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    Mechanisms of late lumen loss after antiproliferative percutaneous coronary intervention using beta-irradiation in a porcine model of restenosis (2007)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Deiner, C.
    Loddenkemper, C.
    Rauch, U.
    Rosenthal, P.
    Pauschinger, M.
    Schwimmbeck, P. L.
    Schultheiss, H. P.
    Pels, K.
    Quelle
    Cardiovascular revascularization medicine; 8(2) — S. 94–98
    ISSN: 1553-8389
    Sprache
    Englisch
    Verweise
    URL (Volltext): http://library.vetmed.fu-berlin.de/pd/files/2007/intern/113/Deiner2007_2.pdf
    DOI: 10.1016/j.carrev.2006.10.004
    Pubmed: 17574167
    Kontakt
    Institut für Veterinär-Physiologie

    Oertzenweg 19 b
    14163 Berlin
    +49 30 838 62600
    physiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    BACKGROUND:
    The short-term results for the prevention of coronary restenosis after intravascular brachytherapy (IVBT) and use of drug-eluting stents (DESs) are excellent. The long-term results either lack or present with late complications (e.g., late thrombosis and late catch-up phenomenon leading to late restenosis even years after the initial procedure). Both IVBT and DESs mediate their potent antirestenotic effects via a cytostatic mechanism, but the cardiovascular pathology at late time points after the use of these antiproliferative therapies is incompletely understood. This study investigated the long-term effects of antiproliferative beta-irradiation in a clinically relevant porcine coronary model to address the pathophysiology of late coronary restenosis after antiproliferative vascular interventions.

    METHODS:
    We performed percutaneous transluminal coronary angioplasty (PTCA) in two major coronary arteries in 12 domestic crossbred pigs. One of the two balloon-injured segments was randomly assigned to receive immediate beta-irradiation (PTCA+IVBT group) using a noncentered delivery catheter (20 Gy; Novoste Beta-Cath System, Novoste, Norcross, GA, USA). The animals were sacrificed after 14 days (n=6) or 3 months (n=6).

    RESULTS:
    The luminal area in the PTCA+IVBT group decreased significantly 3 months after the intervention as compared with that in the PTCA group (PTCA 3.45+/-0.46 mm(2) vs. PTCA+IVBT 1.22+/-0.26 mm(2); P=.0017). This lumen loss was primarily due to shrinkage of the external elastic lamina area (negative arterial remodeling; PTCA 5.22+/-0.27 mm(2) vs. PTCA+IVBT 3.42+/-0.45 mm(2); P=.0064), which was accompanied by an increase in the adventitial area (PTCA 3.07+/-0.2 mm(2) vs. PTCA+IVBT 5.41+/-0.5 mm(2); P=.0049).

    CONCLUSIONS:
    The application of antiproliferative radiation in a porcine coronary model caused an early beneficial effect (reduction of intimal-medial lesion and luminal gain) that was followed by a late lumen loss primarily due to negative arterial remodeling. This mechanism may in part help us understand the pathophysiology of late adverse events occurring after IVBT.