Abstract
Abdominal Aortic Aneurysm (AAA) disease is a growing healthcare burden. Besides theassociated cardiovascular comorbidities, the AAA itself poses a risk for the patient in two fashions. First, it could rupture, which is associated with high mortality and morbidity. This thesis focused on the second, more indirect, hazard the patient with
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an AAA is exposed to: the operative risk. Our aim was to improve patient outcome by seeking discrepancies in AAA expressions and repair. Variance and variants in AAA Screening for patients at risk for adverse events due to aneurysmal disease is currently based on traditional risk factors, which does not allow individual risk stratification. The instability of the vessel wall was previously shown to be a part a systemic process, and we show that local proteins predict postoperative cardiovascular adverse events. Currently no differences among AAAs have been established. In this thesis we demonstrate that half of the AAA had only very low amounts of wall inflammation, more pronounced intimal atherosclerosis, more atherosclerotic risk factors and more postoperative events, when compared to the AAA with moderate to severe inflammation. The low-inflammatory AAAs appeared more closely related to atherosclerosis, and might need a different therapeutic approach. Furthermore, we report that there is a regional variance in wall composition inside the AAA. Inflammation and proteases were more pronounced at the lateral sides of the AAA, suggesting decreased local wall strength. This location coincides with the most frequent site of rupture, and merits a prominent focus of (medication-related) research on the lateral wall. Improving outcome after repair Endovascular aneurysm repair (EVAR) comprises the majority of AAA repairs, and various access types exist, which influence outcome. We compared percutaneous access (pEVAR) and femoral cutdown access (cEVAR) both in a tertiary university center and in a more national database, both in the USA. We found that in our hospital pEVAR is associated with an improved (local) outcome and lower operative time and lower hospital stay. However, these results could not be generalized to a national level as this mixture of centers demonstrated only minimal or absent advantages of pEVAR versus cEVAR. When zooming in on physician specialty and experience in a national database in the USA, we noted that vascular surgeons repaired an increasing proportion of AAA overall from 2001 to 2009. Mortality was higher with lower surgeon volumes, especially for open repair. Medium and high volumes decreased over time, suggesting that it will be increasingly hard to deliver good quality treatment. For EVAR, more physicians had medium or large volumes, thereby significantly improving outcome. Current and future advances in knowledge should lead to an individual approach with a tailored cut off for intervention and management of co-existing diseases. Ultimately, if AAAs are better understood, patients who need treatment because of a higher rupture risk can be identified better. Also, the AAA repair of patients who are at high-risk for postoperative mortality and morbidity should be postponed as long as possible to delay the burden of repair, ideally to be repaired just before AAA rupture.
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