At the 5-year follow-up, a significantly higher varicose vein recurrence rate originated at the SFJ region after EVLA compared with SFL/S. There were no differences in the relief of venous symptoms, CEAP staging, or general QoL between the groups.

Objectives: This systematic review assessed the efficacy of centralisation for the treatment of unruptured and ruptured abdominal aortic aneurysms. Patient outcomes achieved by low and high volume hospitals/ surgeons, including morbidity, mortality and length of hospital stay, were used as proxy measures of efficacy.Design: Systematic review was designed to identify, assess and report on peer-reviewed articles reporting outcomes from unruptured and ruptured abdominal aortic aneurysms. No language restriction was placed on the databases searched.Materials: Only peer-reviewed journals articles were included. Methods: To ensure the contemporary nature of this review, only studies published between January 1997 and June 2007 were sought. Studies were included if they reported on at least one volume type and patient outcome.Results: Twenty two studies were included in this review. In the majority of group assessments, the number of studies reporting statistical significance was similar to the number of studies reporting no statistical significance.Conclusion: The paucity of studies reporting statistically significant results demonstrates that although this evidence exists, its potential to be overstated must also be taken into account when drawing conclusions as to its efficacy for twenty first century healthcare systems.

Both SFL/S and EVLA, using local tumescent anaesthesia, were well tolerated, with no difference in short-term recurrence rate. In the second week after EVLA, patients experienced significantly more pain resulting in restricted mobility, self care and daily activity compared to SFL/S.

These studies give us insight in the pathology but do not lead to the specific genetic factor(s) responsible for (familial) AAA. Considering the supposed autosomal dominant inheritance, a gene mutation in one of the structural proteins of the connective tissue is expected. In the future, linkage analysis may resolve the genetic background of AAA.

Our results identified a candidate locus in three Dutch families with AAA at chromosome 19q13.3. Separate analysis of these three families provides evidence for genetic heterogeneity.