Randomised trial of coronary intervention with antibody against platelet IIb/IIIa iritegrin for reduction of clinical restenosis: results at six months

Local gene transfer of tissue factor pathway inhibitor regulates intimal hyperplasia in atherosclerotic arteries

“…However, these therapies have not been consistently effective, and their dosing is limited given their associated hemorrhagic risk (1,35,36). After local gene transfer of TFPI, we observed no derangements in hemostasis.…”

“…Taken together, these findings warrant reconsideration of systemic anticoagulant and antithrombotic approaches to the problem of recurrent thrombosis and restenosis. With one exception (35), such strategies have failed to reduce the need for repeated revascularization after percutaneous vascular interventions, leading to a quest for more potent and prolonged antithrombotic treatment, especially in the secondary prevention of acute coronary syndromes (37,38). Although we cannot exclude that intense systemic anticoagulation, added to local inhibition of TF, may provide additional protection against postinjury intimal hyperplasia and thrombotic occlusion, in situ expression of TFPI alone is shown in our study to markedly inhibit neointima formation in damaged atherosclerotic arteries without the bleeding risks associated with intense prolonged systemic antithrombotic therapies.…”

Apoptosis in the vasculature: mechanisms and functional importance

“…Death of VSMCs by apoptosis may be viewed as harmful because it may weaken the ®brous cap by decreasing the synthesis of extracellular matrix and therefore may lead to plaque rupture. However, others may argue that plaque stabilization observed with anti-b 3 integrin antibodies (Topol et al, 1994) may involve selective apoptosis of intimal smooth muscle cells that express a v b 3 integrin and whose attachment to the extracellular matrix are disrupted.…”

Inibição do receptor plaquetário glicoproteína (GP) IIb/IIIa em síndromes isquêmicas agudas e intervenções coronárias

“…Esta diferença foi mantida, ou mesmo aumentada, ao longo do tempo. Aos seis meses de seguimento, havia uma redução absoluta de 8% nessas complicações 8 . Contudo, os pacientes que receberam o inibidor plaquetário tiveram maior incidência de sangramento relacionado ao sítio de acesso arterial e receberam mais transfusões.…”

“…Os bloqueadores do receptor plaquetário glicoproteína (GP) IIb/IIIa, que inibem a via comum da agregação plaquetária, possuem um grande potencial terapêutico em pacientes submetidos a intervenções coronárias e no manejo de síndromes coronárias agudas. O anticorpo monoclonal contra a GP IIb/IIIa, ou abciximab, tem sido extensivamente estudado em pacientes submetidos a intervenções coroná-rias [5][6][7][8][9][10][11] , sendo o primeiro de uma série de agentes a ser introduzido para o uso clínico. Um número expressivo de outros bloqueadores peptídicos e não peptídicos do receptor plaquetário GP IIb/IIIa também estão sendo avaliados em estudos clínicos de fase II e III [12][13][14][15][16][17][18][19] .…”