简介：Objective:Implantableportthrombosis(IPT)incancerpatientsisarelativelyrarebutseverecomplication.Severalfactorsarereportedlyassociatedwiththeoccurrenceofthrombosis.WeaimedtodescribetheprevalenceandtheanatomoclinicalfeaturesofIPTobservedincancerpatientswhoweretreatedinamedicaloncologydepartmentinTunisia.Methods:Atotalof600cancerpatientswhohadportimplantationfromJanuary2013toDecember2015wereretrospectivelyidentified.Caseswithsymptomatic/incidentalIPT(radiologicallyconfirmed)werefurtheridentified.Epidemiologicalandanatomoclinicalfeatureswerecollectedfrompatientrecordsandthedepartmentdatabase.Results:Weobservedthat33ofthe600patientshadIPT;thus,theprevalencewas5.5%.Themedianagewas57years,andthegenderratiowas0.43.Overweightorobesitywasobservedin73%ofthepatients.IPToccurredmainlyinpatientswithbreast(36.4%)andcolorectal(33.3%)cancers,whichweremostlynonmetastatic(79%).Atleastoneidentifiedclassicalthromboembolicriskfactorwasfoundin13patients(smokingin9,tamoxifenin2).IPTwassymptomaticin93%ofthecases,occurringwithinanaveragetimeof56days.Implantableportswereremovedbecauseofinfectionin2casesandnonfunctionalityin3cases.IPTtreatmentwasbasedonlow-molecular-weightheparins(94%)andantivitaminK(6%)foranaverageof130days.Fourpatientshadpost-therapycomplications:onethrombosisrecurrenceandthreeinfections.Conclusions:IPTcasesinthe600patientswereobservedtooccurinobesenonmetastaticcancerpatientswithinthefirst3monthsafterIPimplantation.

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简介：BackgroundAfterpercutaneouscoronaryintervention(PCI),somepatientsmaysufferfromrestenosisandstentthrombosis.Manystudiessuggestthatendothelialprogenitorcell(EPC)hasanimportantroleinpreventingrestenosisandstentthrombosis.AnovelstentwhichcanattractEPChasbeendesignedtoprovideabetteroutcomefortheseproblems.MethodThedataofthepresentreviewwasobtainedbysearchingPUBMEDandotherdatabases(1994-2011)usingthekeytermsof'endothelialprogenitorcell','reendothelialization','restenosis','stentthrombosis',and'percutaneouscoronaryintervention'.ResultRapidreendothelializationisessentialinpreventingrestenosisandstentthrombosis.EPCcandifferentiateintoendothelialcellandacceleratethereendothelialization.Afternumerouspreclinicalandclinicalresearches,thecorrelationbetweencirculatingEPCstorestenosisstillremainspoorlyunderstood.However,manystudieshaveshowntheimportantroleofEPCindiminishingtheriskofthrombosisfollowingstentimplantation.Somepharmacologicalagentshavebeenreportedcanincreasethenumberand/orfunctionsofEPC.Recently,CD34+antibodycoatedstenthasbeendevelopedtoattractEPCtothehealingendothelium,andhasshowedfavorableresults.ConclusionEPChasimportantroleinrapidreendothelializationaftervascularinjury.EPCcanpreventstentthrombosisafterPCI,howevertheeffectsofEPCinpreventingrestenosisneedfurtherinvestigations.ThecapturingCD34+stentissafeandsignificantlydecreasesstentthrombosis.

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简介：Useagenesutureimmersedrecombinanttissue-typeplasminogenactivator(r-tPA)expressionplasmidtotransducemyocardiatopreventthethrombosisaftermechanicaltricuspidvalvereplacementinpigs.MethodsAr-tPAgeneplasmidwasconstructedandconjugatedtoanovelcationicphosphonolipidandar-tPAgenesuturewasmade.Eighteenpigswereselectedanddividedintotwogroupsatrandomization.Therewere9pigsintheexperimentalgroupand9inthecontrolgroup,allthe18pigs'tricuspidswerereplacedwithmechanicalvalves.Thegenethreadsweresuturedintotherightventricularwallsnearmechanicalvalvesandanultrasoundwasusedonthesurfacesoftherightventricularwallsforthegenetransferintheexperimentalgroup.Coagulativefunction,D-dimerlevelofthebloodandthethrombosisonthesurfacesofthevalveswereobserved.Resultsr-tPAgeneplasmidwassuccessfullyconstructedandr-tPAproteinwasexpressedintheventricularcellsaroundthegenesutures.D-dimerreacheditspeaklevel(1.67±0.79)μg·mL-1in1weekafteroperationintwogroups,butitdecreasedtopreoperationlevelthereafterincontrolgroupandkeptonthehighlevelandreincreasedtoanewhighlevel(1.89±0.79)μg·mL-1untiltheendoftheexperimentinexperimentalgroup.Thethrombosesaroundthevalveswerefoundinallthecontrolgroup(100%)butonly1(11.11%)caseinexperimentalgroup.Therewerenochangesinprothrombintimepreandpostoperationintwogroups.ConclusionsUsinggenesutureimmersedr-tPAexpressionplasmidtotransducemyocardiamightbeabestsubstitutionforlifelonganti-coagulationtherapyforthepatients,whounderwentoperation.

简介：AbstractBackground:Antiphospholipid syndrome (APS) is an autoimmune prothrombotic condition with significant morbidity. The objective of this study was to identify additional clinical and epidemiological risks of arterial thrombosis, venous thrombosis, and pregnancy morbidities in a large cohort of persistent antiphospholipid antibodies (aPLs)-positive carriers.Methods:This was a cross-sectional cohort study of 453 consecutive patients with a documented positive aPL who attended Peking University People's Hospital. Among 453 patients screened, 297 patients had persistent positive aPL. We compared asymptomatic aPL carriers with thrombotic and obstetric APS patients. And the univariate analysis and multivariable logistic regression were used to evaluate the association between different risk factors and APS clinical manifestations. The levels of circulating markers of neutrophil extracellular traps (NETs) (cell-free DNA and citrullinated histone H3 [Cit-H3]) were assessed and compared among aPL-positive carriers with or without autoimmune disease and APS patients.Results:Additional risk factors associated with arterial thrombosis among aPL-positive carriers included: smoking (odds ratio [OR] = 6.137, 95% confidence interval [CI] = 2.408-15.637, P = 0.0001), hypertension (OR = 2.368, 95% CI = 1.249-4.491, P = 0.008), and the presence of underlying autoimmune disease (OR = 4.401, 95% CI = 2.387-8.113, P < 0.001). Additional risks associated with venous thrombosis among aPL carriers included: smoking (OR = 4.594, 95% CI = 1.681-12.553, P = 0.029) and the presence of underlying autoimmune disease (OR = 6.330, 95% CI = 3.355-11.940, P < 0.001). The presence of underlying autoimmune disease (OR = 3.301, 95% CI= 1.407-7.744, P = 0.006) is the additional risk, which demonstrated a significant association with APS pregnancy morbidity. Higher circulating levels of cell-free DNA and Cit-H3 were observed among APS patients and aPL patients with autoimmune diseases compared with those aPL carriers without underlying autoimmune diseases. Furthermore, control neutrophils that are conditioned with APS patients' sera have more pronounced NET release compared with those treated with aPL carriers' sera without underlying autoimmune diseases.Conclusions:We identified several potential additional risk factors for APS clinical manifestations among a large cohort of Chinese aPL carriers. Our data may help physicians to risk stratify aPL-positive Asian patients.

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简介：BackgroundHeartfailureisoneofthemaincausesofdeathduetoprogressivemusculardystrophyofDuchennemusculardystrophy(DMD)inthemajorityofthecases.ThereishighincidenceofarterialthromboembolisminDMDpatientswithsevereheartfailure.However,ithasbeenreceivinglittleattentionwhetheranticoagulativetherapyinDMDpatientswithsevereheartfailureinsinusrhythmshouldbeperformed.HereinwepresentacaseofDMDpatients,withsevereheartfailureinsinusrhythm,whopresentsalargemuralthrombusformationatleftventricularanteriorwall.

简介：BackgroundTheregulationoft-PAgeneistheessenceandcoreofthrombosis.Therefore,thepresentstudyaimedtopreparenanot-PAgenecoatedstentandtoobserveitseffectoncoronarystentthrombosisindogs.MethodsHighlyexpressedt-PAgeneplasmidwasconstructedandalbuminnanot-PAgenecoatingstentwasprepared.Themajorbranchvesselsofdogcoronaryarterywerepre-expandedwitha3.0mm×20balloonwith8-10atmosphericpressure.10dogsofthecontrolgroupwereimplantedwithbaremetalstent;while12dogsoftheexperimentalgroupwereimplantedwithnanot-PAgenecoatingstent.Bothgroupswerenotgivenanti-coagulationtreatments.Bloodsamplesweretakenfort-PAandD-dimerbeforetheoperation,at1,2,4and8weeksafteroperation.Pathologicalanalysisfoundthrombosisinthecavityandthehyperplasiaoftheintima.t-PAexpressionwasdetectedbyimmunohistochemicalindirectly,andthethicknessoftheintimaofthesectioncrosswasdirectlymeasuredbymorphometry.Liver,heart,kidneysandlungweretakenforpathologicalobservation.ResultsAllexperimentalanimalssurvivedatpostoperative8weeks.Vascularstentthrombosiswasseenin10casesofthecontrolgroupwiththethrombosisrateof100%;whilewasseenin2casesamong12casesoftheexperimentalgroupwiththethrombosisratewas16.67%(P=0.00087).Immunohistochemicalstainingshowedthatthepositivet-PAgenetransfectionoftheexperimentalgroupwasmainlydistributedonthesurfaceofhyperplasiaintima,andvascularwallt-PAexpressionofthecontrolgroupwasnegative.Positivet-PAsignalwasnotfoundintheliver,heart,kidneysandlung.ConclusionNanot-PAgenevectorcoatingstentcaneffectivelyexpresst-PAinvascularwallandeffectivelypreventsstentthrombosis.

简介：AbstractThe coronavirus disease 2019 (COVID-19) pandemic was triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a previously unknown strain of coronavirus. To fully understand the consequences and complications of SARS-CoV-2 infections, we have reviewed current literature on coagulation dysfunctions that are related to the disease and vaccination. While COVID-19 is more commonly considered as a respiratory illness, studies indicate that, in addition to respiratory illness, a coagulation dysfunction may develop in individuals after the initial infection, placing them at the risk of developing thrombotic events. Patients who died of COVID-19 had higher levels of D-dimer, a biomarker for blood clot formation and breakdown. Effective treatments for coagulation dysfunctions are critically needed to improve patient survival. On the other hand, antibodies against platelet factor 4 (PF4)/heparin may be found in patients with rare instances of vaccine-induced immunological thrombotic thrombocytopenia (VITT) following vaccination with adenovirus-based vaccines. VITT is characterized by atypical thrombosis and thrombocytopenia, similar to immune-mediated heparin-induced thrombocytopenia (HIT), but with no need for heparin to trigger the immune response. Although both adenovirus-based and mRNA-based vaccines express the Spike protein of SARS-CoV-2, VITT is exclusively related to adenovirus-based vaccines. Due to the resemblance with HIT, the use of heparin is highly discouraged against treating patients with thrombotic thrombocytopenia after SARS-CoV-2 infection or with VITT after vaccination. Intravenous immunoglobulin therapy coupled with anticoagulation is recommended instead. The well-studied anti-PF4 monoclonal antibody RTO, which does not induce pathologic immune complexes in the presence of heparin and has been humanized for a potential treatment modality for HIT, may provide a nonanticoagulant HIT-specific solution to the problem of increased blood coagulation after SARS-CoV-2 infection or the VITT after immunization.