombi in patients et al Solheim reported a similar incidence of 15% in with or without atenolol.10 the first 3 months in a selected group of AMI 6 It has been demonstrated that mitral regurgita- patients treated by primary PCI. So, the timing of tion prevents thrombus formation in patients LV thrombus assessment is crucial, as assessment with dilated cardiomyopathy.w10 The protective too soon after the onset of myocardial infarction effect of mitral regurgitation may be the conse- will probably lead to failure to detect the thrombus quence of augmented early diastolic flow velocities fi in a signi cant percentage of patients. at the mitral annulus level, as well through the entire length of the left ventricle, protecting the CLINICAL FACTORS CONTRIBUTING TO LV LV cavity from a stagnant, thrombogenic blood http://heart.bmj.com/ THROMBUS FORMATION flow pattern. In addition, studies suggest abnormal Risk factors for the development of LV thrombus flow profiles are associated with the presence of an are consistently irrespective of infarct treatment LV thrombus.11 w11 However, to date no studies and include large infarct size, severe apical asynergy have demonstrated the same association in patients (ie, akinesis or dyskinesis), LV aneurysm, and with AMI. e anterior MI.2 5 8w6This is consistent with an There have been few studies on the use of increased contribution of at least two of the three biomarkers in the setting of LV thrombus forma- components of Virchow’s triad, namely a larger tion. It could be postulated that factors involved in on September 26, 2021 by guest. Protected copyright. area of blood stasis as well as an increased area of the coagulation cascade could serve as biomarkers to injured subendocardium. identify patients at increased risk for LV thrombus In a study of more than 8000 patients with ST development. Data presented at the European elevation myocardial infarction (STEMI), LV Society of Cardiology in 2011 demonstrated higher thrombus was found in 427 patients (5.1%). This soluble tissue factor and d-dimer concentrations in incidence is relatively low compared to other patients with LV thrombus formation.w12 Another studies, probably because of the exclusion of high study observed mildly
Recommended publications
  • Disseminated Intravascular Coagulation (DIC) and Thrombosis: the Critical Role of the Lab Paul Riley, Phd, MBA, Diagnostica Stago, Inc

    Disseminated Intravascular Coagulation (DIC) and Thrombosis: the Critical Role of the Lab Paul Riley, Phd, MBA, Diagnostica Stago, Inc

    Generate Knowledge Disseminated Intravascular Coagulation (DIC) and Thrombosis: The Critical Role of the Lab Paul Riley, PhD, MBA, Diagnostica Stago, Inc. Learning Objectives Describe the basic pathophysiology of DIC Demonstrate a diagnostic and management approach for DIC Compare markers of thrombin & plasmin generation in DIC, including D-Dimer, fibrin monomers (FM; aka soluble fibrin monomers, SFM), and fibrin degradation products (FDPs; aka fibrin split products, FSPs) Correlate DIC theory and testing to specific clinical cases DIC = Death is Coming What is Hemostasis? Blood Circulation Occurs through blood vessels ARTERIES The heart pumps the blood Arteries carry oxygenated blood away from the heart under high pressure VEINS Veins carry de-oxygenated blood back to the heart under low pressure Hemostasis The mechanism that maintains blood fluidity Keeps a balance between bleeding and clotting 2 major roles Stop bleeding by repairing holes in blood vessels Clean up the inside of blood vessels Removes temporary clot that stopped bleeding Sweeps off needless deposits that may cause blood flow blockages Two Major Diseases Linked to Hemostatic Abnormalities Bleeding = Hemorrhage Blood clot = Thrombosis Physiology of Hemostasis Wound Sealing break in vesselEFFRAC PRIMARY PLASMATIC HEMOSTASIS COAGULATION strong clot wound sealing blood FIBRINOLYSIS flow ± stopped clot destruction The Three Steps of Hemostasis Primary Hemostasis Interaction between vessel wall, platelets and adhesive proteins platelet clot Coagulation Consolidation
  • Heart – Thrombus

    Heart – Thrombus

    Heart – Thrombus Figure Legend: Figure 1 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A thrombus is present in the right atrium (arrow). Figure 2 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 1). Multiple layers of fibrin, erythrocytes, and scattered inflammatory cells (arrows) comprise this right atrial thrombus. Figure 3 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study. A large thrombus with two foci of mineral fills the left atrium (arrow). Figure 4 Heart, Atrium - Thrombus in a male Swiss Webster mouse from a chronic study (higher magnification of Figure 3). This thrombus in the left atrium (arrows) has two dark, basophilic areas of mineral (arrowheads). 1 Heart – Thrombus Comment: Although thrombi can be seen in the right (Figure 1 and Figure 2) or left (Figure 3 and Figure 4) atrium, the most common site of spontaneously occurring and chemically induced thrombi is the left atrium. In acute situations, the lumen is distended by a mass of laminated fibrin layers, leukocytes, and red blood cells. In more chronic cases, there is more organization of the thrombus (e.g., presence of vascularized fibrous connective tissue, inflammation, and/or cartilage metaplasia), with potential attachment to the atrial wall. Spontaneous rates of cardiac thrombi were determined for control Fischer 344 rats and B6C3F1 mice: in 90-day studies, 0% in rats and mice; in 2-year studies, 0.7% in both genders of mice, 4% in male rats, and 1% in female rats.
  • Thrombotic Thrombocytopenic Purpura

    Thrombotic Thrombocytopenic Purpura

    Thrombotic thrombocytopenic Purpura Flora Peyvandi Angelo Bianchi Bonomi Hemophilia and Thrombosis Center IRCCS Ca’ Granda Ospedale Maggiore Policlinico University of Milan Milan, Italy Disclosures Research Support/P.I. No relevant conflicts of interest to declare Employee No relevant conflicts of interest to declare Consultant Kedrion, Octapharma Major Stockholder No relevant conflicts of interest to declare Speakers Bureau Shire, Alnylam Honoraria No relevant conflicts of interest to declare Scientific Advisory Ablynx, Shire, Roche Board Objectives • Advances in understanding the pathogenetic mechanisms and the resulting clinical implications in TTP • Which tests need to be done for diagnosis of congenital and acquired TTP • Standard and novel therapies for congenital and acquired TTP • Potential predictive markers of relapse and implications on patient management during remission Thrombotic Thrombocytopenic Purpura (TTP) First described in 1924 by Moschcowitz, TTP is a thrombotic microangiopathy characterized by: • Disseminated formation of platelet- rich thrombi in the microvasculature → Tissue ischemia with neurological, myocardial, renal signs & symptoms • Platelets consumption → Severe thrombocytopenia • Red blood cell fragmentation → Hemolytic anemia TTP epidemiology • Acute onset • Rare: 5-11 cases / million people / year • Two forms: congenital (<5%), acquired (>95%) • M:F ratio 1:3 • Peak of incidence: III-IV decades • Mortality reduced from 90% to 10-20% with appropriate therapy • Risk of recurrence: 30-35% Peyvandi et al, Haematologica 2010 TTP clinical features Bleeding 33 patients with ≥ 3 acute episodes + Thrombosis “Old” diagnostic pentad: • Microangiopathic hemolytic anemia • Thrombocytopenia • Fluctuating neurologic signs • Fever • Renal impairment ScullyLotta et et al, al, BJH BJH 20122010 TTP pathophysiology • Caused by ADAMTS13 deficiency (A Disintegrin And Metalloproteinase with ThromboSpondin type 1 motifs, member 13) • ADAMTS13 cleaves the VWF subunit at the Tyr1605–Met1606 peptide bond in the A2 domain Furlan M, et al.
  • 32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies

    32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies

    32 Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets Joan-Carles Reverter and Dolors Tàssies Introduction Antiphospholipid antibodies (aPL) are related to thrombosis in the antiphospho- lipid syndrome (APS) [1, 2] and numerous pathophysiological mechanisms have been suggested involving cellular effects, plasma coagulation regulatory proteins, and fibrinolysis [3, 4]: aPL may act as blocking agents directly inhibiting antigen enzymatic or co-factor function of hemostasis; may bind fluid-phase antigens of hemostasis involved proteins and then decrease plasma antigen levels by clearance of immune complexes; may form immune complexes with their antigens that may be deposited in blood vessels causing inflammation and tissue injury; may cause dysregulation of antigen–phospholipid binding due to cross-linking of membrane bound antigens; and may trigger cell mediated events by cross-linking of antigen bound to cell surfaces or cell surface receptors [3, 4]. Moreover, several characteris- tics of the aPL, such as the concentration, class/subclass, affinity or charge, and several characteristics of the antigens, as the concentration, size, location or charge, may influence which of the theoretical autoantibody actions will occur in vivo [3]. Among the cellular mechanisms supposed to be involved, platelets have been considered as one of the most promising potential target for circulating aPL that may cause antibody mediated thrombosis as a part of the clinical spectrum of the autoimmune disorder of the APS. In the present chapter we will focus on the inter- actions that involve aPL binding to platelet membrane or platelet membrane bound antigens. Platelets as Target for aPL Platelets play a central role in primary hemostasis involving platelet adhesion to the injured blood vessel wall, followed by platelet activation, granule release, shape change, and rearrangement of the outer membrane phospholipids and proteins, transforming them into a highly efficient procoagulant surface [5].
  • Thrombosis and Embolism After Injury J Clin Pathol: First Published As 10.1136/Jcp.S3-4.1.86 on 1 January 1970

    Thrombosis and Embolism After Injury J Clin Pathol: First Published As 10.1136/Jcp.S3-4.1.86 on 1 January 1970

    J. clin. Path., 23, Suppl. (Roy. Coll. Path.), 4, 86-101 Thrombosis and embolism after injury J Clin Pathol: first published as 10.1136/jcp.s3-4.1.86 on 1 January 1970. Downloaded from S. SEVITT From the Birmingham Accident Hospital Thrombosis is frequent in injured patients. It classified as follows, namely, local thrombosis, takes different forms, and at least one of them, deep vein thrombosis, pulmonary microem- deep vein thrombosis in the lower limbs, is a bolism, glomerular microthrombosis, allied to common cause of morbidity and death through the Schwartzman reaction, occasional cases of embolic detachment. The different kinds may be arterial thrombosis, and rarely, abacterial vege- tative endocarditis. Thrombi form in flowing blood and are layered structures, unlike blood clots which form copyright. in static blood. They contain platelets, fibrin, red cells, and leucocytes, or a variable mixture, the differences depending on size, genesis, age, and venous or arterial location; but whatever the origin, the building blocks of enlarging thrombi are closely packed clumps of platelets with narrow fibrin borders (Fig. 1). Two main pro- http://jcp.bmj.com/ cesses are involved, namely, coagulation and platelet aggregation. These are interlinked and local release of thrombin is probably the key factor; thrombin promotes platelet clumping at a low concentration and fibrin formation at a higher concentration. Further, the release of substances from platelets can set in motion the coagulation on September 30, 2021 by guest. Protected process. Local Thrombosis and Haemostasis Thrombosis is frequent as a direct response to injury. In burned skin, for example, small venous thrombi may become prominent in the subdermis and subcutaneous tissue.
  • Zebrafish Depends on Von Willebrand Factor

    Zebrafish Depends on Von Willebrand Factor

    Hemostasis ARTICLE Histone-induced thrombotic thrombocytopenic Ferrata Storti Foundation purpura in adamts13-/- zebrafish depends on von Willebrand factor Liang Zheng,1 Mohammad S. Abdelgawwad,1 Di Zhang,1 Leimeng Xu,1 Shi Wei,2 Wenjing Cao1 and X. Long Zheng1 Divisions of 1Laboratory Medicine and 2Anatomic Pathology, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA ABSTRACT Haematologica 2020 Volume 105(4):1107-1119 hrombotic thrombocytopenic purpura (TTP) is caused by severe deficiency of ADAMTS13 (A13), a plasma metalloprotease that Tcleaves endothelium-derived von Willebrand factor (VWF). However, severe A13 deficiency alone is often not sufficient to cause an acute TTP; additional factors may be required to trigger the disease. Using CRISPR/Cas9, we created and characterized several novel zebrafish lines carrying a null mutation in a13-/-, vwf, and both. We fur- ther used these zebrafish lines to test the hypothesis that inflammation that results in neutrophil activation and release of histone/DNA com- plexes may trigger TTP. As shown, a13-/- zebrafish exhibit increased lev- els of plasma VWF antigen, multimer size, and ability of thrombocytes to adhere to a fibrillar collagen-coated surface under flow. The a13-/- zebrafish also show an increased rate of occlusive thrombus formation in -/- the caudal venules after FeCl3 injury. More interestingly, a13 zebrafish exhibit ~30% reduction in the number of total, immature, and mature thrombocytes with increased fragmentation of erythrocytes. Administration of a lysine-rich histone results in more severe and persist- Correspondence: ent thrombocytopenia and a significantly increased mortality rate in a13-/- zebrafish than in wildtype (wt) ones. However, both spontaneous and X.
  • Surgical Treatment of Cardiogenic Shock Due to Huge Right Atrial Thrombus

    Surgical Treatment of Cardiogenic Shock Due to Huge Right Atrial Thrombus

    Türk Kareliyol Dem Arş 2000; 28:458-460 CASEREPORT Surgical Treatment of Cardiogenic Shock Due to Huge Right Atrial Thrombus Ahmet BALT ALARLI MD, Bekir Hayrettin Ş İRİN MD, Asuman KAFTAN MD* Pamukkale Universty Medical Faculty Deparimenis o.fCardiovascular Surgery and Cardiology, Denizli DEV SAG ATRİYAL TROMBÜS NEDENiYLE and sero-sanguineous in charactcr. The story of a blunt GELiŞEN KARDiYOJENiK ŞOK VE CERRAHi chest ı rauma due to a ıraffic accidcnt 20 days ago w itlıout TEDAVİSİ any lung complication was obtained from the hospital's transfer note. ÖZET The patient was conscious and oriented. The systolic blood Kardiyojenik şok ve mu/tip/ pulmoner mikroemboliye prcssure was 65 mmHg, the pulse was regular at 130 per neden olan bir sağ atriya/ tromboemboli olgusu, nadir minute, and the respiratory rate was 20 breat lı per minutc. o lması sebebiyle bildirilmiştir. Sağ atriyumda serbestçe His neck veins were distended. The li ver was not enlarged dolaşan, diyasro/ sırasında trikiispit kapaktan sağ but tender. He had a vague calf tenderness on the right, ventrikiile prolabe olan ve sağ ventrikül g iriş (inj7ow) ve and H onıan's sign was considered positive. No pe riplı eral çıkı şmda ( outflow) tıkamklığa yol açan dii:ensiz geniş bir cdema was present. kitle iki boyutlu ekokardiyografi ile tespit edilmiş tir. Acil The ECG s lı owcd sin us tachycardia witlı T wavc invcrsion operasyona alınarak kardiyopulmoner baypasa girilmed­ in leads lll and V t-3.T lı e clıes t x-ray film sh o wed minimal en, tromboembolik materyal sağ atriyumdan başarıyla pleural cffusion at right sin us.
  • Upper-Extremity Deep Venous Thrombosis After Whole Blood Donation: Report of Three Cases from a Single Blood Center

    Upper-Extremity Deep Venous Thrombosis After Whole Blood Donation: Report of Three Cases from a Single Blood Center

    BLOOD DONORS AND BLOOD COLLECTION Upper-extremity deep venous thrombosis after whole blood donation: report of three cases from a single blood center Bruce Newman,1 Madhvi Rajpurkar,2 Bulent Ozgonenel,2 Anup Lal,3 and Philip Kuriakose4 pper-extremity deep venous thrombosis BACKGROUND: There are two upper-extremity deep (UEDVT) after whole blood donation is rarely venous thrombosis (UEDVT) cases after whole blood reported. There are two reported cases in the donation reported in the English medical literature. English medical literature.1-3 Our institution Three additional UEDVT cases after whole blood Uhad three UEDVT cases after whole blood donation within donation were reported to our blood center within a a 13-month period. We report the three cases and also 13-month period. review the two cases reported in the literature. In addition, STUDY DESIGN AND METHODS: A case study was we are aware of 20 more cases reported in a recent done for each case in collaboration with a clinical abstract from 4.2 million whole blood donations in Aus- physician. A description of the donation event, donor tralia,4 and we report on the abstract. demographics, risk factors for thrombosis, treatment, and outcome were described. RESULTS: A 33-year-old woman and two 17-year-old, MATERIALS AND METHODS first-time-donating men presented with arm pain, Three donation events were reported to American Red swelling, and bruising within hours to 3 days after Cross, SE Michigan Region, by the donors, donors’ rela- donation. Two had distal UEDVTs in the basilic or tives, or patients’ physician.
  • Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management

    Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management

    Journal of Clinical Medicine Review Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management Senthil Sukumar 1 , Bernhard Lämmle 2,3,4 and Spero R. Cataland 1,* 1 Division of Hematology, Department of Medicine, The Ohio State University, Columbus, OH 43210, USA; [email protected] 2 Department of Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern, CH 3010 Bern, Switzerland; [email protected] 3 Center for Thrombosis and Hemostasis, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany 4 Haemostasis Research Unit, University College London, London WC1E 6BT, UK * Correspondence: [email protected] Abstract: Thrombotic thrombocytopenic purpura (TTP) is a rare thrombotic microangiopathy charac- terized by microangiopathic hemolytic anemia, severe thrombocytopenia, and ischemic end organ injury due to microvascular platelet-rich thrombi. TTP results from a severe deficiency of the specific von Willebrand factor (VWF)-cleaving protease, ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13). ADAMTS13 deficiency is most commonly acquired due to anti-ADAMTS13 autoantibodies. It can also be inherited in the congenital form as a result of biallelic mutations in the ADAMTS13 gene. In adults, the condition is most often immune-mediated (iTTP) whereas congenital TTP (cTTP) is often detected in childhood or during pregnancy. iTTP occurs more often in women and is potentially lethal without prompt recognition and treatment. Front-line therapy includes daily plasma exchange with fresh frozen plasma replacement and im- munosuppression with corticosteroids. Immunosuppression targeting ADAMTS13 autoantibodies Citation: Sukumar, S.; Lämmle, B.; with the humanized anti-CD20 monoclonal antibody rituximab is frequently added to the initial ther- Cataland, S.R.
  • Platelet and Thrombophilia-Related Risk Factors of Retinal Vein Occlusion

    Platelet and Thrombophilia-Related Risk Factors of Retinal Vein Occlusion

    Journal of Clinical Medicine Review Platelet and Thrombophilia-Related Risk Factors of Retinal Vein Occlusion Adrianna Marcinkowska 1,2, Slawomir Cisiecki 2 and Marcin Rozalski 1,* 1 Department of Haemostasis and Haemostatic Disorders, Chair of Biomedical Sciences, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland; [email protected] 2 Department of Ophthalmology, Karol Jonscher’s Municipal Medical Center, 93-113 Lodz, Poland; [email protected] * Correspondence: [email protected] Abstract: Retinal vein occlusion (RVO) is a heterogenous disorder in which the formation of a thrombus results in the retinal venous system narrowing and obstructing venous return from the retinal circulation. The pathogenesis of RVO remains uncertain, but it is believed to be multifactorial and to depend on both local and systemic factors, which can be divided into vascular, platelet, and hypercoagulable factors. The vascular factors include dyslipidaemia, high blood pressure, and diabetes mellitus. Regarding the platelet factors, platelet function, mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (PLCR) play key roles in the diagnosis of retinal vein occlusion and should be monitored. Nevertheless, the role of a hypercoagulable state in retinal vein occlusion remains unclear and requires further studies. Therefore, the following article will present the risk factors of RVO associated with coagulation disorders, as well as the acquired and genetic risk factors of thrombophilia. According to Virchow’s triad, all factors mentioned above lead Citation: Marcinkowska, A.; Cisiecki, to thrombus formation, which causes pathophysiological changes inside venous vessels in the fundus S.; Rozalski, M. Platelet and of the eye, which in turn results in the vessel occlusion.
  • Protocol for the Prevention of Venous Thromboembolism at the Ivo Pitanguy Institute: Efficacy and Safety in 1351 Patients

    Protocol for the Prevention of Venous Thromboembolism at the Ivo Pitanguy Institute: Efficacy and Safety in 1351 Patients

    ARTIGO ORIGINAL Protocolo de prevenção de tromboembolismoVendraminFranco T FSet al.et venoso al. no Instituto Ivo Pitanguy Protocolo de prevenção de tromboembolismo venoso no Instituto Ivo Pitanguy: eficácia e segurança em 1.351 pacientes Protocol for the prevention of venous thromboembolism at the Ivo Pitanguy Institute: efficacy and safety in 1351 patients RITA A. PAIVA1 RESUMO JIHED CHADRAOUI2 Introdução: Eventos tromboembólicos causam grande preocupação, em decorrência das BArbARA B. MACHADO3 altas taxas de morbidade e mortalidade existentes e da possibilidade de apresentação clínica NATALE F. GONTIJO DE com sintomas escassos e, muitas vezes, inespecíficos. A prevenção é a maneira mais eficaz AMORIM3 de lidar com esse tipo de evento, que, uma vez estabelecido, pode levar rapidamente à HAZEL FISCHDICK4 morte. Método: Foi realizado estudo retrospectivo, no período entre maio de 2009 e maio IVO PITAngUY5 de 2010, com pacientes submetidos a cirurgia plástica no Instituto Ivo Pitanguy. Todos os pacientes foram submetidos ao protocolo de prevenção de tromboembolismo venoso, após serem avaliados quanto aos fatores predisponentes e de risco. A soma desses fatores gerou uma pontuação, que determinou a profilaxia a ser adotada. Resultados: Foram avaliados 1.351 pacientes durante o período de um ano. Não houve incidência de tromboem bolismo venoso. Foram observados 16 casos de hematoma, 9 (56,25%) deles ocorreram após profi- laxia com heparina e 7 (43,75%) sem o uso de quimioprofilaxia. Conclusões: O protocolo para prevenção de tromboembolismo venoso no Instituto Ivo Pitanguy foi eficaz, sem ocor- rência de eventos tromboembólicos e com incidência de hematomas abaixo da encontrada na literatura médica. Descritores: Tromboembolia venosa/prevenção & controle.
  • Protruding Left Ventricular Thrombus Formation Following Blunt Chest Trauma

    Protruding Left Ventricular Thrombus Formation Following Blunt Chest Trauma

    Volume 125, Number 3 American Heart Journal Rechavia et aE. 893 * P c 0.01 vs baseline values A P e 0.005 vs recovery values of nMI r* ; E 40. recovery F maximum ’ 30. MI 5 5 20 nMI I -10 recovery g baseline maximum a ul Rest 0 1 1.5 5 9 minutes Fig. 1. SACE levels in ischemic (IMI) and nonischemic (nMII subjects during exercise test. Table II. SACE activity during the exercise test SACE (nmol/ml/mini Groups -10 0 Maximum Recovery Ischemic (n = 9) "0.78 t 1.99 22.06 f 2.17 ‘25.18 t xv*I I 28.95 t 5.09*i Nonischemic (n = 9) 21.80 c X.70 21.50 k 4.80 2::.30 +- ,'3.10 22.00 k 3.40 *p < 0.01 versus baseline values. tp < 0.005 versus nonischemic at recovery in the event of myocardial ischemia, SACE increases (kininase II) in human endoehelial cells in culture. Adv Exp markedly at maximum effort as well as during recovery. Med Biol 1978;120B:287-90. Our data on SACE activity in nonischemic subjects support 9. Hayes LW, Goguen CA, Ching SF, Slakey LL. Angiotensin- converting enzyme: accumulation in medium from cultured similar results obtained by Milledge and Catley,” who endothelial cells. Biochem Biophys Commun 1978;82:1147-9. found SACE to remain unchanged during extended stress 10. Kasahara Y, Ashihara Y, Harada T. The method for determi- testing (up to 60 minutes) in normal healthy subjects. In nation of angiotensin I converting enzyme (ACE) activity.