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Patency [VERIFIED]
Objective: Patency rates for autogenous accesses are presumed to be better than for polytetrafluoroethylene (PTFE) accesses, although the strength of the supporting evidence is limited. We undertook this study to test the hypothesis that patency rates for upper extremity autogenous hemodialysis arteriovenous accesses in adults are superior to those for PTFE counterparts.
patency
Methods: A systematic review of relevant literature and meta-analysis of the patency data were performed. Studies were considered acceptable if patency data were reported by either life table or Kaplan-Meier method, including number of patients at risk.
Conclusions: The patency rate for autogenous upper extremity arteriovenous hemodialysis accesses in adults is superior to that for PTFE counterparts, although the overall quality of the studies in the meta-analysis was less than ideal. Randomized, controlled studies to further examine the differences in outcome between these two access types are necessary.
Results: Patency at 10 years was 61% for SVGs compared with 85% for IMA grafts (p 2.0 mm in diameter SVG patency was 88% versus 55% in vessels
Conclusions: The 10-year patency of IMA grafts is better than SVGs. The 10-year patency for SVGs is better and the 10-year patency for IMA grafts is worse than expected. The 10-year patency of SVGs to the LAD is better than that to the right or circumflex. The best long-term predictors of SVG graft patency are grafting into the LAD and grafting into a vessel that is >2.0 mm in diameter.
Prostaglandins (PGs) play an important role in maintaining the patency of the ductus arteriosus (DA). Cyclooxygenase (COX) is the first rate-limiting enzyme in PG synthesis and exists as two isoforms, COX-1, a constitutive isoform, and COX-2, an inducible isoform. Nonspecific COX inhibitors such as indomethacin cause postnatal and intrauterine ductal closure, while PG administration to the newborn results in prolonged patency of the DA. Mice deficient for a PGE2 receptor (subtype EP4) die from patent DA complications, yet the mechanisms of fetal DA patency and postnatal closure remain poorly defined. Thus, the expression patterns of COX-1 and COX-2 were examined in the DA of wild type and COX deficient mice on day 18 and 19, prior to the onset of labor (day 1 = vaginal plug), to determine isoform-specific COX expression, and to evaluate whether ductal patency is more influenced by intrinsic PG synthesis or by circulating PGs.
Mortality was not altered by cesarean delivery or by pre- and postnatal oxygen therapy. In-situ hybridization with 35S-labeled COX-1 and COX-2-specific anti-sense RNA probes was performed on cardiac and uterine tissues. Micro-dissected segments of the right ventricular outflow tract, pulmonary artery (PA), DA and aorta from day 18 and 19 wild type showed low level COX expression, with COX-1 signals more abundant than COX-2 in the PA and DA. Whole uterine sections showed dramatic upregulation of COX-1 at the time of labor, with some upregulation of COX-2 signal in COX-1(-/-) placentae. The preferential expression of COX-1 in fetal DA suggests that selective inhibitors of COX-2 may be useful in the management of preterm labor, where occult infection results in COX-2 upregulation. However, the survival of COX-1(-/-) and COX-2(-/-) pups, the excessive perinatal mortality in double knockout pups, and the upregulation of COX-2 expression in COX-1(-/-) placentae indicate that circulating PGs may be more important to DA patency than intrinsic PG production in the DA. 041b061a72