ABSTRACT
<p><b>BACKGROUND</b>The success rate of antegrade approach for chronic total occlusions (CTO) recanalization has not dramatically increased, especially in complex CTO subset. The retrograde technique may hold great promise. This report aimed to describe our experience of retrograde recanalization for CTO, focusing on its safety and feasibility.</p><p><b>METHODS</b>We identified 42 patients who underwent revascularization in CTO with retrograde approach from July 2005 to November 2009 in our center.</p><p><b>RESULTS</b>Three kinds of strategy were applied: retrograde as primary strategy (50.0%), retrograde immediately after antegrade failure (26.2%) and repeat procedure after previous antegrade failure (23.8%). Septal collaterals were more frequently used as the retrograde access route (92.9%). Overall success rate was 88.1%. In patients with successful retrograde wire crossing collateral channel to the distal cap of CTO, the success rate of recanalization was 94.1%. In patient with failure to cross the collaterals, the success rate was 62.5%. Eight different kinds of retrograde techniques were used: kissing wire technique (35.3%), wire trapped and reverse wire trapped technique (17.6%), back-end balloon and microcatheter reversal technique (14.7%), controlled antegrade and retrograde subintimal tracking (CART) technique (8.8%), reverse CART and modified reverse CART technique (8.8%), retrograde wire crossing technique (2.9%). There were 4 complications occurred without in-hospital major adverse cardiac events (MACE). In-hospital MACE was 7.7%. All of them were non-Q wave myocardial infarction. There were no cases of death or target vessel revascularization, either surgery or percutaneous.</p><p><b>CONCLUSIONS</b>The retrograde approach can be an effective tool for increasing the success rate of recanalization in the very complex CTO. To ensure the success and safety of the approach, careful case selection and device handling by experienced operators is essential.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Angioplasty, Balloon, Coronary , Methods , Chronic Disease , Coronary Angiography , Coronary Occlusion , Therapeutics , Models, Theoretical , Treatment OutcomeABSTRACT
<p><b>OBJECTIVE</b>To investigate whether p53 pathway participates in the effect of emodin on vascular smooth muscle cell proliferation.</p><p><b>METHODS</b>The effects of emodin on vascular smooth muscle cell proliferation were evaluated by cell count, senescent-associated beta-galactosidase staining, and annexin V staining. DNA synthesis was determined by (3)H-thymidine corporation, cell cycle was analyzed by FACS, the p53 protein level was measured by Western blot and cDNA expression array technology was used to demonstrate the effect of emodin on the simultaneous expression of a large number of genes in cultured vascular smooth muscle cells.</p><p><b>RESULTS</b>Emodin at 1.6-3.1 microg/ml inhibited VSMC growth, at 6.3-12.5 microg/ml promoted VSMC aging and induced VSMC apoptosis at 25.0 microg/ml 24 hours after exposure. Unscheduled DNA synthesis, which was a sensitive indicator for DNA injury, was observed in VSMC following 24 hours emodin exposure. The mRNA and protein levels of p53 were up-regulated in a concentration-dependent manner. Proliferation/carcinogenesis-related genes were down-regulated and other genes related to cell senescence, apoptosis, and DNA damage/repair were up-regulated in VSMC after exposure to emodin for 24 hours. Emodin readily permeated VSMC membrane and mostly located in the cytoplasm and few of them in the nucleus.</p><p><b>CONCLUSIONS</b>The p53 pathway in VSMC was activated post emodin exposure in a concentration-dependent manner and which might be responsible for the observed antiproliferative effects of emodin in vascular smooth muscle cells.</p>